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ulceration, skin, patients, rheumatoid arthritis, disease, mortality, pathogenesis, ulceration, causes, development, immune complex, vasculitis, treatment, drugs, side effects, treatment, venous insufficiency, ulceration, autoimmune disease, immunosuppressive drugs, plasmapheresis, Adjuvant, treatment, pain, analgesics, blood, perfusion, drugs, therapy, ulcers, inflammatory reaction, surgical, patients, muscle, flaps, skin grafts, ulceration, rheumatoid arthritis, treatment, rheumatoid arthritis, immunotherapy, monoclonal antibodies | DerHautarzt.50460406.eng.abstr_task2 | Sentence: The appearance of severe ulceration of the skin in patients with rheumatoid arthritis is often associated with a tendency to progression of the underlying disease , involvement of internal organs and increased mortality . In the pathogenesis of such ulceration there are multiple causes for their development , persistence and tendency to poor healing . They include localized or generalized immune complex vasculitis , treatment with anti-inflammatory drugs and their side effects following the treatment , arterial and venous insufficiency , and mechanical factors . The management of severe ulceration requires stabilization of the underlying autoimmune disease , e.g. with high doses of glucocorticosteroids or other immunosuppressive drugs or plasmapheresis . Adjuvant treatment of pain with analgesics , improvement of blood perfusion and anti-inflammatory drugs should accompany the topical therapy of ulcers . After suppression of the local inflammatory reaction surgical intervention becomes necessary in most of the patients , and vascularized muscle flaps should be used in preference to meshgrafts or split skin grafts for extensive ulceration in rheumatoid arthritis . A hopeful perspective in the treatment of severe rheumatoid arthritis might be opened up with immunotherapy using monoclonal antibodies .
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IL6 is a Protein, GMCSF is a Protein, IL6 is a Protein, Sharpin is a Protein | 182_task0 | Sentence: Defective production of pro-inflammatory mediators from stimulated cpdm BMDC.
(A-D) Cultured WT and cpdm BMDC (1x105 cells in 0.1 ml complete medium) were washed and stimulated with medium, 100 ng/ml LPS or 25 microg/ml poly I:C for 24 hours. Supernatants were collected for ELISA of IL12P70, IL6, and GMCSF, and for quantification of nitric oxide (NO). (E-F) Gradient numbers (1x104, 2x104, and 4x104 cells in 0.1 mL complete medium) of BMDC were used for100 ng/mL LPS stimulation. After 24 hours, the amounts of IL12P70 and IL6 from the supernatant were measured. (G) The cpdm mice rescued by Sharpin-containing BAC had complete remission of the inflammatory phenotype [2]. BMDC developed from cpdm and rescued cpdm mice were plated (1x106 cells in 0.3 mL) and stimulated with 100 ng/mL LPS. After 24 hours, supernatants were collected for analysis of IL12P70 production. Data are representative of three independent experiments. * P<0.01; ** P<0.005.
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IL6 is a Protein, GMCSF is a Protein, IL6 is a Protein, Sharpin is a Protein | 182_task1 | Sentence: Defective production of pro-inflammatory mediators from stimulated cpdm BMDC.
(A-D) Cultured WT and cpdm BMDC (1x105 cells in 0.1 ml complete medium) were washed and stimulated with medium, 100 ng/ml LPS or 25 microg/ml poly I:C for 24 hours. Supernatants were collected for ELISA of IL12P70, IL6, and GMCSF, and for quantification of nitric oxide (NO). (E-F) Gradient numbers (1x104, 2x104, and 4x104 cells in 0.1 mL complete medium) of BMDC were used for100 ng/mL LPS stimulation. After 24 hours, the amounts of IL12P70 and IL6 from the supernatant were measured. (G) The cpdm mice rescued by Sharpin-containing BAC had complete remission of the inflammatory phenotype [2]. BMDC developed from cpdm and rescued cpdm mice were plated (1x106 cells in 0.3 mL) and stimulated with 100 ng/mL LPS. After 24 hours, supernatants were collected for analysis of IL12P70 production. Data are representative of three independent experiments. * P<0.01; ** P<0.005.
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Apigenin is a CHEMICAL, c - Myc is a GENE-Y | 23376608_task1 | Sentence: Apigenin induces c-Myc-mediated apoptosis in FRO anaplastic thyroid carcinoma cells.
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Pterostilbene is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, Pterostilbene is a CHEMICAL, PTE is a CHEMICAL, resveratrol is a CHEMICAL, PTE is a CHEMICAL, PTE is a CHEMICAL, Janus kinase 2 is a GENE-Y, Signal Transducer and Activator of Transcription 3 is a GENE-Y, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL, PTE is a CHEMICAL, PTE is a CHEMICAL, oxygen is a CHEMICAL, PTE is a CHEMICAL, JAK2 is a GENE-Y, Tyr is a CHEMICAL, STAT3 is a GENE-Y, PTE is a CHEMICAL, STAT3 is a GENE-Y, Bcl - xL is a GENE-Y, Mcl-1 is a GENE-Y, Bax is a GENE-Y, Bak is a GENE-Y, Cytochrome c is a GENE-Y, Caspase3 is a GENE-Y, cyclin - dependent kinase is a GENE-N, p21 is a GENE-Y, p27 is a GENE-Y, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, AG490 is a CHEMICAL, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL | 32868_task0 | Sentence: Pterostilbene exerts antitumor activity against human osteosarcoma cells by inhibiting the JAK2/STAT3 signaling pathway.
Osteosarcoma is a high-grade malignant bone tumor. Pterostilbene (PTE) is a natural, dimethylated analog of resveratrol with higher bioavailability. While PTE has been shown to have potent antitumor activity against various types of cancer, the molecular mechanisms underlying the effects of PTE remain largely unknown. The Janus kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway plays a crucial role in tumorigenesis and immune development. In this study, we assessed the antitumor activity of PTE against human osteosarcoma cells and explored the role of JAK2/STAT3 and apoptosis-related signaling pathways on the activity of PTE. PTE treatment resulted in a dose- and time-dependent inhibition of osteosarcoma cell viability. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration and mitochondrial membrane potential (MMP) but also by increases in the apoptotic index, reactive oxygen species (ROS) and several biochemical parameters. Furthermore, PTE treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of STAT3. PTE also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27. PTE, used in combination with a known JAK2/STAT3 inhibitor, AG490, further decreased the viability of osteosarcoma cells. Taken together, PTE is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/STAT3 signaling pathway. These data suggest that inhibition of JAK2/STAT3 signaling is a novel mechanism of action for PTE during therapeutic intervention in osteosarcoma cancers.
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Pterostilbene is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, Pterostilbene is a CHEMICAL, PTE is a CHEMICAL, resveratrol is a CHEMICAL, PTE is a CHEMICAL, PTE is a CHEMICAL, Janus kinase 2 is a GENE-Y, Signal Transducer and Activator of Transcription 3 is a GENE-Y, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL, PTE is a CHEMICAL, PTE is a CHEMICAL, oxygen is a CHEMICAL, PTE is a CHEMICAL, JAK2 is a GENE-Y, Tyr is a CHEMICAL, STAT3 is a GENE-Y, PTE is a CHEMICAL, STAT3 is a GENE-Y, Bcl - xL is a GENE-Y, Mcl-1 is a GENE-Y, Bax is a GENE-Y, Bak is a GENE-Y, Cytochrome c is a GENE-Y, Caspase3 is a GENE-Y, cyclin - dependent kinase is a GENE-N, p21 is a GENE-Y, p27 is a GENE-Y, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, AG490 is a CHEMICAL, PTE is a CHEMICAL, JAK2 is a GENE-Y, STAT3 is a GENE-Y, JAK2 is a GENE-Y, STAT3 is a GENE-Y, PTE is a CHEMICAL | 32868_task1 | Sentence: Pterostilbene exerts antitumor activity against human osteosarcoma cells by inhibiting the JAK2/STAT3 signaling pathway.
Osteosarcoma is a high-grade malignant bone tumor. Pterostilbene (PTE) is a natural, dimethylated analog of resveratrol with higher bioavailability. While PTE has been shown to have potent antitumor activity against various types of cancer, the molecular mechanisms underlying the effects of PTE remain largely unknown. The Janus kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway plays a crucial role in tumorigenesis and immune development. In this study, we assessed the antitumor activity of PTE against human osteosarcoma cells and explored the role of JAK2/STAT3 and apoptosis-related signaling pathways on the activity of PTE. PTE treatment resulted in a dose- and time-dependent inhibition of osteosarcoma cell viability. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration and mitochondrial membrane potential (MMP) but also by increases in the apoptotic index, reactive oxygen species (ROS) and several biochemical parameters. Furthermore, PTE treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of STAT3. PTE also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27. PTE, used in combination with a known JAK2/STAT3 inhibitor, AG490, further decreased the viability of osteosarcoma cells. Taken together, PTE is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/STAT3 signaling pathway. These data suggest that inhibition of JAK2/STAT3 signaling is a novel mechanism of action for PTE during therapeutic intervention in osteosarcoma cancers.
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Osteosarcoma is a high-grade malignant bone tumor. Pterostilbene (PTE) is a natural, dimethylated analog of resveratrol with higher bioavailability. While PTE has been shown to have potent antitumor activity against various types of cancer, the molecular mechanisms underlying the effects of PTE remain largely unknown. The Janus kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway plays a crucial role in tumorigenesis and immune development. In this study, we assessed the antitumor activity of PTE against human osteosarcoma cells and explored the role of JAK2/STAT3 and apoptosis-related signaling pathways on the activity of PTE. PTE treatment resulted in a dose- and time-dependent inhibition of osteosarcoma cell viability. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration and mitochondrial membrane potential (MMP) but also by increases in the apoptotic index, reactive oxygen species (ROS) and several biochemical parameters. Furthermore, PTE treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of STAT3. PTE also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27. PTE, used in combination with a known JAK2/STAT3 inhibitor, AG490, further decreased the viability of osteosarcoma cells. Taken together, PTE is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/STAT3 signaling pathway. These data suggest that inhibition of JAK2/STAT3 signaling is a novel mechanism of action for PTE during therapeutic intervention in osteosarcoma cancers. | [
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Pterostilbene, JAK2, STAT3, Pterostilbene, PTE, resveratrol, PTE, PTE, Janus kinase 2, Signal Transducer and Activator of Transcription 3, JAK2, STAT3, PTE, JAK2, STAT3, PTE, PTE, PTE, oxygen, PTE, JAK2, Tyr, STAT3, PTE, STAT3, Bcl - xL, Mcl-1, Bax, Bak, Cytochrome c, Caspase3, cyclin - dependent kinase, p21, p27, PTE, JAK2, STAT3, AG490, PTE, JAK2, STAT3, JAK2, STAT3, PTE | 32868_task2 | Sentence: Pterostilbene exerts antitumor activity against human osteosarcoma cells by inhibiting the JAK2/STAT3 signaling pathway.
Osteosarcoma is a high-grade malignant bone tumor. Pterostilbene (PTE) is a natural, dimethylated analog of resveratrol with higher bioavailability. While PTE has been shown to have potent antitumor activity against various types of cancer, the molecular mechanisms underlying the effects of PTE remain largely unknown. The Janus kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway plays a crucial role in tumorigenesis and immune development. In this study, we assessed the antitumor activity of PTE against human osteosarcoma cells and explored the role of JAK2/STAT3 and apoptosis-related signaling pathways on the activity of PTE. PTE treatment resulted in a dose- and time-dependent inhibition of osteosarcoma cell viability. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration and mitochondrial membrane potential (MMP) but also by increases in the apoptotic index, reactive oxygen species (ROS) and several biochemical parameters. Furthermore, PTE treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of STAT3. PTE also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27. PTE, used in combination with a known JAK2/STAT3 inhibitor, AG490, further decreased the viability of osteosarcoma cells. Taken together, PTE is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/STAT3 signaling pathway. These data suggest that inhibition of JAK2/STAT3 signaling is a novel mechanism of action for PTE during therapeutic intervention in osteosarcoma cancers.
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Osteosarcoma is a high-grade malignant bone tumor. Pterostilbene (PTE) is a natural, dimethylated analog of resveratrol with higher bioavailability. While PTE has been shown to have potent antitumor activity against various types of cancer, the molecular mechanisms underlying the effects of PTE remain largely unknown. The Janus kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway plays a crucial role in tumorigenesis and immune development. In this study, we assessed the antitumor activity of PTE against human osteosarcoma cells and explored the role of JAK2/STAT3 and apoptosis-related signaling pathways on the activity of PTE. PTE treatment resulted in a dose- and time-dependent inhibition of osteosarcoma cell viability. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration and mitochondrial membrane potential (MMP) but also by increases in the apoptotic index, reactive oxygen species (ROS) and several biochemical parameters. Furthermore, PTE treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of STAT3. PTE also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27. PTE, used in combination with a known JAK2/STAT3 inhibitor, AG490, further decreased the viability of osteosarcoma cells. Taken together, PTE is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/STAT3 signaling pathway. These data suggest that inhibition of JAK2/STAT3 signaling is a novel mechanism of action for PTE during therapeutic intervention in osteosarcoma cancers. | [
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publication is an umlsterm, research is an umlsterm, controlled clinical trials is an umlsterm, standards is an umlsterm, research is an umlsterm, clinical studies is an umlsterm | MedizinischeKlinik.00950171.eng.abstr_task0 | Sentence: The publication of the CONSORT Statement was aimed at the improvement of the quality of research reports of randomized controlled clinical trials . It contains the most important standards of high quality research . Although originally meant for randomized studies only most aspects of this statement can be applied to other kinds of clinical studies .
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physiotherapy service is an intervention, rate of hospital admission , rate of re - presentation to the ED , use of community healthcare resources is an outcome, rate of return to usual work / home / leisure activities or patient satisfaction is an outcome | 1475_task0 | Sentence: A physiotherapy service for EECU patients , as provided in this study , did not reduce the rate of hospital admission , rate of re-presentation to the ED , use of community healthcare resources , or improve the rate of return to usual work/home/leisure activities or patient satisfaction .
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HSV-2 is an umlsterm, Virustyp is an umlsterm, Praevalenz is an umlsterm, Antikoerpern is an umlsterm, Bevoelkerung is an umlsterm, anonym is an umlsterm, Blutspendern is an umlsterm, Klinikpatienten is an umlsterm, Patienten is an umlsterm, Risikofaktoren is an umlsterm, sexuell uebertragbare Krankheiten is an umlsterm, Infektionskrankheiten is an umlsterm, Therapie is an umlsterm, Glykoproteinen is an umlsterm, Glykoproteinen is an umlsterm | Bundesgesundheitsblatt.90420776.ger.abstr_task0 | Sentence: Herpes-simplex-Viren ( HSV-1, HSV-2) sind die haeufigste infektioese Ursache von genitalen Ulzerationen . Trotz einer Zunahme primaerer genitaler HSV-1-Infektionen ist HSV-2 der dominante Virustyp bei rezidivierenden Erkrankungen . Rueckschluesse auf die Haeufigkeit des genitalen Herpes koennen daher aus der Praevalenz von HSV-2-spezifischen Antikoerpern in der Bevoelkerung gezogen werden . Diese Studie wurde an einem Panel von Serumproben durchgefuehrt , das 1996 und 1997 anonym von 1979 Blutspendern und 3079 Klinikpatienten gesammelt worden war . Die Patienten hatten keine bekannten Risikofaktoren bezueglich HSV-Infektionen wie sexuell uebertragbare Krankheiten , andere Infektionskrankheiten oder eine immunsuppressive Therapie . Die Serumproben wurden mit typenspezifischen ELISA-Testen , die auf den gereinigten nativen Glykoproteinen gG1 bzw. gG2 basieren sowie einem Immunoblot mit typenspezifischen rekombinanten Glykoproteinen untersucht . Die Abklaerung fraglicher Reaktionsausfaelle erfolgte mit einem In-Haus-Westernblot .
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HSV-2 is an umlsterm, Virustyp is an umlsterm, Praevalenz is an umlsterm, Antikoerpern is an umlsterm, Bevoelkerung is an umlsterm, anonym is an umlsterm, Blutspendern is an umlsterm, Klinikpatienten is an umlsterm, Patienten is an umlsterm, Risikofaktoren is an umlsterm, sexuell uebertragbare Krankheiten is an umlsterm, Infektionskrankheiten is an umlsterm, Therapie is an umlsterm, Glykoproteinen is an umlsterm, Glykoproteinen is an umlsterm | Bundesgesundheitsblatt.90420776.ger.abstr_task1 | Sentence: Herpes-simplex-Viren ( HSV-1, HSV-2) sind die haeufigste infektioese Ursache von genitalen Ulzerationen . Trotz einer Zunahme primaerer genitaler HSV-1-Infektionen ist HSV-2 der dominante Virustyp bei rezidivierenden Erkrankungen . Rueckschluesse auf die Haeufigkeit des genitalen Herpes koennen daher aus der Praevalenz von HSV-2-spezifischen Antikoerpern in der Bevoelkerung gezogen werden . Diese Studie wurde an einem Panel von Serumproben durchgefuehrt , das 1996 und 1997 anonym von 1979 Blutspendern und 3079 Klinikpatienten gesammelt worden war . Die Patienten hatten keine bekannten Risikofaktoren bezueglich HSV-Infektionen wie sexuell uebertragbare Krankheiten , andere Infektionskrankheiten oder eine immunsuppressive Therapie . Die Serumproben wurden mit typenspezifischen ELISA-Testen , die auf den gereinigten nativen Glykoproteinen gG1 bzw. gG2 basieren sowie einem Immunoblot mit typenspezifischen rekombinanten Glykoproteinen untersucht . Die Abklaerung fraglicher Reaktionsausfaelle erfolgte mit einem In-Haus-Westernblot .
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HSV-2, Virustyp, Praevalenz, Antikoerpern, Bevoelkerung, anonym, Blutspendern, Klinikpatienten, Patienten, Risikofaktoren, sexuell uebertragbare Krankheiten, Infektionskrankheiten, Therapie, Glykoproteinen, Glykoproteinen | Bundesgesundheitsblatt.90420776.ger.abstr_task2 | Sentence: Herpes-simplex-Viren ( HSV-1, HSV-2) sind die haeufigste infektioese Ursache von genitalen Ulzerationen . Trotz einer Zunahme primaerer genitaler HSV-1-Infektionen ist HSV-2 der dominante Virustyp bei rezidivierenden Erkrankungen . Rueckschluesse auf die Haeufigkeit des genitalen Herpes koennen daher aus der Praevalenz von HSV-2-spezifischen Antikoerpern in der Bevoelkerung gezogen werden . Diese Studie wurde an einem Panel von Serumproben durchgefuehrt , das 1996 und 1997 anonym von 1979 Blutspendern und 3079 Klinikpatienten gesammelt worden war . Die Patienten hatten keine bekannten Risikofaktoren bezueglich HSV-Infektionen wie sexuell uebertragbare Krankheiten , andere Infektionskrankheiten oder eine immunsuppressive Therapie . Die Serumproben wurden mit typenspezifischen ELISA-Testen , die auf den gereinigten nativen Glykoproteinen gG1 bzw. gG2 basieren sowie einem Immunoblot mit typenspezifischen rekombinanten Glykoproteinen untersucht . Die Abklaerung fraglicher Reaktionsausfaelle erfolgte mit einem In-Haus-Westernblot .
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aspartate aminotransferase is a GENE-Y, kynurenate is a CHEMICAL | 17442055_task0 | Sentence: Mitochondrial aspartate aminotransferase: a third kynurenate-producing enzyme in the mammalian brain.
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aspartate aminotransferase is a GENE-Y, kynurenate is a CHEMICAL | 17442055_task1 | Sentence: Mitochondrial aspartate aminotransferase: a third kynurenate-producing enzyme in the mammalian brain.
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PILOT is a Protein, IL-2 is a Protein, IL-8 family is a Entity, interferon - gamma is a Protein, genes is a Entity, PILOT is a Protein, PILOT is a Protein, PILOT is a Protein, zinc fingers is a Entity, C2H2-type is a Entity, carboxyl - terminus is a Entity, zinc finger regions is a Entity, EGR1 is a Protein, EGR2 is a Protein, pAT 133 is a Protein, PILOT is a Protein, Ca2 + signal - dependent regulatory element is a Entity, genes is a Entity | 417_task0 | Sentence: Expression of PILOT, a putative transcription factor, requires two signals and is cyclosporin A sensitive in T cells.
Few known genes (IL-2, members of the IL-8 family, interferon-gamma) are induced in T cells only through the combined effect of phorbol myristic acetate (PMA) and a Ca(2+)-ionophore, and expression of only these genes can be fully suppressed by Cyclosporin A (CyA). We have identified a putative transcription factor, designated PILOT, with an identical dual signal requirement for expression. Induction of the PILOT gene is detectable in human T cells 20 min following activation in the presence of cycloheximide and is fully suppressed by CyA. The PILOT protein has a calculated M(r) of 42.6 kDa and contains three zinc fingers of the C2H2-type at the carboxyl-terminus which are highly homologous to the zinc finger regions of the transcription factors EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT gene expression requires only one signal (PMA) and is not affected by CyA. This observation directly demonstrates the existence of a Ca2+ signal-dependent regulatory element obligatory for expression of some genes in T cells but not in fibroblasts. This differential expression model will be valuable in the dissection of the dual signal pathway in T cells and the effects of CyA upon it.
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PILOT is a Protein, IL-2 is a Protein, IL-8 family is a Entity, interferon - gamma is a Protein, genes is a Entity, PILOT is a Protein, PILOT is a Protein, PILOT is a Protein, zinc fingers is a Entity, C2H2-type is a Entity, carboxyl - terminus is a Entity, zinc finger regions is a Entity, EGR1 is a Protein, EGR2 is a Protein, pAT 133 is a Protein, PILOT is a Protein, Ca2 + signal - dependent regulatory element is a Entity, genes is a Entity | 417_task1 | Sentence: Expression of PILOT, a putative transcription factor, requires two signals and is cyclosporin A sensitive in T cells.
Few known genes (IL-2, members of the IL-8 family, interferon-gamma) are induced in T cells only through the combined effect of phorbol myristic acetate (PMA) and a Ca(2+)-ionophore, and expression of only these genes can be fully suppressed by Cyclosporin A (CyA). We have identified a putative transcription factor, designated PILOT, with an identical dual signal requirement for expression. Induction of the PILOT gene is detectable in human T cells 20 min following activation in the presence of cycloheximide and is fully suppressed by CyA. The PILOT protein has a calculated M(r) of 42.6 kDa and contains three zinc fingers of the C2H2-type at the carboxyl-terminus which are highly homologous to the zinc finger regions of the transcription factors EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT gene expression requires only one signal (PMA) and is not affected by CyA. This observation directly demonstrates the existence of a Ca2+ signal-dependent regulatory element obligatory for expression of some genes in T cells but not in fibroblasts. This differential expression model will be valuable in the dissection of the dual signal pathway in T cells and the effects of CyA upon it.
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Few known genes (IL-2, members of the IL-8 family, interferon-gamma) are induced in T cells only through the combined effect of phorbol myristic acetate (PMA) and a Ca(2+)-ionophore, and expression of only these genes can be fully suppressed by Cyclosporin A (CyA). We have identified a putative transcription factor, designated PILOT, with an identical dual signal requirement for expression. Induction of the PILOT gene is detectable in human T cells 20 min following activation in the presence of cycloheximide and is fully suppressed by CyA. The PILOT protein has a calculated M(r) of 42.6 kDa and contains three zinc fingers of the C2H2-type at the carboxyl-terminus which are highly homologous to the zinc finger regions of the transcription factors EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT gene expression requires only one signal (PMA) and is not affected by CyA. This observation directly demonstrates the existence of a Ca2+ signal-dependent regulatory element obligatory for expression of some genes in T cells but not in fibroblasts. This differential expression model will be valuable in the dissection of the dual signal pathway in T cells and the effects of CyA upon it.
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] | Expression of PILOT, a putative transcription factor, requires two signals and is cyclosporin A sensitive in T cells.
Few known genes (IL-2, members of the IL-8 family, interferon-gamma) are induced in T cells only through the combined effect of phorbol myristic acetate (PMA) and a Ca(2+)-ionophore, and expression of only these genes can be fully suppressed by Cyclosporin A (CyA). We have identified a putative transcription factor, designated PILOT, with an identical dual signal requirement for expression. Induction of the PILOT gene is detectable in human T cells 20 min following activation in the presence of cycloheximide and is fully suppressed by CyA. The PILOT protein has a calculated M(r) of 42.6 kDa and contains three zinc fingers of the C2H2-type at the carboxyl-terminus which are highly homologous to the zinc finger regions of the transcription factors EGR1, EGR2, and pAT 133. In contrast to T cells, in fibroblasts PILOT gene expression requires only one signal (PMA) and is not affected by CyA. This observation directly demonstrates the existence of a Ca2+ signal-dependent regulatory element obligatory for expression of some genes in T cells but not in fibroblasts. This differential expression model will be valuable in the dissection of the dual signal pathway in T cells and the effects of CyA upon it.
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Spermine is a DRUG, Spermine is a DRUG, spermidine is a DRUG_N, putrescine is a DRUG_N, Spermine is a DRUG, spermidine is a DRUG_N | 2981704_task0 | Sentence: Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: DRUG_N, DRUG
| [
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] | Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids. | [
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"DRUG_N",
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Spermine is a DRUG, Spermine is a DRUG, spermidine is a DRUG_N, putrescine is a DRUG_N, Spermine is a DRUG, spermidine is a DRUG_N | 2981704_task1 | Sentence: Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids.
Instructions: please typing these entity words according to sentence: Spermine, Spermine, spermidine, putrescine, Spermine, spermidine
Options: DRUG_N, DRUG
| [
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] | Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids. | [
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Spermine, Spermine, spermidine, putrescine, Spermine, spermidine | 2981704_task2 | Sentence: Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids.
Instructions: please extract entity words from the input sentence
| [
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] | Spermine promotes the translocation of phosphatidate phosphohydrolase from the cytosol to the microsomal fraction of rat liver and it enhances the effects of oleate in this respect. Spermine (0.5-2 mM) promoted the translocation of phosphatidate phosphohydrolase from the soluble to the microsomal fraction in a cell-free system derived from rat liver. By contrast, spermidine (1 mM) and putrescine (1 mM) had no significant effect on the translocation when added alone. Spermine, and to a lesser extent, spermidine, enhanced the translocating action of oleate and increased its effectiveness in transferring the phosphohydrolase from the soluble to the microsomal fraction. It is proposed that the phosphohydrolase becomes metabolically active when it combines with membranes and that polyamines might help to regulate this interaction. This could facilitate the action of fatty acids and enable cells to increase their capacity for triacylglycerol synthesis to match an increased availability of fatty acids. | [
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Bronchial matrix and inflammation is a Outcome_Physical, inhaled steroids is a Intervention_Pharmacological, asthma is a Participant_Condition, Inflammatory and structural changes of the airway mucosa is a Outcome_Physical, patients with mild asthma is a Participant_Condition, low - dose allergen is a Intervention_Pharmacological, concomitant inhaled steroid is a Intervention_Pharmacological, placebo treatment is a Intervention_Control, bronchial epithelial macrophages is a Outcome_Physical, numbers of mucosal eosinophils , neutrophils and T lymphocytes is a Outcome_Physical, density of the proteoglycans ( PGS ) biglycan and decorin is a Outcome_Physical, Steroid is a Intervention_Pharmacological, mean density of the PGS biglycan and versican is a Outcome_Physical, mucosal inflammatory cells is a Outcome_Physical, steroid - induced changes is a Outcome_Other, patients with asthma . is a Participant_Condition | 24270_task0 | Sentence: Bronchial matrix and inflammation respond to inhaled steroids despite ongoing allergen exposure in asthma . BACKGROUND Inflammatory and structural changes of the airway mucosa are chronic features of asthma . The mechanisms underlying these changes and their modulation by steroid prophylaxis have not been clarified . OBJECTIVE We postulated that asymptomatic ongoing allergen exposure could drive airway inflammation as well as changes in the extracellular matrix ( ECM ) , and that inhaled steroids could prevent this . METHODS Therefore , we exposed patients with mild asthma to 2 weeks of repeated low-dose allergen , with concomitant inhaled steroid or placebo treatment . Bronchial biopsies , which were taken before and after this exposure , were stained and digitally analysed . The ECM proteins in asthmatics were also compared with a normal control group . RESULTS Low-dose allergen exposure alone resulted in a significant increase of bronchial epithelial macrophages . Despite ongoing allergen exposure , inhaled steroids reduced the numbers of mucosal eosinophils , neutrophils and T lymphocytes . At baseline , the mean density of the proteoglycans ( PGS ) biglycan and decorin were , respectively , higher and lower in the bronchial mucosa of asthmatics as compared with normal controls . Steroid treatment , during allergen exposure , increased the mean density of the PGS biglycan and versican . CONCLUSION We conclude that chronic allergen exposure induces inflammatory changes in the bronchial mucosa . Despite ongoing allergen exposure , steroid treatment decreases mucosal inflammatory cells while altering PG density . The latter observation highlights the need to examine steroid-induced changes closely in the airway structure in patients with asthma .
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Bronchial matrix and inflammation is a Outcome_Physical, inhaled steroids is a Intervention_Pharmacological, asthma is a Participant_Condition, Inflammatory and structural changes of the airway mucosa is a Outcome_Physical, patients with mild asthma is a Participant_Condition, low - dose allergen is a Intervention_Pharmacological, concomitant inhaled steroid is a Intervention_Pharmacological, placebo treatment is a Intervention_Control, bronchial epithelial macrophages is a Outcome_Physical, numbers of mucosal eosinophils , neutrophils and T lymphocytes is a Outcome_Physical, density of the proteoglycans ( PGS ) biglycan and decorin is a Outcome_Physical, Steroid is a Intervention_Pharmacological, mean density of the PGS biglycan and versican is a Outcome_Physical, mucosal inflammatory cells is a Outcome_Physical, steroid - induced changes is a Outcome_Other, patients with asthma . is a Participant_Condition | 24270_task1 | Sentence: Bronchial matrix and inflammation respond to inhaled steroids despite ongoing allergen exposure in asthma . BACKGROUND Inflammatory and structural changes of the airway mucosa are chronic features of asthma . The mechanisms underlying these changes and their modulation by steroid prophylaxis have not been clarified . OBJECTIVE We postulated that asymptomatic ongoing allergen exposure could drive airway inflammation as well as changes in the extracellular matrix ( ECM ) , and that inhaled steroids could prevent this . METHODS Therefore , we exposed patients with mild asthma to 2 weeks of repeated low-dose allergen , with concomitant inhaled steroid or placebo treatment . Bronchial biopsies , which were taken before and after this exposure , were stained and digitally analysed . The ECM proteins in asthmatics were also compared with a normal control group . RESULTS Low-dose allergen exposure alone resulted in a significant increase of bronchial epithelial macrophages . Despite ongoing allergen exposure , inhaled steroids reduced the numbers of mucosal eosinophils , neutrophils and T lymphocytes . At baseline , the mean density of the proteoglycans ( PGS ) biglycan and decorin were , respectively , higher and lower in the bronchial mucosa of asthmatics as compared with normal controls . Steroid treatment , during allergen exposure , increased the mean density of the PGS biglycan and versican . CONCLUSION We conclude that chronic allergen exposure induces inflammatory changes in the bronchial mucosa . Despite ongoing allergen exposure , steroid treatment decreases mucosal inflammatory cells while altering PG density . The latter observation highlights the need to examine steroid-induced changes closely in the airway structure in patients with asthma .
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Abstract is an umlsterm, metastasis is an umlsterm, chondrosarcoma is an umlsterm, metastasis is an umlsterm, neoplasm is an umlsterm, metastases is an umlsterm, literature is an umlsterm, prognosis is an umlsterm | DerHautarzt.40450722.eng.abstr_task0 | Sentence: Abstract . We report on a rare case of a solitary subcutaneous metastasis from a chondrosarcoma . The metastasis occurred 7 years after excision of the primary neoplasm . Further investigations revealed no evidence of other metastases . Nevertheless , according to data in the literature , the prognosis has to be considered very poor .
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Abstract, metastasis, chondrosarcoma, metastasis, neoplasm, metastases, literature, prognosis | DerHautarzt.40450722.eng.abstr_task2 | Sentence: Abstract . We report on a rare case of a solitary subcutaneous metastasis from a chondrosarcoma . The metastasis occurred 7 years after excision of the primary neoplasm . Further investigations revealed no evidence of other metastases . Nevertheless , according to data in the literature , the prognosis has to be considered very poor .
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tumor necrosis factor - alpha is a Protein, interleukin 1-beta is a Protein, granulocyte - macrophage colony - stimulating factor is a Protein, interleukin-6 is a Protein, nitric oxide synthase is a Protein | 686_task0 | Sentence: Suppression by azelastine hydrochloride of NF-kappa B activation involved in generation of cytokines and nitric oxide.
The influence of the anti-allergy agent azelastine hydrochloride (Azeptin) on NF-kappa B activation associated with the generation of cytokines and nitric oxide (NO) was investigated in various kinds of human and mouse cells. Azeptin dose-dependently suppressed both DNA and protein synthesis in human gingival fibroblasts (HF) and also suppressed blastogenesis of human peripheral blood lymphocytes (PBL). Generation of tumor necrosis factor-alpha, interleukin 1-beta, granulocyte-macrophage colony-stimulating factor and interleukin-6 from 10(-5) M Azeptin-treated PBL and human monocytes (HM) was decreased to approximately 1/3 to 2/3 of the control levels. In parallel with the decreased cytokine generation, each cytokine mRNA was less expressed in the presence of 10(-5) M Azeptin. In addition, both inducible nitric oxide synthase-mRNA level and NO generation in mouse peritoneal macrophages were suppressed by 10(-5) M Azeptin. Being compatible with those results, Azeptin (10(-5) M) suppressed activation of NF-kappa B in PBL, HM and HF. These results appear to indicate that suppression of cytokine and NO generation by Azeptin results at least partially from the inhibition of NF-kappa B activation.
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tumor necrosis factor - alpha is a Protein, interleukin 1-beta is a Protein, granulocyte - macrophage colony - stimulating factor is a Protein, interleukin-6 is a Protein, nitric oxide synthase is a Protein | 686_task1 | Sentence: Suppression by azelastine hydrochloride of NF-kappa B activation involved in generation of cytokines and nitric oxide.
The influence of the anti-allergy agent azelastine hydrochloride (Azeptin) on NF-kappa B activation associated with the generation of cytokines and nitric oxide (NO) was investigated in various kinds of human and mouse cells. Azeptin dose-dependently suppressed both DNA and protein synthesis in human gingival fibroblasts (HF) and also suppressed blastogenesis of human peripheral blood lymphocytes (PBL). Generation of tumor necrosis factor-alpha, interleukin 1-beta, granulocyte-macrophage colony-stimulating factor and interleukin-6 from 10(-5) M Azeptin-treated PBL and human monocytes (HM) was decreased to approximately 1/3 to 2/3 of the control levels. In parallel with the decreased cytokine generation, each cytokine mRNA was less expressed in the presence of 10(-5) M Azeptin. In addition, both inducible nitric oxide synthase-mRNA level and NO generation in mouse peritoneal macrophages were suppressed by 10(-5) M Azeptin. Being compatible with those results, Azeptin (10(-5) M) suppressed activation of NF-kappa B in PBL, HM and HF. These results appear to indicate that suppression of cytokine and NO generation by Azeptin results at least partially from the inhibition of NF-kappa B activation.
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tumor necrosis factor - alpha, interleukin 1-beta, granulocyte - macrophage colony - stimulating factor, interleukin-6, nitric oxide synthase | 686_task2 | Sentence: Suppression by azelastine hydrochloride of NF-kappa B activation involved in generation of cytokines and nitric oxide.
The influence of the anti-allergy agent azelastine hydrochloride (Azeptin) on NF-kappa B activation associated with the generation of cytokines and nitric oxide (NO) was investigated in various kinds of human and mouse cells. Azeptin dose-dependently suppressed both DNA and protein synthesis in human gingival fibroblasts (HF) and also suppressed blastogenesis of human peripheral blood lymphocytes (PBL). Generation of tumor necrosis factor-alpha, interleukin 1-beta, granulocyte-macrophage colony-stimulating factor and interleukin-6 from 10(-5) M Azeptin-treated PBL and human monocytes (HM) was decreased to approximately 1/3 to 2/3 of the control levels. In parallel with the decreased cytokine generation, each cytokine mRNA was less expressed in the presence of 10(-5) M Azeptin. In addition, both inducible nitric oxide synthase-mRNA level and NO generation in mouse peritoneal macrophages were suppressed by 10(-5) M Azeptin. Being compatible with those results, Azeptin (10(-5) M) suppressed activation of NF-kappa B in PBL, HM and HF. These results appear to indicate that suppression of cytokine and NO generation by Azeptin results at least partially from the inhibition of NF-kappa B activation.
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] | Suppression by azelastine hydrochloride of NF-kappa B activation involved in generation of cytokines and nitric oxide.
The influence of the anti-allergy agent azelastine hydrochloride (Azeptin) on NF-kappa B activation associated with the generation of cytokines and nitric oxide (NO) was investigated in various kinds of human and mouse cells. Azeptin dose-dependently suppressed both DNA and protein synthesis in human gingival fibroblasts (HF) and also suppressed blastogenesis of human peripheral blood lymphocytes (PBL). Generation of tumor necrosis factor-alpha, interleukin 1-beta, granulocyte-macrophage colony-stimulating factor and interleukin-6 from 10(-5) M Azeptin-treated PBL and human monocytes (HM) was decreased to approximately 1/3 to 2/3 of the control levels. In parallel with the decreased cytokine generation, each cytokine mRNA was less expressed in the presence of 10(-5) M Azeptin. In addition, both inducible nitric oxide synthase-mRNA level and NO generation in mouse peritoneal macrophages were suppressed by 10(-5) M Azeptin. Being compatible with those results, Azeptin (10(-5) M) suppressed activation of NF-kappa B in PBL, HM and HF. These results appear to indicate that suppression of cytokine and NO generation by Azeptin results at least partially from the inhibition of NF-kappa B activation. | [
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olanzapine is a CHEMICAL, neurotrophic factor is a GENE-N, quinpirole is a CHEMICAL, quinpirole is a CHEMICAL, D2 receptor is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, Dopamine D2 receptor is a GENE-Y, D2 receptor is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, D2 is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, NGF is a GENE-Y, BDNF is a GENE-Y, ChAT is a GENE-Y, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, BDNF is a GENE-Y, ChAT is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, D2 receptor is a GENE-Y, D2 is a GENE-Y | 29905_task0 | Sentence: The effects of adulthood olanzapine treatment on cognitive performance and neurotrophic factor content in male and female rats neonatally treated with quinpirole.
Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus.
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Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus. | [
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olanzapine is a CHEMICAL, neurotrophic factor is a GENE-N, quinpirole is a CHEMICAL, quinpirole is a CHEMICAL, D2 receptor is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, Dopamine D2 receptor is a GENE-Y, D2 receptor is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, D2 is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, NGF is a GENE-Y, BDNF is a GENE-Y, ChAT is a GENE-Y, olanzapine is a CHEMICAL, quinpirole is a CHEMICAL, BDNF is a GENE-Y, ChAT is a GENE-Y, olanzapine is a CHEMICAL, olanzapine is a CHEMICAL, D2 receptor is a GENE-Y, D2 is a GENE-Y | 29905_task1 | Sentence: The effects of adulthood olanzapine treatment on cognitive performance and neurotrophic factor content in male and female rats neonatally treated with quinpirole.
Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus.
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] | The effects of adulthood olanzapine treatment on cognitive performance and neurotrophic factor content in male and female rats neonatally treated with quinpirole.
Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus. | [
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olanzapine, neurotrophic factor, quinpirole, quinpirole, D2 receptor, olanzapine, olanzapine, Dopamine D2 receptor, D2 receptor, olanzapine, olanzapine, quinpirole, D2, olanzapine, olanzapine, olanzapine, quinpirole, NGF, BDNF, ChAT, olanzapine, quinpirole, BDNF, ChAT, olanzapine, olanzapine, D2 receptor, D2 | 29905_task2 | Sentence: The effects of adulthood olanzapine treatment on cognitive performance and neurotrophic factor content in male and female rats neonatally treated with quinpirole.
Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus.
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] | The effects of adulthood olanzapine treatment on cognitive performance and neurotrophic factor content in male and female rats neonatally treated with quinpirole.
Male and female Sprague-Dawley rats were administered quinpirole (1 mg/kg, i.p.) or saline once daily from postnatal day (P)1 to P21. This drug treatment has been shown to produce long-term priming of the D2 receptor. Beginning on P62, rats were administered the atypical antipsychotic olanzapine (2.5 mg/kg) or saline twice daily (i.p.) for 28 days. One day after olanzapine treatment ceased, rats were tested on the place and match-to-place versions of the Morris water maze (MWM) for seven consecutive days. Dopamine D2 receptor priming was verified through a yawning behavioural test, a D2 receptor-mediated event, before olanzapine was administered as well as after olanzapine treatment and behavioural testing were complete. Results showed that neonatal quinpirole treatment induced D2 priming that was eliminated by olanzapine treatment. On the MWM place version, D2-primed rats demonstrated a significant impairment that was eliminated by olanzapine treatment, but olanzapine treatment to animals neonatally treated with saline produced a significant deficit on the place version of the MWM. There were no significant deficits on the match-to-place version. Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and ChAT that was eliminated by olanzapine treatment. Neonatal quinpirole treatment produced a significant decrease in BDNF and ChAT in the frontal cortex that was unaffected by olanzapine treatment. These results show that olanzapine eliminates D2 receptor priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus. | [
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paper is an umlsterm, fistula is an umlsterm, implantation is an umlsterm, hip is an umlsterm, old is an umlsterm, woman is an umlsterm, fracture is an umlsterm, thigh is an umlsterm, bone is an umlsterm, paraproctic is an umlsterm, fistula is an umlsterm, implantation is an umlsterm, hip prosthesis is an umlsterm, knowledge is an umlsterm, cases reported is an umlsterm, complication is an umlsterm, wound is an umlsterm, symptoms is an umlsterm, treatment is an umlsterm | DerUnfallchirurg.71000402.eng.abstr_task0 | Sentence: In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: umlsterm
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] | In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment . | [
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paper is an umlsterm, fistula is an umlsterm, implantation is an umlsterm, hip is an umlsterm, old is an umlsterm, woman is an umlsterm, fracture is an umlsterm, thigh is an umlsterm, bone is an umlsterm, paraproctic is an umlsterm, fistula is an umlsterm, implantation is an umlsterm, hip prosthesis is an umlsterm, knowledge is an umlsterm, cases reported is an umlsterm, complication is an umlsterm, wound is an umlsterm, symptoms is an umlsterm, treatment is an umlsterm | DerUnfallchirurg.71000402.eng.abstr_task1 | Sentence: In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment .
Instructions: please typing these entity words according to sentence: paper, fistula, implantation, hip, old, woman, fracture, thigh, bone, paraproctic, fistula, implantation, hip prosthesis, knowledge, cases reported, complication, wound, symptoms, treatment
Options: umlsterm
| [
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] | In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment . | [
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] | [
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paper, fistula, implantation, hip, old, woman, fracture, thigh, bone, paraproctic, fistula, implantation, hip prosthesis, knowledge, cases reported, complication, wound, symptoms, treatment | DerUnfallchirurg.71000402.eng.abstr_task2 | Sentence: In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment .
Instructions: please extract entity words from the input sentence
| [
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] | In this paper we present the unusual case of a fistula after implantation of a total hip prothesis . In a 75-year old woman with a fracture of the thigh bone , we observed a paraproctic fistula 42 months after implantation of a total hip prosthesis . To our knowledge there have been no such cases reported with this complication . Thus , we wound like to demonstrate the progress of the illness , the first symptoms , and the kind and success of the treatment . | [
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morbidity is an umlsterm, Germany is an umlsterm, electronic is an umlsterm, work is an umlsterm, classification is an umlsterm, research is an umlsterm, thesaurus is an umlsterm, diagnostic is an umlsterm, charge is an umlsterm, INTERNET is an umlsterm | Bundesgesundheitsblatt.90420827.eng.abstr_task0 | Sentence: ICD-10 is to be implemented for morbidity coding in Germany soon . The electronic versions of ICD-10 are introduced . For everyday work with the classification and for epidemiological research further tools are provided by DIMDI : ICD-10 meta files , ICD conversion tables , ICD-10 thesaurus of diagnostic terms . All files are available free of charge via the INTERNET .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: umlsterm
| [
"O",
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] | ICD-10 is to be implemented for morbidity coding in Germany soon . The electronic versions of ICD-10 are introduced . For everyday work with the classification and for epidemiological research further tools are provided by DIMDI : ICD-10 meta files , ICD conversion tables , ICD-10 thesaurus of diagnostic terms . All files are available free of charge via the INTERNET . | [
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morbidity is an umlsterm, Germany is an umlsterm, electronic is an umlsterm, work is an umlsterm, classification is an umlsterm, research is an umlsterm, thesaurus is an umlsterm, diagnostic is an umlsterm, charge is an umlsterm, INTERNET is an umlsterm | Bundesgesundheitsblatt.90420827.eng.abstr_task1 | Sentence: ICD-10 is to be implemented for morbidity coding in Germany soon . The electronic versions of ICD-10 are introduced . For everyday work with the classification and for epidemiological research further tools are provided by DIMDI : ICD-10 meta files , ICD conversion tables , ICD-10 thesaurus of diagnostic terms . All files are available free of charge via the INTERNET .
Instructions: please typing these entity words according to sentence: morbidity, Germany, electronic, work, classification, research, thesaurus, diagnostic, charge, INTERNET
Options: umlsterm
| [
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morbidity, Germany, electronic, work, classification, research, thesaurus, diagnostic, charge, INTERNET | Bundesgesundheitsblatt.90420827.eng.abstr_task2 | Sentence: ICD-10 is to be implemented for morbidity coding in Germany soon . The electronic versions of ICD-10 are introduced . For everyday work with the classification and for epidemiological research further tools are provided by DIMDI : ICD-10 meta files , ICD conversion tables , ICD-10 thesaurus of diagnostic terms . All files are available free of charge via the INTERNET .
Instructions: please extract entity words from the input sentence
| [
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"B-umlsterm",
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] | ICD-10 is to be implemented for morbidity coding in Germany soon . The electronic versions of ICD-10 are introduced . For everyday work with the classification and for epidemiological research further tools are provided by DIMDI : ICD-10 meta files , ICD conversion tables , ICD-10 thesaurus of diagnostic terms . All files are available free of charge via the INTERNET . | [
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paraganglioma is an umlsterm, cauda equina is an umlsterm, man is an umlsterm, tumours is an umlsterm, lumbago is an umlsterm, paraesthesia is an umlsterm, Paragangliomas is an umlsterm, cauda equina is an umlsterm, cells is an umlsterm, cell is an umlsterm, cluster is an umlsterm, architecture is an umlsterm, connective tissue is an umlsterm, cells is an umlsterm, tumours is an umlsterm, morphological is an umlsterm, ependymomas is an umlsterm, paragangliomas is an umlsterm, cauda equina is an umlsterm, incidence is an umlsterm, Immunohistochemistry is an umlsterm, findings is an umlsterm, neuron - specific enolase is an umlsterm, chromogranin is an umlsterm, markers is an umlsterm, neuropeptides is an umlsterm, cells is an umlsterm, S-100 protein is an umlsterm, cells is an umlsterm, GFAP is an umlsterm, Paragangliomas is an umlsterm, cauda equina is an umlsterm, literature is an umlsterm, differential diagnosis is an umlsterm, cauda equina is an umlsterm | DerPathologe.70180484.eng.abstr_task0 | Sentence: We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina .
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] | We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina . | [
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paraganglioma is an umlsterm, cauda equina is an umlsterm, man is an umlsterm, tumours is an umlsterm, lumbago is an umlsterm, paraesthesia is an umlsterm, Paragangliomas is an umlsterm, cauda equina is an umlsterm, cells is an umlsterm, cell is an umlsterm, cluster is an umlsterm, architecture is an umlsterm, connective tissue is an umlsterm, cells is an umlsterm, tumours is an umlsterm, morphological is an umlsterm, ependymomas is an umlsterm, paragangliomas is an umlsterm, cauda equina is an umlsterm, incidence is an umlsterm, Immunohistochemistry is an umlsterm, findings is an umlsterm, neuron - specific enolase is an umlsterm, chromogranin is an umlsterm, markers is an umlsterm, neuropeptides is an umlsterm, cells is an umlsterm, S-100 protein is an umlsterm, cells is an umlsterm, GFAP is an umlsterm, Paragangliomas is an umlsterm, cauda equina is an umlsterm, literature is an umlsterm, differential diagnosis is an umlsterm, cauda equina is an umlsterm | DerPathologe.70180484.eng.abstr_task1 | Sentence: We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina .
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] | We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina . | [
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paraganglioma, cauda equina, man, tumours, lumbago, paraesthesia, Paragangliomas, cauda equina, cells, cell, cluster, architecture, connective tissue, cells, tumours, morphological, ependymomas, paragangliomas, cauda equina, incidence, Immunohistochemistry, findings, neuron - specific enolase, chromogranin, markers, neuropeptides, cells, S-100 protein, cells, GFAP, Paragangliomas, cauda equina, literature, differential diagnosis, cauda equina | DerPathologe.70180484.eng.abstr_task2 | Sentence: We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina .
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] | We report on a case of paraganglioma of the cauda equina in a 48-year-old man . These slow-growing , mostly benign and encapsulated intradural-extramedullar tumours are clinically characterized by lumbago , paraesthesia and motor deficits as well as occasi-onally by incontinence . Paragangliomas of the cauda equina show monomorphous ( main ) cells arranged in a typical cell cluster pattern , demonstrating a lobular architecture and a fine net of connective tissue formed by so-called sustentacular cells ; some tumours show focal ganglionic differentiation . Because of their morphological similarity to the more common ependymomas , paragangliomas of the cauda equina are sometimes misdiagnosed so that their incidence is likely to be higher than previously estimated . Immunohistochemistry findings are positive for neuron-specific enolase , chromogranin and other neuronal markers as well as neuropeptides ( main cells ) and S-100 protein ( sustentacular cells ) while widely lacking reactivity for GFAP . Paragangliomas of the cauda equina represent a rare entity , of which only 80 cases have been described in the literature . Because they only occur sporadically , they are often not included in the differential diagnosis of mass lesions of the region of the cauda equina . | [
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artificial tear formulations is a Intervention_Physical, two artificial eye - drop formulations is a Intervention_Pharmacological, Tear meniscus volume is a Outcome_Physical | 51834_task0 | Sentence: Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation .
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] | Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation . | [
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"Intervention_Pharmacological",
"Intervention_Physical",
"Outcome_Physical"
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artificial tear formulations is a Intervention_Physical, two artificial eye - drop formulations is a Intervention_Pharmacological, Tear meniscus volume is a Outcome_Physical | 51834_task1 | Sentence: Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation .
Instructions: please typing these entity words according to sentence: artificial tear formulations, two artificial eye - drop formulations, Tear meniscus volume
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] | Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation . | [
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artificial tear formulations, two artificial eye - drop formulations, Tear meniscus volume | 51834_task2 | Sentence: Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation .
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] | Comparison of two artificial tear formulations for dry eye through high-resolution optical coherence tomography . PURPOSE The aim was to determine the efficacy of two artificial eye-drop formulations by analysing the lower tear film meniscus volume through a commercial high-resolution spectral-domain optical coherence tomographer . METHODS Twenty dry eye patients ( 12 men , eight women , aged 57.5 ± 8.4 years ) with refractive errors from -2.50 to +0.75 D ( mean -1.34 ± 1.02 D ) and cylinders lower than 1.00 D were examined . Tear meniscus volume was measured before , immediately after and 10 , 30 and 60 minutes after instillation using the Copernicus high-resolution spectral-domain optical coherence tomographer ( Optopol Tech SA , Zawiercie , Poland ) . Volume was calculated from the local area obtained from tomograms considering a regular distribution of the tear meniscus across the eyelid . Ten subjects were randomly assigned to first receive either polyethylene glycol ( Blink Intensive , Abbot Medical Optics Inc , CA , USA ) or hypromellose ( Artific , Farma-Lepori SA , Barcelona , Spain ) three times daily in both eyes for one month . Measures were then repeated and after a one-week wash-out period they were switched to the other eye-drop for another month . RESULTS Mean baseline volume was 0.38 ± 0.10 µL , while mean baseline volume after the wash-out period was slightly higher , 0.39 ± 0.10 µL ( p = 0.638 ) . Analysis of variance showed significant differences in meniscus volume with time after instillation with both formulations ( p < 0.001 ) , mean volume decreasing with time . At 30 and 60 minutes following instillation , values decreased to almost baseline ( average difference 0.02 ± 0.03 µL at t ( 30 ) , p = 0.016 and 0.01 ± 0.01 µL at t ( 60 ) , p = 0.098 ) . CONCLUSION An increase in tear film meniscus volume in dry eyes from the use of eye-drops has been shown . High resolution imaging of lower tear film meniscus with clinical optical coherence tomography systems provides useful measures of tear volume . Both formulations assessed in the present study are efficient in increasing tear meniscus volume and reducing dry eye signs and symptoms , although results in terms of increase in meniscus volume were higher with the polyethylene glycol formulation . | [
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] | [
"Intervention_Pharmacological",
"Intervention_Physical",
"Outcome_Physical"
] |
environment is an umlsterm, environment is an umlsterm, older is an umlsterm, people is an umlsterm, older is an umlsterm, people is an umlsterm, environment is an umlsterm, older is an umlsterm, people is an umlsterm, maintenance is an umlsterm, competence is an umlsterm | ZfuerGerontologie+Geriatrie.80310104.eng.abstr_task0 | Sentence: An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: umlsterm
| [
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] | An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged . | [
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] | [
"umlsterm"
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environment is an umlsterm, environment is an umlsterm, older is an umlsterm, people is an umlsterm, older is an umlsterm, people is an umlsterm, environment is an umlsterm, older is an umlsterm, people is an umlsterm, maintenance is an umlsterm, competence is an umlsterm | ZfuerGerontologie+Geriatrie.80310104.eng.abstr_task1 | Sentence: An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged .
Instructions: please typing these entity words according to sentence: environment, environment, older, people, older, people, environment, older, people, maintenance, competence
Options: umlsterm
| [
"O",
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] | An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged . | [
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] | [
"umlsterm"
] |
environment, environment, older, people, older, people, environment, older, people, maintenance, competence | ZfuerGerontologie+Geriatrie.80310104.eng.abstr_task2 | Sentence: An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged .
Instructions: please extract entity words from the input sentence
| [
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] | An ecological theory of remembering is formulated which is based on the patterns of meaningfulness in the social and spatial environment . The specific ecological relationship to the environment is affinitive , and also opens access to the ressources of the past . In the present study , conditions for this access ( in particular with older people ) were investigated . It is assumed that older people , especially , when they lose someone with whom they had a fixed relationship seek counselling and that abrupt changes in the spatial environment , such as moving to a home , are rejected by older people . These hypotheses were checked on the basis of material ( N=120) gathered in a counselling service for the aged and they were essentially confirmed . To make matters clear , " typical " and thus every-day experiences of maintenance and loss of competence are cited from the material . Finally , practical conclusions are drawn with regard to work with the aged . | [
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Arsenic is a CHEMICAL, endothelin-1 is a GENE-Y, Gi protein - coupled receptor is a GENE-N, glucose is a CHEMICAL, Arsenic is a CHEMICAL, As(III ) is a CHEMICAL, As(III ) is a CHEMICAL, Pertussis toxin is a GENE-N, Ptx is a GENE-N, Gi protein - coupled receptor is a GENE-N, GPCR is a GENE-N, As(III ) is a CHEMICAL, GPCR is a GENE-N, As(III ) is a CHEMICAL, dexamethasone is a CHEMICAL, adiponectin is a GENE-Y, perilipin is a GENE-Y, Ptx is a GENE-N, As(III ) is a CHEMICAL, Gi is a GENE-N, endothelin-1 type A and B receptors is a GENE-N, As(III ) is a CHEMICAL, sphingosine-1-phosphate type 1 receptor is a GENE-Y, As(III ) is a CHEMICAL, angiotensin II type 1 receptor is a GENE-Y, As(III ) is a CHEMICAL, arsenic is a CHEMICAL, endothelin-1 is a GENE-Y, GPCRs is a GENE-N, As(III ) is a CHEMICAL, GPCR is a GENE-N, arsenic is a CHEMICAL | 32103_task0 | Sentence: Arsenic activates endothelin-1 Gi protein-coupled receptor signaling to inhibit stem cell differentiation in adipogenesis.
Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases.
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Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases. | [
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Arsenic is a CHEMICAL, endothelin-1 is a GENE-Y, Gi protein - coupled receptor is a GENE-N, glucose is a CHEMICAL, Arsenic is a CHEMICAL, As(III ) is a CHEMICAL, As(III ) is a CHEMICAL, Pertussis toxin is a GENE-N, Ptx is a GENE-N, Gi protein - coupled receptor is a GENE-N, GPCR is a GENE-N, As(III ) is a CHEMICAL, GPCR is a GENE-N, As(III ) is a CHEMICAL, dexamethasone is a CHEMICAL, adiponectin is a GENE-Y, perilipin is a GENE-Y, Ptx is a GENE-N, As(III ) is a CHEMICAL, Gi is a GENE-N, endothelin-1 type A and B receptors is a GENE-N, As(III ) is a CHEMICAL, sphingosine-1-phosphate type 1 receptor is a GENE-Y, As(III ) is a CHEMICAL, angiotensin II type 1 receptor is a GENE-Y, As(III ) is a CHEMICAL, arsenic is a CHEMICAL, endothelin-1 is a GENE-Y, GPCRs is a GENE-N, As(III ) is a CHEMICAL, GPCR is a GENE-N, arsenic is a CHEMICAL | 32103_task1 | Sentence: Arsenic activates endothelin-1 Gi protein-coupled receptor signaling to inhibit stem cell differentiation in adipogenesis.
Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases.
Instructions: please typing these entity words according to sentence: Arsenic, endothelin-1, Gi protein - coupled receptor, glucose, Arsenic, As(III ), As(III ), Pertussis toxin, Ptx, Gi protein - coupled receptor, GPCR, As(III ), GPCR, As(III ), dexamethasone, adiponectin, perilipin, Ptx, As(III ), Gi, endothelin-1 type A and B receptors, As(III ), sphingosine-1-phosphate type 1 receptor, As(III ), angiotensin II type 1 receptor, As(III ), arsenic, endothelin-1, GPCRs, As(III ), GPCR, arsenic
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Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases. | [
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Arsenic, endothelin-1, Gi protein - coupled receptor, glucose, Arsenic, As(III ), As(III ), Pertussis toxin, Ptx, Gi protein - coupled receptor, GPCR, As(III ), GPCR, As(III ), dexamethasone, adiponectin, perilipin, Ptx, As(III ), Gi, endothelin-1 type A and B receptors, As(III ), sphingosine-1-phosphate type 1 receptor, As(III ), angiotensin II type 1 receptor, As(III ), arsenic, endothelin-1, GPCRs, As(III ), GPCR, arsenic | 32103_task2 | Sentence: Arsenic activates endothelin-1 Gi protein-coupled receptor signaling to inhibit stem cell differentiation in adipogenesis.
Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases.
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Dysfunctional lipid and glucose metabolism contribute to metabolic syndrome-a major public health concern that enhances cardiovascular disease risk. Arsenic (As(III)) exposure may increase metabolic syndrome and cardiovascular disease risk by impairing adipose tissue differentiation, function, and insulin sensitivity through pathogenic mechanisms that remain unclear. We hypothesized that As(III) signals through the Pertussis toxin (Ptx) sensitive, Gi protein-coupled receptor (GPCR) to impair adipogenesis, as previously demonstrated for its stimulation of vascular oxidant generation, angiogenesis, and remodeling. Because both As(III) and GPCR ligands inhibit progenitor cell differentiation into adipocytes, we investigated the hypothesis in a model of low-passage human mesenchymal stem cells (hMSC). As(III) (0.1-1.0 µM) suppressed dexamethasone/insulin-induced hMSC adipogenesis, as indicated by decreased transcriptional promoters of differentiation, decreased fat droplet formation, and decreased expression of differentiated adipocyte markers, such as adiponectin and perilipin. Preincubating hMSC with Ptx prevented 90% of the suppressive effect of As(III). Selective competitive antagonists of Gi-coupled endothelin-1 type A and B receptors were ~60% effective in blocking As(III) inhibition and combination of antagonists to both receptors were 85% effective. In contrast, antagonists to the sphingosine-1-phosphate type 1 receptor (previously shown to mediate As(III) vascular effects) or the angiotensin II type 1 receptor were ineffective in blocking As(III) effects. These studies suggest a majority of arsenic-inhibited adipocyte differentiation, and metabolism requires endothelin-1 GPCRs and that As(III) effects on GPCR signaling are tissue and context specific. This may represent a significant mechanism for the contribution of arsenic exposure to increased metabolic and cardiovascular diseases. | [
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patient is an umlsterm, hypoglossal nerve is an umlsterm, paralysis is an umlsterm, head trauma is an umlsterm, CT scan is an umlsterm, fractures is an umlsterm, posterior is an umlsterm, skull base is an umlsterm, traction is an umlsterm, nerve is an umlsterm, injury is an umlsterm | DerNervenarzt.90700357.eng.abstr_task0 | Sentence: We report a 72-year-old patient who developed an isolated bilateral hypoglossal nerve paralysis following head trauma with complete recovery after three months . Since the CT scan did not show any fractures of the posterior skull base , we discuss a traction nerve injury as a possible mechanism .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
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patient is an umlsterm, hypoglossal nerve is an umlsterm, paralysis is an umlsterm, head trauma is an umlsterm, CT scan is an umlsterm, fractures is an umlsterm, posterior is an umlsterm, skull base is an umlsterm, traction is an umlsterm, nerve is an umlsterm, injury is an umlsterm | DerNervenarzt.90700357.eng.abstr_task1 | Sentence: We report a 72-year-old patient who developed an isolated bilateral hypoglossal nerve paralysis following head trauma with complete recovery after three months . Since the CT scan did not show any fractures of the posterior skull base , we discuss a traction nerve injury as a possible mechanism .
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] | We report a 72-year-old patient who developed an isolated bilateral hypoglossal nerve paralysis following head trauma with complete recovery after three months . Since the CT scan did not show any fractures of the posterior skull base , we discuss a traction nerve injury as a possible mechanism . | [
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patient, hypoglossal nerve, paralysis, head trauma, CT scan, fractures, posterior, skull base, traction, nerve, injury | DerNervenarzt.90700357.eng.abstr_task2 | Sentence: We report a 72-year-old patient who developed an isolated bilateral hypoglossal nerve paralysis following head trauma with complete recovery after three months . Since the CT scan did not show any fractures of the posterior skull base , we discuss a traction nerve injury as a possible mechanism .
Instructions: please extract entity words from the input sentence
| [
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] | We report a 72-year-old patient who developed an isolated bilateral hypoglossal nerve paralysis following head trauma with complete recovery after three months . Since the CT scan did not show any fractures of the posterior skull base , we discuss a traction nerve injury as a possible mechanism . | [
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Gram - negative is a Phenotype, yeast communities is a Habitat, Gram - negative is a Phenotype, D. hansenii is a Microorganism, G. candidum is a Microorganism, cheese surface is a Habitat, G. candidum is a Microorganism, D. hansenii is a Microorganism, Y. lipolytica is a Microorganism | 80_task0 | Sentence: Growth of two Gram-negative bacteria during ripening had no effect on the growth of the yeasts studied (data not shown). All yeast communities, with or without Gram-negative bacteria, reached viable cell numbers above 7.9–8.0 log10 cfu/g after 5 days of ripening. D. hansenii followed by G. candidum dominated the cheese surface on day 5 with 7.6 log10 cfu/g and 7.1 log10 cfu/g, respectively. After day 5, G. candidum levels remained close to 7.8 log10 cfu/g while the D. hansenii population decreased by 1.0 to 1.5 log10 cfu/g between day 15 and day 35. Y. lipolytica levels slightly increased after day 5 and reached a maximum after 35 days with counts of 7.5 log10 cfu/g.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: Habitat, Microorganism, Phenotype
| [
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] | Growth of two Gram-negative bacteria during ripening had no effect on the growth of the yeasts studied (data not shown). All yeast communities, with or without Gram-negative bacteria, reached viable cell numbers above 7.9–8.0 log10 cfu/g after 5 days of ripening. D. hansenii followed by G. candidum dominated the cheese surface on day 5 with 7.6 log10 cfu/g and 7.1 log10 cfu/g, respectively. After day 5, G. candidum levels remained close to 7.8 log10 cfu/g while the D. hansenii population decreased by 1.0 to 1.5 log10 cfu/g between day 15 and day 35. Y. lipolytica levels slightly increased after day 5 and reached a maximum after 35 days with counts of 7.5 log10 cfu/g. | [
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Gram - negative is a Phenotype, yeast communities is a Habitat, Gram - negative is a Phenotype, D. hansenii is a Microorganism, G. candidum is a Microorganism, cheese surface is a Habitat, G. candidum is a Microorganism, D. hansenii is a Microorganism, Y. lipolytica is a Microorganism | 80_task1 | Sentence: Growth of two Gram-negative bacteria during ripening had no effect on the growth of the yeasts studied (data not shown). All yeast communities, with or without Gram-negative bacteria, reached viable cell numbers above 7.9–8.0 log10 cfu/g after 5 days of ripening. D. hansenii followed by G. candidum dominated the cheese surface on day 5 with 7.6 log10 cfu/g and 7.1 log10 cfu/g, respectively. After day 5, G. candidum levels remained close to 7.8 log10 cfu/g while the D. hansenii population decreased by 1.0 to 1.5 log10 cfu/g between day 15 and day 35. Y. lipolytica levels slightly increased after day 5 and reached a maximum after 35 days with counts of 7.5 log10 cfu/g.
Instructions: please typing these entity words according to sentence: Gram - negative, yeast communities, Gram - negative, D. hansenii, G. candidum, cheese surface, G. candidum, D. hansenii, Y. lipolytica
Options: Habitat, Microorganism, Phenotype
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] | Growth of two Gram-negative bacteria during ripening had no effect on the growth of the yeasts studied (data not shown). All yeast communities, with or without Gram-negative bacteria, reached viable cell numbers above 7.9–8.0 log10 cfu/g after 5 days of ripening. D. hansenii followed by G. candidum dominated the cheese surface on day 5 with 7.6 log10 cfu/g and 7.1 log10 cfu/g, respectively. After day 5, G. candidum levels remained close to 7.8 log10 cfu/g while the D. hansenii population decreased by 1.0 to 1.5 log10 cfu/g between day 15 and day 35. Y. lipolytica levels slightly increased after day 5 and reached a maximum after 35 days with counts of 7.5 log10 cfu/g. | [
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Gram - negative, yeast communities, Gram - negative, D. hansenii, G. candidum, cheese surface, G. candidum, D. hansenii, Y. lipolytica | 80_task2 | Sentence: Growth of two Gram-negative bacteria during ripening had no effect on the growth of the yeasts studied (data not shown). All yeast communities, with or without Gram-negative bacteria, reached viable cell numbers above 7.9–8.0 log10 cfu/g after 5 days of ripening. D. hansenii followed by G. candidum dominated the cheese surface on day 5 with 7.6 log10 cfu/g and 7.1 log10 cfu/g, respectively. After day 5, G. candidum levels remained close to 7.8 log10 cfu/g while the D. hansenii population decreased by 1.0 to 1.5 log10 cfu/g between day 15 and day 35. Y. lipolytica levels slightly increased after day 5 and reached a maximum after 35 days with counts of 7.5 log10 cfu/g.
Instructions: please extract entity words from the input sentence
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ethambutol is a DRUG, aluminum hydroxide is a DRUG, antacid is a GROUP, ethambutol is a DRUG, ethambutol is a DRUG, antacid products is a GROUP, ethambutol is a DRUG, aluminum hydroxide is a DRUG, antacids is a GROUP, ethambutol is a DRUG | Ethambutol_ddi_task0 | Sentence: The results of a study of coadministration of ethambutol (50 mg/kg) with an aluminum hydroxide containing antacid to 13 patients with tuberculosis showed a reduction of mean serum concentrations and urinary excretion of ethambutol of approximately 20% and 13%, respectively, suggesting that the oral absorption of ethambutol may be reduced by these antacid products. It is recommended to avoid concurrent administration of ethambutol with aluminum hydroxide containing antacids for at least 4 hours following ethambutol administration.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: GROUP, DRUG
| [
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ethambutol is a DRUG, aluminum hydroxide is a DRUG, antacid is a GROUP, ethambutol is a DRUG, ethambutol is a DRUG, antacid products is a GROUP, ethambutol is a DRUG, aluminum hydroxide is a DRUG, antacids is a GROUP, ethambutol is a DRUG | Ethambutol_ddi_task1 | Sentence: The results of a study of coadministration of ethambutol (50 mg/kg) with an aluminum hydroxide containing antacid to 13 patients with tuberculosis showed a reduction of mean serum concentrations and urinary excretion of ethambutol of approximately 20% and 13%, respectively, suggesting that the oral absorption of ethambutol may be reduced by these antacid products. It is recommended to avoid concurrent administration of ethambutol with aluminum hydroxide containing antacids for at least 4 hours following ethambutol administration.
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ethambutol, aluminum hydroxide, antacid, ethambutol, ethambutol, antacid products, ethambutol, aluminum hydroxide, antacids, ethambutol | Ethambutol_ddi_task2 | Sentence: The results of a study of coadministration of ethambutol (50 mg/kg) with an aluminum hydroxide containing antacid to 13 patients with tuberculosis showed a reduction of mean serum concentrations and urinary excretion of ethambutol of approximately 20% and 13%, respectively, suggesting that the oral absorption of ethambutol may be reduced by these antacid products. It is recommended to avoid concurrent administration of ethambutol with aluminum hydroxide containing antacids for at least 4 hours following ethambutol administration.
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YY1 is a Protein, Oct1 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, hIL-5 is a Protein, IL-5 is a Protein, hIL-5 is a Protein, hIL-5 is a Protein, promoter is a Entity, IL-5 is a Protein, hIL-5 is a Protein, promoter is a Entity, Oct1 is a Protein, YY1 is a Protein, hIL-5 is a Protein, promoter is a Entity, Oct1 is a Protein, YY1 is a Protein, IL-5 is a Protein, promoter is a Entity, IL-5 is a Protein | 10359895_task0 | Sentence: Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.
BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells.
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] | Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.
BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells. | [
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YY1 is a Protein, Oct1 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, IL-5 is a Protein, hIL-5 is a Protein, IL-5 is a Protein, hIL-5 is a Protein, hIL-5 is a Protein, promoter is a Entity, IL-5 is a Protein, hIL-5 is a Protein, promoter is a Entity, Oct1 is a Protein, YY1 is a Protein, hIL-5 is a Protein, promoter is a Entity, Oct1 is a Protein, YY1 is a Protein, IL-5 is a Protein, promoter is a Entity, IL-5 is a Protein | 10359895_task1 | Sentence: Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.
BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells.
Instructions: please typing these entity words according to sentence: YY1, Oct1, IL-5, IL-5, IL-5, IL-5, IL-5, hIL-5, IL-5, hIL-5, hIL-5, promoter, IL-5, hIL-5, promoter, Oct1, YY1, hIL-5, promoter, Oct1, YY1, IL-5, promoter, IL-5
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BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells. | [
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BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells.
Instructions: please extract entity words from the input sentence
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BACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level. OBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells. METHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis. RESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells. CONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells. | [
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Denmark is an umlsterm, France is an umlsterm, Germany is an umlsterm, Great Britain is an umlsterm, Italy is an umlsterm, ophthalmology is an umlsterm, internal medicine is an umlsterm, institute is an umlsterm, medical informatics is an umlsterm, health services research is an umlsterm, publishing is an umlsterm, market is an umlsterm | DerOpthalmologe.70940523.eng.abstr_task0 | Sentence: Background : In Denmark , France , Germany , Great Britain and Italy , the OPHTEL project combines clinical centers of ophthalmology and internal medicine , an institute for medical informatics and health services research , a publishing company and different industrial partners in the EDP market .
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Denmark is an umlsterm, France is an umlsterm, Germany is an umlsterm, Great Britain is an umlsterm, Italy is an umlsterm, ophthalmology is an umlsterm, internal medicine is an umlsterm, institute is an umlsterm, medical informatics is an umlsterm, health services research is an umlsterm, publishing is an umlsterm, market is an umlsterm | DerOpthalmologe.70940523.eng.abstr_task1 | Sentence: Background : In Denmark , France , Germany , Great Britain and Italy , the OPHTEL project combines clinical centers of ophthalmology and internal medicine , an institute for medical informatics and health services research , a publishing company and different industrial partners in the EDP market .
Instructions: please typing these entity words according to sentence: Denmark, France, Germany, Great Britain, Italy, ophthalmology, internal medicine, institute, medical informatics, health services research, publishing, market
Options: umlsterm
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Denmark, France, Germany, Great Britain, Italy, ophthalmology, internal medicine, institute, medical informatics, health services research, publishing, market | DerOpthalmologe.70940523.eng.abstr_task2 | Sentence: Background : In Denmark , France , Germany , Great Britain and Italy , the OPHTEL project combines clinical centers of ophthalmology and internal medicine , an institute for medical informatics and health services research , a publishing company and different industrial partners in the EDP market .
Instructions: please extract entity words from the input sentence
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beta 1 triiodothyronine receptor mRNA is a RNA_molecule, human tissues is a tissue, competitive reverse transcription polymerase chain reaction is an other_name | 101349_task0 | Sentence: Quantitation of beta 1 triiodothyronine receptor mRNA in human tissues by competitive reverse transcription polymerase chain reaction.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: RNA_molecule, other_name, tissue
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beta 1 triiodothyronine receptor mRNA is a RNA_molecule, human tissues is a tissue, competitive reverse transcription polymerase chain reaction is an other_name | 101349_task1 | Sentence: Quantitation of beta 1 triiodothyronine receptor mRNA in human tissues by competitive reverse transcription polymerase chain reaction.
Instructions: please typing these entity words according to sentence: beta 1 triiodothyronine receptor mRNA, human tissues, competitive reverse transcription polymerase chain reaction
Options: RNA_molecule, other_name, tissue
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beta 1 triiodothyronine receptor mRNA, human tissues, competitive reverse transcription polymerase chain reaction | 101349_task2 | Sentence: Quantitation of beta 1 triiodothyronine receptor mRNA in human tissues by competitive reverse transcription polymerase chain reaction.
Instructions: please extract entity words from the input sentence
| [
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Behandlungkonzepts is an umlsterm, Ekzem is an umlsterm, Basistherapie is an umlsterm, Oelbaedern is an umlsterm, Kindern is an umlsterm, Behandlung is an umlsterm, Hautveraenderungen is an umlsterm, Glukokortikoide is an umlsterm, Antihistaminika is an umlsterm, Antibiotikagabe is an umlsterm, Ekzem is an umlsterm, Ekzem is an umlsterm, Antibiotikaanwendung is an umlsterm, Antiseptika is an umlsterm | DerHautarzt.70480379.ger.abstr_task0 | Sentence: Im Mittelpunkt des Behandlungkonzepts fuer das atopische Ekzem im Kindesalter steht die adjuvante Basistherapie . Hierunter versteht man die regelmaessige , stadiengerechte Anwendung von wirkstofffreien Externa und Oelbaedern . Harnstoffhaltige Zubereitungen sind v.a. bei juengeren Kindern aufgrund des " Stinging " -Effektes nur bedingt einsetzbar . Zur Behandlung ekzematoeser Hautveraenderungen sind Glukokortikoide Mittel der 1. Wahl und anderen Externa mit antiinflammatorischer Wirkung ueberlegen . Antihistaminika , vorzugsweise mit sedierender Komponente , werden zeitlich begrenzt bei Exazerbationen erfolgreich als unterstuetzende Massnahme eingesetzt . Die systemische Antibiotikagabe beim impetiginisierten atopischen Ekzem ist etabliert . In Faellen von bakteriell getriggertem atopischem Ekzem kann darueber hinaus eine oertlich begrenzte topische Antibiotikaanwendung bzw. der grossflaechige Einsatz von Antiseptika indiziert sein .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: umlsterm
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Instructions: please typing these entity words according to sentence: Behandlungkonzepts, Ekzem, Basistherapie, Oelbaedern, Kindern, Behandlung, Hautveraenderungen, Glukokortikoide, Antihistaminika, Antibiotikagabe, Ekzem, Ekzem, Antibiotikaanwendung, Antiseptika
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Behandlungkonzepts, Ekzem, Basistherapie, Oelbaedern, Kindern, Behandlung, Hautveraenderungen, Glukokortikoide, Antihistaminika, Antibiotikagabe, Ekzem, Ekzem, Antibiotikaanwendung, Antiseptika | DerHautarzt.70480379.ger.abstr_task2 | Sentence: Im Mittelpunkt des Behandlungkonzepts fuer das atopische Ekzem im Kindesalter steht die adjuvante Basistherapie . Hierunter versteht man die regelmaessige , stadiengerechte Anwendung von wirkstofffreien Externa und Oelbaedern . Harnstoffhaltige Zubereitungen sind v.a. bei juengeren Kindern aufgrund des " Stinging " -Effektes nur bedingt einsetzbar . Zur Behandlung ekzematoeser Hautveraenderungen sind Glukokortikoide Mittel der 1. Wahl und anderen Externa mit antiinflammatorischer Wirkung ueberlegen . Antihistaminika , vorzugsweise mit sedierender Komponente , werden zeitlich begrenzt bei Exazerbationen erfolgreich als unterstuetzende Massnahme eingesetzt . Die systemische Antibiotikagabe beim impetiginisierten atopischen Ekzem ist etabliert . In Faellen von bakteriell getriggertem atopischem Ekzem kann darueber hinaus eine oertlich begrenzte topische Antibiotikaanwendung bzw. der grossflaechige Einsatz von Antiseptika indiziert sein .
Instructions: please extract entity words from the input sentence
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Meclofenamic acid is a CHEMICAL, diclofenac is a CHEMICAL, KCNQ2 / Q3 is a GENE-N, potassium channel is a GENE-N | 15598972_task0 | Sentence: Meclofenamic acid and diclofenac, novel templates of KCNQ2/Q3 potassium channel openers, depress cortical neuron activity and exhibit anticonvulsant properties.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: GENE-N, CHEMICAL
| [
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Meclofenamic acid is a CHEMICAL, diclofenac is a CHEMICAL, KCNQ2 / Q3 is a GENE-N, potassium channel is a GENE-N | 15598972_task1 | Sentence: Meclofenamic acid and diclofenac, novel templates of KCNQ2/Q3 potassium channel openers, depress cortical neuron activity and exhibit anticonvulsant properties.
Instructions: please typing these entity words according to sentence: Meclofenamic acid, diclofenac, KCNQ2 / Q3, potassium channel
Options: GENE-N, CHEMICAL
| [
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Meclofenamic acid, diclofenac, KCNQ2 / Q3, potassium channel | 15598972_task2 | Sentence: Meclofenamic acid and diclofenac, novel templates of KCNQ2/Q3 potassium channel openers, depress cortical neuron activity and exhibit anticonvulsant properties.
Instructions: please extract entity words from the input sentence
| [
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] | Meclofenamic acid and diclofenac, novel templates of KCNQ2/Q3 potassium channel openers, depress cortical neuron activity and exhibit anticonvulsant properties. | [
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"GENE-Y",
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nerve agent toxicity is a ADVERSE | example-173_task0 | Sentence: Comparison of oxime reactivation and aging of nerve agent-inhibited monkey and human acetylcholinesterases. Non-human primates are valuable animal models that are used for the evaluation of nerve agent toxicity as well as antidotes and results from animal experiments are extrapolated to humans. It has been demonstrated that the efficacy of an oxime primarily depends on its ability to reactivate nerve agent-inhibited acetylcholinesterase (AChE). If the in vitro oxime reactivation of nerve agent-inhibited animal AChE is similar to that of human AChE, it is likely that the results of an in vivo animal study will reliably extrapolate to humans. Therefore, the goal of this study was to compare the aging and reactivation of human and different monkey (Rhesus, Cynomolgus, and African Green) AChEs inhibited by GF, GD, and VR. The oximes examined include the traditional oxime 2-PAM, two H-oximes HI-6 and HLo-7, and the new candidate oxime MMB4. Results indicate that oxime reactivation of all three monkey AChEs was very similar to human AChE. The maximum difference in the second-order reactivation rate constant between human and three monkey AChEs or between AChEs from different monkey species was 5-fold. Aging rate constants of GF-, GD-, and VR-inhibited monkey AChEs were very similar to human AChE except for GF-inhibited monkey AChEs, which aged 2-3 times faster than the human enzyme. The results of this study suggest that all three monkey species are suitable animal models for nerve agent antidote evaluation since monkey AChEs possess similar biochemical/pharmacological properties to human AChE.
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: ADVERSE
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"ADVERSE"
] |
nerve agent toxicity is a ADVERSE | example-173_task1 | Sentence: Comparison of oxime reactivation and aging of nerve agent-inhibited monkey and human acetylcholinesterases. Non-human primates are valuable animal models that are used for the evaluation of nerve agent toxicity as well as antidotes and results from animal experiments are extrapolated to humans. It has been demonstrated that the efficacy of an oxime primarily depends on its ability to reactivate nerve agent-inhibited acetylcholinesterase (AChE). If the in vitro oxime reactivation of nerve agent-inhibited animal AChE is similar to that of human AChE, it is likely that the results of an in vivo animal study will reliably extrapolate to humans. Therefore, the goal of this study was to compare the aging and reactivation of human and different monkey (Rhesus, Cynomolgus, and African Green) AChEs inhibited by GF, GD, and VR. The oximes examined include the traditional oxime 2-PAM, two H-oximes HI-6 and HLo-7, and the new candidate oxime MMB4. Results indicate that oxime reactivation of all three monkey AChEs was very similar to human AChE. The maximum difference in the second-order reactivation rate constant between human and three monkey AChEs or between AChEs from different monkey species was 5-fold. Aging rate constants of GF-, GD-, and VR-inhibited monkey AChEs were very similar to human AChE except for GF-inhibited monkey AChEs, which aged 2-3 times faster than the human enzyme. The results of this study suggest that all three monkey species are suitable animal models for nerve agent antidote evaluation since monkey AChEs possess similar biochemical/pharmacological properties to human AChE.
Instructions: please typing these entity words according to sentence: nerve agent toxicity
Options: ADVERSE
| [
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nerve agent toxicity | example-173_task2 | Sentence: Comparison of oxime reactivation and aging of nerve agent-inhibited monkey and human acetylcholinesterases. Non-human primates are valuable animal models that are used for the evaluation of nerve agent toxicity as well as antidotes and results from animal experiments are extrapolated to humans. It has been demonstrated that the efficacy of an oxime primarily depends on its ability to reactivate nerve agent-inhibited acetylcholinesterase (AChE). If the in vitro oxime reactivation of nerve agent-inhibited animal AChE is similar to that of human AChE, it is likely that the results of an in vivo animal study will reliably extrapolate to humans. Therefore, the goal of this study was to compare the aging and reactivation of human and different monkey (Rhesus, Cynomolgus, and African Green) AChEs inhibited by GF, GD, and VR. The oximes examined include the traditional oxime 2-PAM, two H-oximes HI-6 and HLo-7, and the new candidate oxime MMB4. Results indicate that oxime reactivation of all three monkey AChEs was very similar to human AChE. The maximum difference in the second-order reactivation rate constant between human and three monkey AChEs or between AChEs from different monkey species was 5-fold. Aging rate constants of GF-, GD-, and VR-inhibited monkey AChEs were very similar to human AChE except for GF-inhibited monkey AChEs, which aged 2-3 times faster than the human enzyme. The results of this study suggest that all three monkey species are suitable animal models for nerve agent antidote evaluation since monkey AChEs possess similar biochemical/pharmacological properties to human AChE.
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Indinavir is a DRUG, CRIXIVAN is a BRAND, Indinavir is a DRUG, indinavir is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, indinavir is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, Antiarrhythmics is a GROUP, amiodarone is a DRUG, dihydroergotamine is a DRUG, ergonovine is a DRUG, ergotamine is a DRUG, methylergonovine is a DRUG, Sedative is a GROUP, hypnotics is a GROUP, midazolam is a DRUG, triazolam is a DRUG, cisapride is a DRUG, Neuroleptic is a GROUP, pimozide is a DRUG, CRIXIVAN is a BRAND, protease inhibitors is a GROUP, Antimycobacterial is a GROUP, rifampin is a DRUG, CRIXIVAN is a BRAND, protease inhibitors is a GROUP, antiretroviral agents is a GROUP, HMG - CoA Reductase inhibitors is a GROUP, lovastatin is a DRUG, simvastatin is a DRUG, Protease inhibitor is a GROUP, atazanavir is a DRUG, CRIXIVAN is a BRAND, atazanavir is a DRUG, CRIXIVAN is a BRAND, atazanavir is a DRUG, HIV Antiviral Agents is a GROUP, Delavirdine is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, delavirdine is a DRUG, Didanosine is a DRUG, Indinavir is a DRUG, didanosine is a DRUG, Efavirenz is a DRUG, indinavir is a DRUG, indinavir is a DRUG, efavirenz is a DRUG, indinavir is a DRUG, indinavir is a DRUG, efavirenz is a DRUG, Nelfinavir is a DRUG, indinavir is a DRUG, Nevirapine is a DRUG, indinavir is a DRUG, Indinavir is a DRUG, nevirapine is a DRUG, Ritonavir is a DRUG, indinavir is a DRUG, ritonavir is a DRUG, indinavir is a DRUG, ritonavir is a DRUG, CRIXIVAN is a BRAND, Saquinavir is a DRUG, saquinavir is a DRUG, Antiarrhythmics is a GROUP, bepridil is a DRUG, lidocaine is a DRUG, quinidine is a DRUG, antiarrhythmic agents is a GROUP, antiarrhythmics is a GROUP, CRIXIVAN is a BRAND, Anticonvulsants is a GROUP, carbamazepine is a DRUG, phenobarbital is a DRUG, phenytoin is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, indinavir is a DRUG, Calcium Channel Blockers is a GROUP, Dihydropyridine is a GROUP, felodipine is a DRUG, nifedipine is a DRUG, nicardipine is a DRUG, dihydropyridine calcium channel blockers is a GROUP, Clarithromycin is a DRUG, clarithromycin is a DRUG, indinavir is a DRUG, HMG - CoA Reductase Inhibitor is a GROUP, atorvastatin is a DRUG, atorvastatin is a DRUG, atorvastatin is a DRUG, HMG - CoA reductase inhibitors is a GROUP, pravastatin is a DRUG, fluvastatin is a DRUG, rosuvastatin is a DRUG, CRIXIVAN is a BRAND, Immunosuppressants is a GROUP, cyclosporine is a DRUG, tacrolimus is a DRUG, sirolimus is a DRUG, immunosuppressant agents is a GROUP, CRIXIVAN is a BRAND, Itraconazole is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, itraconazole is a DRUG, Ketoconazole is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, Rifabutin is a DRUG, indinavir is a DRUG, rifabutin is a DRUG, rifabutin is a DRUG, CRIXIVAN is a BRAND, rifabutin is a DRUG, CRIXIVAN is a BRAND, Sildenafil is a DRUG, sildenafil is a DRUG, Sildenafil is a DRUG, indinavir is a DRUG, Tadalafil is a DRUG, tadalafil is a DRUG, Tadalafil is a DRUG, indinavir is a DRUG, Vardenafil is a DRUG, vardenafil is a DRUG, Vardenafil is a DRUG, indinavir is a DRUG | Indinavir_ddi_task0 | Sentence: Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease
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] | Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease | [
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"Comment",
"Antiarrhythmics",
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"amiodarone",
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"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
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"as",
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".",
"Ergot",
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":",
"dihydroergotamine",
",",
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",",
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"methylergonovine",
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"and",
"/",
"or",
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"-",
"threatening",
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"midazolam",
",",
"triazolam",
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"/",
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"-",
"threatening",
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"/",
"or",
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"-",
"threatening",
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"Neuroleptic",
":",
"pimozide",
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"/",
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"-",
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"Herbal",
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":",
"St",
".",
"John",
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"wort",
"(",
"Hypericum",
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"Antimycobacterial",
":",
"rifampin",
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"HMG",
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"lovastatin",
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"Potential",
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"Protease",
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"atazanavir",
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"(",
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"and",
"atazanavir",
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"not",
"recommended",
".",
"Table",
"9",
"Established",
"and",
"Other",
"Potentially",
"Significant",
"Drug",
"Interactions",
":",
"Alteration",
"in",
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"or",
"Regimen",
"May",
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"on",
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"Interaction",
"Studies",
"or",
"Predicted",
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"Name",
"Effect",
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"Antiviral",
"Agents",
"Delavirdine",
"indinavir",
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"Dose",
"reduction",
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"600",
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"400",
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"Didanosine",
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"Nelfinavir",
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",",
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"and",
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",",
"have",
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"The",
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"Ritonavir",
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"ritonavir",
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",",
"with",
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",",
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"Preliminary",
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"800",
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".",
"Saquinavir",
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",",
"with",
"respect",
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"safety",
",",
"have",
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"Other",
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"Antiarrhythmics",
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"bepridil",
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"(",
"systemic",
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".",
"Calcium",
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"Dihydropyridine",
":",
"e.g",
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",",
"felodipine",
",",
"nifedipine",
",",
"nicardipine",
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"Caution",
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".",
"Clarithromycin",
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" ",
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"doses",
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",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
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".",
"HMG",
"-",
"CoA",
"Reductase",
"Inhibitor",
":",
"atorvastatin",
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"lowest",
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"inhibitors",
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"Immunosuppressants",
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"cyclosporine",
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"tacrolimus",
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"sirolimus",
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"Plasma",
"concentrations",
"may",
"be",
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".",
"Itraconazole",
"indinavir",
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"Dose",
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"600",
"mg",
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"8",
"hours",
"is",
"recommended",
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".",
"Ketoconazole",
"indinavir",
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"Dose",
"reduction",
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"CRIXIVAN",
"to",
"600",
"mg",
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"8",
"hours",
"should",
"be",
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".",
"Rifabutin",
"indinavir",
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" ",
"rifabutin",
"concentration",
"Dose",
"reduction",
"of",
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"CRIXIVAN",
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"(",
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".",
"Sildenafil",
"sildenafil",
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"exceed",
"a",
"maximum",
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"25",
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"a",
"48-",
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"indinavir",
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".",
"Tadalafil",
"tadalafil",
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"72-",
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".",
"Vardenafil",
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".",
"Note",
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"=",
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";",
"=",
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] | [
"GROUP",
"DRUG",
"BRAND"
] |
Indinavir is a DRUG, CRIXIVAN is a BRAND, Indinavir is a DRUG, indinavir is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, indinavir is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, Antiarrhythmics is a GROUP, amiodarone is a DRUG, dihydroergotamine is a DRUG, ergonovine is a DRUG, ergotamine is a DRUG, methylergonovine is a DRUG, Sedative is a GROUP, hypnotics is a GROUP, midazolam is a DRUG, triazolam is a DRUG, cisapride is a DRUG, Neuroleptic is a GROUP, pimozide is a DRUG, CRIXIVAN is a BRAND, protease inhibitors is a GROUP, Antimycobacterial is a GROUP, rifampin is a DRUG, CRIXIVAN is a BRAND, protease inhibitors is a GROUP, antiretroviral agents is a GROUP, HMG - CoA Reductase inhibitors is a GROUP, lovastatin is a DRUG, simvastatin is a DRUG, Protease inhibitor is a GROUP, atazanavir is a DRUG, CRIXIVAN is a BRAND, atazanavir is a DRUG, CRIXIVAN is a BRAND, atazanavir is a DRUG, HIV Antiviral Agents is a GROUP, Delavirdine is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, delavirdine is a DRUG, Didanosine is a DRUG, Indinavir is a DRUG, didanosine is a DRUG, Efavirenz is a DRUG, indinavir is a DRUG, indinavir is a DRUG, efavirenz is a DRUG, indinavir is a DRUG, indinavir is a DRUG, efavirenz is a DRUG, Nelfinavir is a DRUG, indinavir is a DRUG, Nevirapine is a DRUG, indinavir is a DRUG, Indinavir is a DRUG, nevirapine is a DRUG, Ritonavir is a DRUG, indinavir is a DRUG, ritonavir is a DRUG, indinavir is a DRUG, ritonavir is a DRUG, CRIXIVAN is a BRAND, Saquinavir is a DRUG, saquinavir is a DRUG, Antiarrhythmics is a GROUP, bepridil is a DRUG, lidocaine is a DRUG, quinidine is a DRUG, antiarrhythmic agents is a GROUP, antiarrhythmics is a GROUP, CRIXIVAN is a BRAND, Anticonvulsants is a GROUP, carbamazepine is a DRUG, phenobarbital is a DRUG, phenytoin is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, indinavir is a DRUG, Calcium Channel Blockers is a GROUP, Dihydropyridine is a GROUP, felodipine is a DRUG, nifedipine is a DRUG, nicardipine is a DRUG, dihydropyridine calcium channel blockers is a GROUP, Clarithromycin is a DRUG, clarithromycin is a DRUG, indinavir is a DRUG, HMG - CoA Reductase Inhibitor is a GROUP, atorvastatin is a DRUG, atorvastatin is a DRUG, atorvastatin is a DRUG, HMG - CoA reductase inhibitors is a GROUP, pravastatin is a DRUG, fluvastatin is a DRUG, rosuvastatin is a DRUG, CRIXIVAN is a BRAND, Immunosuppressants is a GROUP, cyclosporine is a DRUG, tacrolimus is a DRUG, sirolimus is a DRUG, immunosuppressant agents is a GROUP, CRIXIVAN is a BRAND, Itraconazole is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, itraconazole is a DRUG, Ketoconazole is a DRUG, indinavir is a DRUG, CRIXIVAN is a BRAND, Rifabutin is a DRUG, indinavir is a DRUG, rifabutin is a DRUG, rifabutin is a DRUG, CRIXIVAN is a BRAND, rifabutin is a DRUG, CRIXIVAN is a BRAND, Sildenafil is a DRUG, sildenafil is a DRUG, Sildenafil is a DRUG, indinavir is a DRUG, Tadalafil is a DRUG, tadalafil is a DRUG, Tadalafil is a DRUG, indinavir is a DRUG, Vardenafil is a DRUG, vardenafil is a DRUG, Vardenafil is a DRUG, indinavir is a DRUG | Indinavir_ddi_task1 | Sentence: Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease
Instructions: please typing these entity words according to sentence: Indinavir, CRIXIVAN, Indinavir, indinavir, indinavir, CRIXIVAN, indinavir, indinavir, CRIXIVAN, Antiarrhythmics, amiodarone, dihydroergotamine, ergonovine, ergotamine, methylergonovine, Sedative, hypnotics, midazolam, triazolam, cisapride, Neuroleptic, pimozide, CRIXIVAN, protease inhibitors, Antimycobacterial, rifampin, CRIXIVAN, protease inhibitors, antiretroviral agents, HMG - CoA Reductase inhibitors, lovastatin, simvastatin, Protease inhibitor, atazanavir, CRIXIVAN, atazanavir, CRIXIVAN, atazanavir, HIV Antiviral Agents, Delavirdine, indinavir, CRIXIVAN, delavirdine, Didanosine, Indinavir, didanosine, Efavirenz, indinavir, indinavir, efavirenz, indinavir, indinavir, efavirenz, Nelfinavir, indinavir, Nevirapine, indinavir, Indinavir, nevirapine, Ritonavir, indinavir, ritonavir, indinavir, ritonavir, CRIXIVAN, Saquinavir, saquinavir, Antiarrhythmics, bepridil, lidocaine, quinidine, antiarrhythmic agents, antiarrhythmics, CRIXIVAN, Anticonvulsants, carbamazepine, phenobarbital, phenytoin, indinavir, CRIXIVAN, indinavir, Calcium Channel Blockers, Dihydropyridine, felodipine, nifedipine, nicardipine, dihydropyridine calcium channel blockers, Clarithromycin, clarithromycin, indinavir, HMG - CoA Reductase Inhibitor, atorvastatin, atorvastatin, atorvastatin, HMG - CoA reductase inhibitors, pravastatin, fluvastatin, rosuvastatin, CRIXIVAN, Immunosuppressants, cyclosporine, tacrolimus, sirolimus, immunosuppressant agents, CRIXIVAN, Itraconazole, indinavir, CRIXIVAN, itraconazole, Ketoconazole, indinavir, CRIXIVAN, Rifabutin, indinavir, rifabutin, rifabutin, CRIXIVAN, rifabutin, CRIXIVAN, Sildenafil, sildenafil, Sildenafil, indinavir, Tadalafil, tadalafil, Tadalafil, indinavir, Vardenafil, vardenafil, Vardenafil, indinavir
Options: GROUP, BRAND, DRUG
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"B-DRUG",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-DRUG",
"O",
"O",
"B-DRUG",
"B-DRUG",
"O",
"B-DRUG",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-DRUG",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O"
] | Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease | [
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".",
"Coadministration",
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",",
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"Drugs",
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"indinavir",
",",
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".",
"Coadministration",
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"CYP3A4",
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"indinavir",
"and",
"may",
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"in",
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"concentrations",
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"indinavir",
".",
"Table",
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"That",
"Should",
"Not",
"Be",
"Coadministered",
"with",
"CRIXIVAN",
"Drug",
"Class",
":",
"Drug",
"Name",
"Clinical",
"Comment",
"Antiarrhythmics",
":",
"amiodarone",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Ergot",
"derivatives",
":",
"dihydroergotamine",
",",
"ergonovine",
",",
"ergotamine",
",",
"methylergonovine",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"acute",
"ergot",
"toxicity",
"characterized",
"by",
"peripheral",
"vasospasm",
"and",
"ischemia",
"of",
"the",
"extremities",
"and",
"other",
"tissues",
".",
"Sedative",
"/",
"hypnotics",
":",
"midazolam",
",",
"triazolam",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"prolonged",
"or",
"increased",
"sedation",
"or",
"respiratory",
"depression",
".",
"GI",
"motility",
"agents",
":",
"cisapride",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Neuroleptic",
":",
"pimozide",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Herbal",
"products",
":",
"St",
".",
"John",
"s",
"wort",
"(",
"Hypericum",
"perforatum",
")",
"May",
"lead",
"to",
"loss",
"of",
"virologic",
"response",
"and",
"possible",
"resistance",
"to",
"CRIXIVAN",
"or",
"to",
"the",
"class",
"of",
"protease",
"inhibitors",
".",
"Antimycobacterial",
":",
"rifampin",
"May",
"lead",
"to",
"loss",
"of",
"virologic",
"response",
"and",
"possible",
"resistance",
"to",
"CRIXIVAN",
"or",
"to",
"the",
"class",
"of",
"protease",
"inhibitors",
"or",
"other",
"coadministered",
"antiretroviral",
"agents",
".",
"HMG",
"-",
"CoA",
"Reductase",
"inhibitors",
":",
"lovastatin",
",",
"simvastatin",
"Potential",
"for",
"serious",
"reactions",
"such",
"as",
"risk",
"of",
"myopathy",
"including",
"rhabdomyolysis",
".",
"Protease",
"inhibitor",
":",
"atazanavir",
"Both",
"CRIXIVAN",
"and",
"atazanavir",
"are",
"associated",
"with",
"indirect",
"(",
"unconjugated",
")",
"hyperbilirubinemia",
".",
"Combinations",
"of",
"these",
"drugs",
"have",
"not",
"been",
"studied",
"and",
"coadministration",
"of",
"CRIXIVAN",
"and",
"atazanavir",
"is",
"not",
"recommended",
".",
"Table",
"9",
"Established",
"and",
"Other",
"Potentially",
"Significant",
"Drug",
"Interactions",
":",
"Alteration",
"in",
"Dose",
"or",
"Regimen",
"May",
"Be",
"Recommended",
"Based",
"on",
"Drug",
"Interaction",
"Studies",
"or",
"Predicted",
"Interaction",
"Drug",
"Name",
"Effect",
"Clinical",
"Comment",
"HIV",
"Antiviral",
"Agents",
"Delavirdine",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"should",
"be",
"considered",
"when",
"taking",
"delavirdine",
"400",
"mg",
"three",
"times",
"a",
"day",
".",
"Didanosine",
"Indinavir",
"and",
"didanosine",
"formulations",
"containing",
"buffer",
"should",
"be",
"administered",
"at",
"least",
"one",
"hour",
"apart",
"on",
"an",
"empty",
"stomach",
".",
"Efavirenz",
"indinavir",
"concentration",
"The",
"optimal",
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"of",
"indinavir",
",",
"when",
"given",
"in",
"combination",
"with",
"efavirenz",
",",
"is",
"not",
"known",
".",
"Increasing",
"the",
"indinavir",
"dose",
"to",
"1000",
"mg",
"every",
"8",
"hours",
"does",
"not",
"compensate",
"for",
"the",
"increased",
"indinavir",
"metabolism",
"due",
"to",
"efavirenz",
".",
"Nelfinavir",
"indinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Nevirapine",
"indinavir",
"concentration",
"Indinavir",
"concentrations",
"may",
"be",
"decreased",
"in",
"the",
"presence",
"of",
"nevirapine",
".",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Ritonavir",
"indinavir",
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" ",
"ritonavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Preliminary",
"clinical",
"data",
"suggest",
"that",
"the",
"incidence",
"of",
"nephrolithiasis",
"is",
"higher",
"in",
"patients",
"receiving",
"indinavir",
"in",
"combination",
"with",
"ritonavir",
"than",
"those",
"receiving",
"CRIXIVAN",
"800",
"mg",
"q8h",
".",
"Saquinavir",
"saquinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Other",
"Agents",
"Antiarrhythmics",
":",
"bepridil",
",",
"lidocaine",
"(",
"systemic",
")",
"and",
"quinidine",
"antiarrhythmic",
"agents",
"concentration",
"Caution",
"is",
"warranted",
"and",
"therapeutic",
"concentration",
"monitoring",
"is",
"recommended",
"for",
"antiarrhythmics",
"when",
"coadministered",
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".",
"Anticonvulsants",
":",
"carbamazepine",
",",
"phenobarbital",
",",
"phenytoin",
"indinavir",
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"Use",
"with",
"caution",
".",
"CRIXIVAN",
"may",
"not",
"be",
"effective",
"due",
"to",
"decreased",
"indinavir",
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"in",
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"taking",
"these",
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"concomitantly",
".",
"Calcium",
"Channel",
"Blockers",
",",
"Dihydropyridine",
":",
"e.g",
".",
",",
"felodipine",
",",
"nifedipine",
",",
"nicardipine",
"dihydropyridine",
"calcium",
"channel",
"blockers",
"concentration",
"Caution",
"is",
"warranted",
"and",
"clinical",
"monitoring",
"of",
"patients",
"is",
"recommended",
".",
"Clarithromycin",
"clarithromycin",
"concentration",
" ",
"indinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"HMG",
"-",
"CoA",
"Reductase",
"Inhibitor",
":",
"atorvastatin",
"atorvastatin",
"concentration",
"Use",
"lowest",
"possible",
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"with",
"careful",
"monitoring",
",",
"or",
"consider",
"HMG",
"-",
"CoA",
"reductase",
"inhibitors",
"that",
"are",
"not",
"primarily",
"metabolized",
"by",
"CYP3A4",
",",
"such",
"as",
"pravastatin",
",",
"fluvastatin",
",",
"or",
"rosuvastatin",
"in",
"combination",
"with",
"CRIXIVAN",
".",
"Immunosuppressants",
":",
"cyclosporine",
",",
"tacrolimus",
",",
"sirolimus",
"immunosuppressant",
"agents",
"concentration",
"Plasma",
"concentrations",
"may",
"be",
"increased",
"by",
"CRIXIVAN",
".",
"Itraconazole",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"is",
"recommended",
"when",
"administering",
"itraconazole",
"concurrently",
".",
"Ketoconazole",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"should",
"be",
"considered",
".",
"Rifabutin",
"indinavir",
"concentration",
" ",
"rifabutin",
"concentration",
"Dose",
"reduction",
"of",
"rifabutin",
"to",
"half",
"the",
"standard",
"dose",
"and",
"a",
"dose",
"increase",
"of",
"CRIXIVAN",
"to",
"1000",
"mg",
"(",
"three",
"333-mg",
"capsules",
")",
"every",
"8",
"hours",
"are",
"recommended",
"when",
"rifabutin",
"and",
"CRIXIVAN",
"are",
"coadministered",
".",
"Sildenafil",
"sildenafil",
"concentration",
"Sildenafil",
"dose",
"should",
"not",
"exceed",
"a",
"maximum",
"of",
"25",
"mg",
"in",
"a",
"48-",
"hour",
"period",
"in",
"patients",
"receiving",
"concomitant",
"indinavir",
"therapy",
".",
"Tadalafil",
"tadalafil",
"concentration",
"Tadalafil",
"dose",
"should",
"not",
"exceed",
"a",
"maximum",
"of",
"10",
"mg",
"in",
"a",
"72-",
"hour",
"period",
"in",
"patients",
"receiving",
"concomitant",
"indinavir",
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".",
"Vardenafil",
"vardenafil",
"concentration",
"Vardenafil",
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"not",
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"a",
"maximum",
"of",
"2.5",
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"a",
"24-hour",
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"in",
"patients",
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"concomitant",
"indinavir",
"therapy",
".",
"Note",
":",
"=",
"increase",
";",
"=",
"decrease"
] | [
"GROUP",
"DRUG",
"BRAND"
] |
Indinavir, CRIXIVAN, Indinavir, indinavir, indinavir, CRIXIVAN, indinavir, indinavir, CRIXIVAN, Antiarrhythmics, amiodarone, dihydroergotamine, ergonovine, ergotamine, methylergonovine, Sedative, hypnotics, midazolam, triazolam, cisapride, Neuroleptic, pimozide, CRIXIVAN, protease inhibitors, Antimycobacterial, rifampin, CRIXIVAN, protease inhibitors, antiretroviral agents, HMG - CoA Reductase inhibitors, lovastatin, simvastatin, Protease inhibitor, atazanavir, CRIXIVAN, atazanavir, CRIXIVAN, atazanavir, HIV Antiviral Agents, Delavirdine, indinavir, CRIXIVAN, delavirdine, Didanosine, Indinavir, didanosine, Efavirenz, indinavir, indinavir, efavirenz, indinavir, indinavir, efavirenz, Nelfinavir, indinavir, Nevirapine, indinavir, Indinavir, nevirapine, Ritonavir, indinavir, ritonavir, indinavir, ritonavir, CRIXIVAN, Saquinavir, saquinavir, Antiarrhythmics, bepridil, lidocaine, quinidine, antiarrhythmic agents, antiarrhythmics, CRIXIVAN, Anticonvulsants, carbamazepine, phenobarbital, phenytoin, indinavir, CRIXIVAN, indinavir, Calcium Channel Blockers, Dihydropyridine, felodipine, nifedipine, nicardipine, dihydropyridine calcium channel blockers, Clarithromycin, clarithromycin, indinavir, HMG - CoA Reductase Inhibitor, atorvastatin, atorvastatin, atorvastatin, HMG - CoA reductase inhibitors, pravastatin, fluvastatin, rosuvastatin, CRIXIVAN, Immunosuppressants, cyclosporine, tacrolimus, sirolimus, immunosuppressant agents, CRIXIVAN, Itraconazole, indinavir, CRIXIVAN, itraconazole, Ketoconazole, indinavir, CRIXIVAN, Rifabutin, indinavir, rifabutin, rifabutin, CRIXIVAN, rifabutin, CRIXIVAN, Sildenafil, sildenafil, Sildenafil, indinavir, Tadalafil, tadalafil, Tadalafil, indinavir, Vardenafil, vardenafil, Vardenafil, indinavir | Indinavir_ddi_task2 | Sentence: Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease
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] | Indinavir is an inhibitor of the cytochrome P450 isoform CYP3A4. Coadministration of CRIXIVAN and drugs primarily metabolized by CYP3A4 may result in increased plasma concentrations of the other drug, which could increase or prolong its therapeutic and adverse effects. Indinavir is metabolized by CYP3A4. Drugs that induce CYP3A4 activity would be expected to increase the clearance of indinavir, resulting in lowered plasma concentrations of indinavir. Coadministration of CRIXIVAN and other drugs that inhibit CYP3A4 may decrease the clearance of indinavir and may result in increased plasma concentrations of indinavir. Table 8 Drugs That Should Not Be Coadministered with CRIXIVAN Drug Class: Drug Name Clinical Comment Antiarrhythmics: amiodarone CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as acute ergot toxicity characterized by peripheral vasospasm and ischemia of the extremities and other tissues. Sedative/hypnotics: midazolam, triazolam CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as prolonged or increased sedation or respiratory depression. GI motility agents: cisapride CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Neuroleptic: pimozide CONTRAINDICATED due to potential for serious and/or life-threatening reactions such as cardiac arrhythmias. Herbal products: St. John s wort (Hypericum perforatum) May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors. Antimycobacterial: rifampin May lead to loss of virologic response and possible resistance to CRIXIVAN or to the class of protease inhibitors or other coadministered antiretroviral agents. HMG-CoA Reductase inhibitors: lovastatin, simvastatin Potential for serious reactions such as risk of myopathy including rhabdomyolysis. Protease inhibitor: atazanavir Both CRIXIVAN and atazanavir are associated with indirect (unconjugated) hyperbilirubinemia. Combinations of these drugs have not been studied and coadministration of CRIXIVAN and atazanavir is not recommended. Table 9 Established and Other Potentially Significant Drug Interactions: Alteration in Dose or Regimen May Be Recommended Based on Drug Interaction Studies or Predicted Interaction Drug Name Effect Clinical Comment HIV Antiviral Agents Delavirdine indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered when taking delavirdine 400 mg three times a day. Didanosine Indinavir and didanosine formulations containing buffer should be administered at least one hour apart on an empty stomach. Efavirenz indinavir concentration The optimal dose of indinavir, when given in combination with efavirenz, is not known. Increasing the indinavir dose to 1000 mg every 8 hours does not compensate for the increased indinavir metabolism due to efavirenz. Nelfinavir indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Nevirapine indinavir concentration Indinavir concentrations may be decreased in the presence of nevirapine. The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Ritonavir indinavir concentration ritonavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Preliminary clinical data suggest that the incidence of nephrolithiasis is higher in patients receiving indinavir in combination with ritonavir than those receiving CRIXIVAN 800 mg q8h. Saquinavir saquinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. Other Agents Antiarrhythmics: bepridil, lidocaine (systemic) and quinidine antiarrhythmic agents concentration Caution is warranted and therapeutic concentration monitoring is recommended for antiarrhythmics when coadministered with CRIXIVAN. Anticonvulsants: carbamazepine, phenobarbital, phenytoin indinavir concentration Use with caution. CRIXIVAN may not be effective due to decreased indinavir concentrations in patients taking these agents concomitantly. Calcium Channel Blockers, Dihydropyridine: e.g., felodipine, nifedipine, nicardipine dihydropyridine calcium channel blockers concentration Caution is warranted and clinical monitoring of patients is recommended. Clarithromycin clarithromycin concentration indinavir concentration The appropriate doses for this combination, with respect to efficacy and safety, have not been established. HMG-CoA Reductase Inhibitor: atorvastatin atorvastatin concentration Use lowest possible dose of atorvastatin with careful monitoring, or consider HMG-CoA reductase inhibitors that are not primarily metabolized by CYP3A4, such as pravastatin, fluvastatin, or rosuvastatin in combination with CRIXIVAN. Immunosuppressants: cyclosporine, tacrolimus, sirolimus immunosuppressant agents concentration Plasma concentrations may be increased by CRIXIVAN. Itraconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours is recommended when administering itraconazole concurrently. Ketoconazole indinavir concentration Dose reduction of CRIXIVAN to 600 mg every 8 hours should be considered. Rifabutin indinavir concentration rifabutin concentration Dose reduction of rifabutin to half the standard dose and a dose increase of CRIXIVAN to 1000 mg (three 333-mg capsules) every 8 hours are recommended when rifabutin and CRIXIVAN are coadministered. Sildenafil sildenafil concentration Sildenafil dose should not exceed a maximum of 25 mg in a 48- hour period in patients receiving concomitant indinavir therapy. Tadalafil tadalafil concentration Tadalafil dose should not exceed a maximum of 10 mg in a 72- hour period in patients receiving concomitant indinavir therapy. Vardenafil vardenafil concentration Vardenafil dose should not exceed a maximum of 2.5 mg in a 24-hour period in patients receiving concomitant indinavir therapy. Note: = increase; = decrease | [
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"metabolized",
"by",
"CYP3A4",
"may",
"result",
"in",
"increased",
"plasma",
"concentrations",
"of",
"the",
"other",
"drug",
",",
"which",
"could",
"increase",
"or",
"prolong",
"its",
"therapeutic",
"and",
"adverse",
"effects",
".",
"Indinavir",
"is",
"metabolized",
"by",
"CYP3A4",
".",
"Drugs",
"that",
"induce",
"CYP3A4",
"activity",
"would",
"be",
"expected",
"to",
"increase",
"the",
"clearance",
"of",
"indinavir",
",",
"resulting",
"in",
"lowered",
"plasma",
"concentrations",
"of",
"indinavir",
".",
"Coadministration",
"of",
"CRIXIVAN",
"and",
"other",
"drugs",
"that",
"inhibit",
"CYP3A4",
"may",
"decrease",
"the",
"clearance",
"of",
"indinavir",
"and",
"may",
"result",
"in",
"increased",
"plasma",
"concentrations",
"of",
"indinavir",
".",
"Table",
"8",
"Drugs",
"That",
"Should",
"Not",
"Be",
"Coadministered",
"with",
"CRIXIVAN",
"Drug",
"Class",
":",
"Drug",
"Name",
"Clinical",
"Comment",
"Antiarrhythmics",
":",
"amiodarone",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Ergot",
"derivatives",
":",
"dihydroergotamine",
",",
"ergonovine",
",",
"ergotamine",
",",
"methylergonovine",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"acute",
"ergot",
"toxicity",
"characterized",
"by",
"peripheral",
"vasospasm",
"and",
"ischemia",
"of",
"the",
"extremities",
"and",
"other",
"tissues",
".",
"Sedative",
"/",
"hypnotics",
":",
"midazolam",
",",
"triazolam",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"prolonged",
"or",
"increased",
"sedation",
"or",
"respiratory",
"depression",
".",
"GI",
"motility",
"agents",
":",
"cisapride",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Neuroleptic",
":",
"pimozide",
"CONTRAINDICATED",
"due",
"to",
"potential",
"for",
"serious",
"and",
"/",
"or",
"life",
"-",
"threatening",
"reactions",
"such",
"as",
"cardiac",
"arrhythmias",
".",
"Herbal",
"products",
":",
"St",
".",
"John",
"s",
"wort",
"(",
"Hypericum",
"perforatum",
")",
"May",
"lead",
"to",
"loss",
"of",
"virologic",
"response",
"and",
"possible",
"resistance",
"to",
"CRIXIVAN",
"or",
"to",
"the",
"class",
"of",
"protease",
"inhibitors",
".",
"Antimycobacterial",
":",
"rifampin",
"May",
"lead",
"to",
"loss",
"of",
"virologic",
"response",
"and",
"possible",
"resistance",
"to",
"CRIXIVAN",
"or",
"to",
"the",
"class",
"of",
"protease",
"inhibitors",
"or",
"other",
"coadministered",
"antiretroviral",
"agents",
".",
"HMG",
"-",
"CoA",
"Reductase",
"inhibitors",
":",
"lovastatin",
",",
"simvastatin",
"Potential",
"for",
"serious",
"reactions",
"such",
"as",
"risk",
"of",
"myopathy",
"including",
"rhabdomyolysis",
".",
"Protease",
"inhibitor",
":",
"atazanavir",
"Both",
"CRIXIVAN",
"and",
"atazanavir",
"are",
"associated",
"with",
"indirect",
"(",
"unconjugated",
")",
"hyperbilirubinemia",
".",
"Combinations",
"of",
"these",
"drugs",
"have",
"not",
"been",
"studied",
"and",
"coadministration",
"of",
"CRIXIVAN",
"and",
"atazanavir",
"is",
"not",
"recommended",
".",
"Table",
"9",
"Established",
"and",
"Other",
"Potentially",
"Significant",
"Drug",
"Interactions",
":",
"Alteration",
"in",
"Dose",
"or",
"Regimen",
"May",
"Be",
"Recommended",
"Based",
"on",
"Drug",
"Interaction",
"Studies",
"or",
"Predicted",
"Interaction",
"Drug",
"Name",
"Effect",
"Clinical",
"Comment",
"HIV",
"Antiviral",
"Agents",
"Delavirdine",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"should",
"be",
"considered",
"when",
"taking",
"delavirdine",
"400",
"mg",
"three",
"times",
"a",
"day",
".",
"Didanosine",
"Indinavir",
"and",
"didanosine",
"formulations",
"containing",
"buffer",
"should",
"be",
"administered",
"at",
"least",
"one",
"hour",
"apart",
"on",
"an",
"empty",
"stomach",
".",
"Efavirenz",
"indinavir",
"concentration",
"The",
"optimal",
"dose",
"of",
"indinavir",
",",
"when",
"given",
"in",
"combination",
"with",
"efavirenz",
",",
"is",
"not",
"known",
".",
"Increasing",
"the",
"indinavir",
"dose",
"to",
"1000",
"mg",
"every",
"8",
"hours",
"does",
"not",
"compensate",
"for",
"the",
"increased",
"indinavir",
"metabolism",
"due",
"to",
"efavirenz",
".",
"Nelfinavir",
"indinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Nevirapine",
"indinavir",
"concentration",
"Indinavir",
"concentrations",
"may",
"be",
"decreased",
"in",
"the",
"presence",
"of",
"nevirapine",
".",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Ritonavir",
"indinavir",
"concentration",
" ",
"ritonavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Preliminary",
"clinical",
"data",
"suggest",
"that",
"the",
"incidence",
"of",
"nephrolithiasis",
"is",
"higher",
"in",
"patients",
"receiving",
"indinavir",
"in",
"combination",
"with",
"ritonavir",
"than",
"those",
"receiving",
"CRIXIVAN",
"800",
"mg",
"q8h",
".",
"Saquinavir",
"saquinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"Other",
"Agents",
"Antiarrhythmics",
":",
"bepridil",
",",
"lidocaine",
"(",
"systemic",
")",
"and",
"quinidine",
"antiarrhythmic",
"agents",
"concentration",
"Caution",
"is",
"warranted",
"and",
"therapeutic",
"concentration",
"monitoring",
"is",
"recommended",
"for",
"antiarrhythmics",
"when",
"coadministered",
"with",
"CRIXIVAN",
".",
"Anticonvulsants",
":",
"carbamazepine",
",",
"phenobarbital",
",",
"phenytoin",
"indinavir",
"concentration",
"Use",
"with",
"caution",
".",
"CRIXIVAN",
"may",
"not",
"be",
"effective",
"due",
"to",
"decreased",
"indinavir",
"concentrations",
"in",
"patients",
"taking",
"these",
"agents",
"concomitantly",
".",
"Calcium",
"Channel",
"Blockers",
",",
"Dihydropyridine",
":",
"e.g",
".",
",",
"felodipine",
",",
"nifedipine",
",",
"nicardipine",
"dihydropyridine",
"calcium",
"channel",
"blockers",
"concentration",
"Caution",
"is",
"warranted",
"and",
"clinical",
"monitoring",
"of",
"patients",
"is",
"recommended",
".",
"Clarithromycin",
"clarithromycin",
"concentration",
" ",
"indinavir",
"concentration",
"The",
"appropriate",
"doses",
"for",
"this",
"combination",
",",
"with",
"respect",
"to",
"efficacy",
"and",
"safety",
",",
"have",
"not",
"been",
"established",
".",
"HMG",
"-",
"CoA",
"Reductase",
"Inhibitor",
":",
"atorvastatin",
"atorvastatin",
"concentration",
"Use",
"lowest",
"possible",
"dose",
"of",
"atorvastatin",
"with",
"careful",
"monitoring",
",",
"or",
"consider",
"HMG",
"-",
"CoA",
"reductase",
"inhibitors",
"that",
"are",
"not",
"primarily",
"metabolized",
"by",
"CYP3A4",
",",
"such",
"as",
"pravastatin",
",",
"fluvastatin",
",",
"or",
"rosuvastatin",
"in",
"combination",
"with",
"CRIXIVAN",
".",
"Immunosuppressants",
":",
"cyclosporine",
",",
"tacrolimus",
",",
"sirolimus",
"immunosuppressant",
"agents",
"concentration",
"Plasma",
"concentrations",
"may",
"be",
"increased",
"by",
"CRIXIVAN",
".",
"Itraconazole",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"is",
"recommended",
"when",
"administering",
"itraconazole",
"concurrently",
".",
"Ketoconazole",
"indinavir",
"concentration",
"Dose",
"reduction",
"of",
"CRIXIVAN",
"to",
"600",
"mg",
"every",
"8",
"hours",
"should",
"be",
"considered",
".",
"Rifabutin",
"indinavir",
"concentration",
" ",
"rifabutin",
"concentration",
"Dose",
"reduction",
"of",
"rifabutin",
"to",
"half",
"the",
"standard",
"dose",
"and",
"a",
"dose",
"increase",
"of",
"CRIXIVAN",
"to",
"1000",
"mg",
"(",
"three",
"333-mg",
"capsules",
")",
"every",
"8",
"hours",
"are",
"recommended",
"when",
"rifabutin",
"and",
"CRIXIVAN",
"are",
"coadministered",
".",
"Sildenafil",
"sildenafil",
"concentration",
"Sildenafil",
"dose",
"should",
"not",
"exceed",
"a",
"maximum",
"of",
"25",
"mg",
"in",
"a",
"48-",
"hour",
"period",
"in",
"patients",
"receiving",
"concomitant",
"indinavir",
"therapy",
".",
"Tadalafil",
"tadalafil",
"concentration",
"Tadalafil",
"dose",
"should",
"not",
"exceed",
"a",
"maximum",
"of",
"10",
"mg",
"in",
"a",
"72-",
"hour",
"period",
"in",
"patients",
"receiving",
"concomitant",
"indinavir",
"therapy",
".",
"Vardenafil",
"vardenafil",
"concentration",
"Vardenafil",
"dose",
"should",
"not",
"exceed",
"a",
"maximum",
"of",
"2.5",
"mg",
"in",
"a",
"24-hour",
"period",
"in",
"patients",
"receiving",
"concomitant",
"indinavir",
"therapy",
".",
"Note",
":",
"=",
"increase",
";",
"=",
"decrease"
] | [
"GROUP",
"DRUG",
"BRAND"
] |
enterostatin intake is a Intervention_Pharmacological, food intake and energy expenditure . is a Outcome_Physical, Enterostatin ( ENT ) is a Intervention_Pharmacological, fat intake is a Participant_Condition, rats is a Participant_Condition, body weight is a Outcome_Physical, subjects with a preference for a high - fat diet . is a Participant_Condition, placebo - controlled is a Intervention_Control, nine is a Participant_Sample-size, female is a Participant_Sex, three is a Participant_Sample-size, age 34 ( sd 11 ) is a Participant_Age, high - fat diet ingested ENT is a Intervention_Pharmacological, placebo ( PLA ) is a Intervention_Control, consuming a high - fat diet ad libitum is a Intervention_Pharmacological, Body - weight loss is a Outcome_Physical, total energy intake is a Outcome_Physical, macronutrient composition , hunger , satiety and hedonic scores is a Outcome_Physical, Energy expenditure is a Outcome_Other, sleeping and resting metabolic rate , diet - induced thermogenesis , activity - induced energy expenditure and 24 h RQ is a Outcome_Physical | 13432_task0 | Sentence: The effects of enterostatin intake on food intake and energy expenditure . Enterostatin ( ENT ) has been found to inhibit food intake and selectively inhibit fat intake in rats . Both peripheral and central mechanisms have been proposed . It also has been suggested that ENT may increase thermogenesis . The present study investigated the effects of oral ENT administration on food intake , energy expenditure and body weight in subjects with a preference for a high-fat diet . In a double-blind , placebo-controlled , randomized and crossover design , nine female and three male healthy subjects ( age 34 ( sd 11 ) years , BMI 24.5 ( sd 2.5 ) kg/m ( 2 ) ) with a preference for a high-fat diet ingested ENT ( 3 x 15 mg/d ) or placebo ( PLA ) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber , continuing the diet and treatment . Body-weight loss was significant ( ENT 0.8 ( se 0.3 ) kg , P < 0.05 ; PLA 1.3 ( se 0.3 ) kg , P < 0.001 ) , but not different between treatments . There was no difference between treatments in total energy intake ( ENT 37.1 ( se 2.6 ) , PLA 35.9 ( se 3.2 ) MJ ) , macronutrient composition , hunger , satiety and hedonic scores during the 4 d high-fat diet . Energy expenditure ( 24 h ) ( ENT 9.6 ( se 0.4 ) , PLA 9.5 ( se 0.4 ) MJ ) , sleeping and resting metabolic rate , diet-induced thermogenesis , activity-induced energy expenditure and 24 h RQ ( ENT 0.77 ( se 0.01 ) , PLA 0.77 ( se 0.01 ) ) were similar for both treatments . We conclude that oral ENT administration did not affect food intake , energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance .
Instructions: please extract entities and their types from the input sentence, all entity types are in options
Options: Intervention_Pharmacological, Intervention_Control, Participant_Condition, Participant_Sex, Outcome_Physical, Participant_Age, Participant_Sample-size, Outcome_Other
| [
"O",
"O",
"O",
"B-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"B-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Participant_Condition",
"I-Participant_Condition",
"O",
"B-Participant_Condition",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"O",
"B-Participant_Condition",
"I-Participant_Condition",
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"O",
"O",
"O",
"O",
"O",
"O",
"B-Intervention_Control",
"I-Intervention_Control",
"I-Intervention_Control",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Participant_Sample-size",
"B-Participant_Sex",
"O",
"B-Participant_Sample-size",
"O",
"O",
"O",
"O",
"B-Participant_Age",
"I-Participant_Age",
"I-Participant_Age",
"I-Participant_Age",
"I-Participant_Age",
"I-Participant_Age",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Intervention_Control",
"I-Intervention_Control",
"I-Intervention_Control",
"I-Intervention_Control",
"O",
"B-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"I-Intervention_Pharmacological",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Other",
"I-Outcome_Other",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"B-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"I-Outcome_Physical",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
"O",
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] | The effects of enterostatin intake on food intake and energy expenditure . Enterostatin ( ENT ) has been found to inhibit food intake and selectively inhibit fat intake in rats . Both peripheral and central mechanisms have been proposed . It also has been suggested that ENT may increase thermogenesis . The present study investigated the effects of oral ENT administration on food intake , energy expenditure and body weight in subjects with a preference for a high-fat diet . In a double-blind , placebo-controlled , randomized and crossover design , nine female and three male healthy subjects ( age 34 ( sd 11 ) years , BMI 24.5 ( sd 2.5 ) kg/m ( 2 ) ) with a preference for a high-fat diet ingested ENT ( 3 x 15 mg/d ) or placebo ( PLA ) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber , continuing the diet and treatment . Body-weight loss was significant ( ENT 0.8 ( se 0.3 ) kg , P < 0.05 ; PLA 1.3 ( se 0.3 ) kg , P < 0.001 ) , but not different between treatments . There was no difference between treatments in total energy intake ( ENT 37.1 ( se 2.6 ) , PLA 35.9 ( se 3.2 ) MJ ) , macronutrient composition , hunger , satiety and hedonic scores during the 4 d high-fat diet . Energy expenditure ( 24 h ) ( ENT 9.6 ( se 0.4 ) , PLA 9.5 ( se 0.4 ) MJ ) , sleeping and resting metabolic rate , diet-induced thermogenesis , activity-induced energy expenditure and 24 h RQ ( ENT 0.77 ( se 0.01 ) , PLA 0.77 ( se 0.01 ) ) were similar for both treatments . We conclude that oral ENT administration did not affect food intake , energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance . | [
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enterostatin intake is a Intervention_Pharmacological, food intake and energy expenditure . is a Outcome_Physical, Enterostatin ( ENT ) is a Intervention_Pharmacological, fat intake is a Participant_Condition, rats is a Participant_Condition, body weight is a Outcome_Physical, subjects with a preference for a high - fat diet . is a Participant_Condition, placebo - controlled is a Intervention_Control, nine is a Participant_Sample-size, female is a Participant_Sex, three is a Participant_Sample-size, age 34 ( sd 11 ) is a Participant_Age, high - fat diet ingested ENT is a Intervention_Pharmacological, placebo ( PLA ) is a Intervention_Control, consuming a high - fat diet ad libitum is a Intervention_Pharmacological, Body - weight loss is a Outcome_Physical, total energy intake is a Outcome_Physical, macronutrient composition , hunger , satiety and hedonic scores is a Outcome_Physical, Energy expenditure is a Outcome_Other, sleeping and resting metabolic rate , diet - induced thermogenesis , activity - induced energy expenditure and 24 h RQ is a Outcome_Physical | 13432_task1 | Sentence: The effects of enterostatin intake on food intake and energy expenditure . Enterostatin ( ENT ) has been found to inhibit food intake and selectively inhibit fat intake in rats . Both peripheral and central mechanisms have been proposed . It also has been suggested that ENT may increase thermogenesis . The present study investigated the effects of oral ENT administration on food intake , energy expenditure and body weight in subjects with a preference for a high-fat diet . In a double-blind , placebo-controlled , randomized and crossover design , nine female and three male healthy subjects ( age 34 ( sd 11 ) years , BMI 24.5 ( sd 2.5 ) kg/m ( 2 ) ) with a preference for a high-fat diet ingested ENT ( 3 x 15 mg/d ) or placebo ( PLA ) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber , continuing the diet and treatment . Body-weight loss was significant ( ENT 0.8 ( se 0.3 ) kg , P < 0.05 ; PLA 1.3 ( se 0.3 ) kg , P < 0.001 ) , but not different between treatments . There was no difference between treatments in total energy intake ( ENT 37.1 ( se 2.6 ) , PLA 35.9 ( se 3.2 ) MJ ) , macronutrient composition , hunger , satiety and hedonic scores during the 4 d high-fat diet . Energy expenditure ( 24 h ) ( ENT 9.6 ( se 0.4 ) , PLA 9.5 ( se 0.4 ) MJ ) , sleeping and resting metabolic rate , diet-induced thermogenesis , activity-induced energy expenditure and 24 h RQ ( ENT 0.77 ( se 0.01 ) , PLA 0.77 ( se 0.01 ) ) were similar for both treatments . We conclude that oral ENT administration did not affect food intake , energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance .
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enterostatin intake, food intake and energy expenditure ., Enterostatin ( ENT ), fat intake, rats, body weight, subjects with a preference for a high - fat diet ., placebo - controlled, nine, female, three, age 34 ( sd 11 ), high - fat diet ingested ENT, placebo ( PLA ), consuming a high - fat diet ad libitum, Body - weight loss, total energy intake, macronutrient composition , hunger , satiety and hedonic scores, Energy expenditure, sleeping and resting metabolic rate , diet - induced thermogenesis , activity - induced energy expenditure and 24 h RQ | 13432_task2 | Sentence: The effects of enterostatin intake on food intake and energy expenditure . Enterostatin ( ENT ) has been found to inhibit food intake and selectively inhibit fat intake in rats . Both peripheral and central mechanisms have been proposed . It also has been suggested that ENT may increase thermogenesis . The present study investigated the effects of oral ENT administration on food intake , energy expenditure and body weight in subjects with a preference for a high-fat diet . In a double-blind , placebo-controlled , randomized and crossover design , nine female and three male healthy subjects ( age 34 ( sd 11 ) years , BMI 24.5 ( sd 2.5 ) kg/m ( 2 ) ) with a preference for a high-fat diet ingested ENT ( 3 x 15 mg/d ) or placebo ( PLA ) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber , continuing the diet and treatment . Body-weight loss was significant ( ENT 0.8 ( se 0.3 ) kg , P < 0.05 ; PLA 1.3 ( se 0.3 ) kg , P < 0.001 ) , but not different between treatments . There was no difference between treatments in total energy intake ( ENT 37.1 ( se 2.6 ) , PLA 35.9 ( se 3.2 ) MJ ) , macronutrient composition , hunger , satiety and hedonic scores during the 4 d high-fat diet . Energy expenditure ( 24 h ) ( ENT 9.6 ( se 0.4 ) , PLA 9.5 ( se 0.4 ) MJ ) , sleeping and resting metabolic rate , diet-induced thermogenesis , activity-induced energy expenditure and 24 h RQ ( ENT 0.77 ( se 0.01 ) , PLA 0.77 ( se 0.01 ) ) were similar for both treatments . We conclude that oral ENT administration did not affect food intake , energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance .
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] | The effects of enterostatin intake on food intake and energy expenditure . Enterostatin ( ENT ) has been found to inhibit food intake and selectively inhibit fat intake in rats . Both peripheral and central mechanisms have been proposed . It also has been suggested that ENT may increase thermogenesis . The present study investigated the effects of oral ENT administration on food intake , energy expenditure and body weight in subjects with a preference for a high-fat diet . In a double-blind , placebo-controlled , randomized and crossover design , nine female and three male healthy subjects ( age 34 ( sd 11 ) years , BMI 24.5 ( sd 2.5 ) kg/m ( 2 ) ) with a preference for a high-fat diet ingested ENT ( 3 x 15 mg/d ) or placebo ( PLA ) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber , continuing the diet and treatment . Body-weight loss was significant ( ENT 0.8 ( se 0.3 ) kg , P < 0.05 ; PLA 1.3 ( se 0.3 ) kg , P < 0.001 ) , but not different between treatments . There was no difference between treatments in total energy intake ( ENT 37.1 ( se 2.6 ) , PLA 35.9 ( se 3.2 ) MJ ) , macronutrient composition , hunger , satiety and hedonic scores during the 4 d high-fat diet . Energy expenditure ( 24 h ) ( ENT 9.6 ( se 0.4 ) , PLA 9.5 ( se 0.4 ) MJ ) , sleeping and resting metabolic rate , diet-induced thermogenesis , activity-induced energy expenditure and 24 h RQ ( ENT 0.77 ( se 0.01 ) , PLA 0.77 ( se 0.01 ) ) were similar for both treatments . We conclude that oral ENT administration did not affect food intake , energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance . | [
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patients is an umlsterm, myelomeningocele is an umlsterm, hydrocephalus is an umlsterm, growth hormone is an umlsterm, deficiency is an umlsterm, dysfunction is an umlsterm, patients is an umlsterm, human growth hormone is an umlsterm, age is an umlsterm, growth is an umlsterm, bone is an umlsterm, age is an umlsterm, arm is an umlsterm, IGFBP-3 is an umlsterm, growth hormone is an umlsterm, therapy is an umlsterm, patients is an umlsterm, growth is an umlsterm, arm is an umlsterm, scoliosis is an umlsterm, deformity is an umlsterm, syringomyelia is an umlsterm | MonatsschriftKinderheilkunde.91470255.eng.abstr_task0 | Sentence: We report on two patients with myelomeningocele and hydrocephalus in whom hypothalamo-pituitary growth hormone deficiency and neurosecretory dysfunction were diagnosed . The patients were treated with human growth hormone ( 0.5-0.7 IU/ kg/week ) since the age of 4.2 and 8.7 years . Short stature , retarded growth velocity , retarded bone age , reduced arm span and low IGF1 and IGFBP-3 serum levels were found . During growth hormone therapy ( duration : 24-33 months ) patients improved in growth velocity , supine length and arm span . In one girl with thoraco-lumbar scoliosis a rapid progression of the deformity developed . Tethered cord and syringomyelia were present .
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patients is an umlsterm, myelomeningocele is an umlsterm, hydrocephalus is an umlsterm, growth hormone is an umlsterm, deficiency is an umlsterm, dysfunction is an umlsterm, patients is an umlsterm, human growth hormone is an umlsterm, age is an umlsterm, growth is an umlsterm, bone is an umlsterm, age is an umlsterm, arm is an umlsterm, IGFBP-3 is an umlsterm, growth hormone is an umlsterm, therapy is an umlsterm, patients is an umlsterm, growth is an umlsterm, arm is an umlsterm, scoliosis is an umlsterm, deformity is an umlsterm, syringomyelia is an umlsterm | MonatsschriftKinderheilkunde.91470255.eng.abstr_task1 | Sentence: We report on two patients with myelomeningocele and hydrocephalus in whom hypothalamo-pituitary growth hormone deficiency and neurosecretory dysfunction were diagnosed . The patients were treated with human growth hormone ( 0.5-0.7 IU/ kg/week ) since the age of 4.2 and 8.7 years . Short stature , retarded growth velocity , retarded bone age , reduced arm span and low IGF1 and IGFBP-3 serum levels were found . During growth hormone therapy ( duration : 24-33 months ) patients improved in growth velocity , supine length and arm span . In one girl with thoraco-lumbar scoliosis a rapid progression of the deformity developed . Tethered cord and syringomyelia were present .
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] | We report on two patients with myelomeningocele and hydrocephalus in whom hypothalamo-pituitary growth hormone deficiency and neurosecretory dysfunction were diagnosed . The patients were treated with human growth hormone ( 0.5-0.7 IU/ kg/week ) since the age of 4.2 and 8.7 years . Short stature , retarded growth velocity , retarded bone age , reduced arm span and low IGF1 and IGFBP-3 serum levels were found . During growth hormone therapy ( duration : 24-33 months ) patients improved in growth velocity , supine length and arm span . In one girl with thoraco-lumbar scoliosis a rapid progression of the deformity developed . Tethered cord and syringomyelia were present . | [
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patients, myelomeningocele, hydrocephalus, growth hormone, deficiency, dysfunction, patients, human growth hormone, age, growth, bone, age, arm, IGFBP-3, growth hormone, therapy, patients, growth, arm, scoliosis, deformity, syringomyelia | MonatsschriftKinderheilkunde.91470255.eng.abstr_task2 | Sentence: We report on two patients with myelomeningocele and hydrocephalus in whom hypothalamo-pituitary growth hormone deficiency and neurosecretory dysfunction were diagnosed . The patients were treated with human growth hormone ( 0.5-0.7 IU/ kg/week ) since the age of 4.2 and 8.7 years . Short stature , retarded growth velocity , retarded bone age , reduced arm span and low IGF1 and IGFBP-3 serum levels were found . During growth hormone therapy ( duration : 24-33 months ) patients improved in growth velocity , supine length and arm span . In one girl with thoraco-lumbar scoliosis a rapid progression of the deformity developed . Tethered cord and syringomyelia were present .
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Arzneimittelwirkungen is an umlsterm, Behandlung is an umlsterm, alten Menschen is an umlsterm, Risiko is an umlsterm, Rolle is an umlsterm, Patienten is an umlsterm, Patienten is an umlsterm, Arzneimittelwirkung is an umlsterm, Behandlung is an umlsterm, Ofloxacin is an umlsterm, Ciprofloxacin is an umlsterm, Syndromen is an umlsterm, Syndrome is an umlsterm, Schlafstoerungen is an umlsterm, Syndrom is an umlsterm, Patienten is an umlsterm, Syndrome is an umlsterm, Patienten is an umlsterm, affektive Stoerungen is an umlsterm, Leber- is an umlsterm, Nierenerkrankungen is an umlsterm, Behandlung is an umlsterm, Antibiotika is an umlsterm, Immunsuppressiva is an umlsterm, Risikoanalyse is an umlsterm | DerNervenarzt.70680038.ger.abstr_task0 | Sentence: Psychische und neurologische unerwuenschte Arzneimittelwirkungen ( UAW ) wurden unter Behandlung mit Gyrasehemmern ( Fluorquinolone ) wiederholt beschrieben . Ergebnisse frueherer Untersuchungen erbrachten Hinweise dafuer , dass v. a. bei alten Menschen , bei hoher Dosierung , bei psychiatrischer Vorgeschichte und bei Nierenfunktionsstoerungen mit einem hohen Risiko fuer solche UAW zu rechnen ist . Die pathophysiologischen Mechanismen , die bei der Entstehung von unerwuenschten ZNS-Effekten mitwirken , sind noch unzureichend geklaert . Eine wichtige Rolle koennten GABAerge und monoaminerge Mechanismen spielen . In einer eigenen retrospektiven Studie wurden konsiliarpsychiatrische Befunde von 4189 Patienten ausgewertet . Bei 29 Patienten wurde der Verdacht auf das Vorliegen einer psychischen unerwuenschten Arzneimittelwirkung ( UAW ) unter Behandlung mit Ofloxacin oder Ciprofloxacin dokumentiert . Neben deliranten Syndromen wurden paranoide Syndrome , depressive und manische Bilder , Unruhezustaende Schlafstoerungen sowie , je ein soporoeses und ein stuporoeses Syndrom ermittelt . Bei aelteren Patienten ueberwogen delirante und paranoide Syndrome , waehrend bei juengeren Patienten haeufiger affektive Stoerungen auftraten . Meist lagen Multimorbiditaet Leber- oder Nierenerkrankungen , gleichzeitige Behandlung , mit anderen Antibiotika und Immunsuppressiva , psychiatrische Vorerkrankungen oder psychosoziale Belastungsfaktoren vor . Die Ergebnisse der Untersuchung , methodische Probleme , Aspekte der Risikoanalyse und Konsequenzen fuer die aerztliche Behandlungspraxis werden diskutiert .
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Arzneimittelwirkungen, Behandlung, alten Menschen, Risiko, Rolle, Patienten, Patienten, Arzneimittelwirkung, Behandlung, Ofloxacin, Ciprofloxacin, Syndromen, Syndrome, Schlafstoerungen, Syndrom, Patienten, Syndrome, Patienten, affektive Stoerungen, Leber-, Nierenerkrankungen, Behandlung, Antibiotika, Immunsuppressiva, Risikoanalyse | DerNervenarzt.70680038.ger.abstr_task2 | Sentence: Psychische und neurologische unerwuenschte Arzneimittelwirkungen ( UAW ) wurden unter Behandlung mit Gyrasehemmern ( Fluorquinolone ) wiederholt beschrieben . Ergebnisse frueherer Untersuchungen erbrachten Hinweise dafuer , dass v. a. bei alten Menschen , bei hoher Dosierung , bei psychiatrischer Vorgeschichte und bei Nierenfunktionsstoerungen mit einem hohen Risiko fuer solche UAW zu rechnen ist . Die pathophysiologischen Mechanismen , die bei der Entstehung von unerwuenschten ZNS-Effekten mitwirken , sind noch unzureichend geklaert . Eine wichtige Rolle koennten GABAerge und monoaminerge Mechanismen spielen . In einer eigenen retrospektiven Studie wurden konsiliarpsychiatrische Befunde von 4189 Patienten ausgewertet . Bei 29 Patienten wurde der Verdacht auf das Vorliegen einer psychischen unerwuenschten Arzneimittelwirkung ( UAW ) unter Behandlung mit Ofloxacin oder Ciprofloxacin dokumentiert . Neben deliranten Syndromen wurden paranoide Syndrome , depressive und manische Bilder , Unruhezustaende Schlafstoerungen sowie , je ein soporoeses und ein stuporoeses Syndrom ermittelt . Bei aelteren Patienten ueberwogen delirante und paranoide Syndrome , waehrend bei juengeren Patienten haeufiger affektive Stoerungen auftraten . Meist lagen Multimorbiditaet Leber- oder Nierenerkrankungen , gleichzeitige Behandlung , mit anderen Antibiotika und Immunsuppressiva , psychiatrische Vorerkrankungen oder psychosoziale Belastungsfaktoren vor . Die Ergebnisse der Untersuchung , methodische Probleme , Aspekte der Risikoanalyse und Konsequenzen fuer die aerztliche Behandlungspraxis werden diskutiert .
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