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CFI is a GENERIF
1172_0
Sentence: CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: GENERIF
[ "B-GENERIF", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome.
[ "CFI", "-", "rs7356506", "polymorphisms", "associated", "with", "Vogt", "-", "Koyanagi", "-", "Harada", "syndrome", "." ]
[ "Gene", "GENERIF" ]
CFI is a GENERIF
1172_1
Sentence: CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome. Instructions: please typing these entity words according to sentence: CFI Options: GENERIF
[ "B-GENERIF", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome.
[ "CFI", "-", "rs7356506", "polymorphisms", "associated", "with", "Vogt", "-", "Koyanagi", "-", "Harada", "syndrome", "." ]
[ "Gene", "GENERIF" ]
CFI
1172_2
Sentence: CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome. Instructions: please extract entity words from the input sentence
[ "B-GENERIF", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
CFI-rs7356506 polymorphisms associated with Vogt-Koyanagi-Harada syndrome.
[ "CFI", "-", "rs7356506", "polymorphisms", "associated", "with", "Vogt", "-", "Koyanagi", "-", "Harada", "syndrome", "." ]
[ "Gene", "GENERIF" ]
amantadine vs . trihexyphenidyl is a Intervention_Pharmacological, memory is a Outcome_Mental, elderly is a Participant_Age
76459_0
Sentence: The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers . Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Outcome_Mental, Participant_Age, Intervention_Pharmacological
[ "O", "O", "O", "B-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "O", "B-Outcome_Mental", "O", "B-Participant_Age", "O", "O", "O" ]
The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers .
[ "The", "effects", "of", "amantadine", "vs", ".", "trihexyphenidyl", "on", "memory", "in", "elderly", "normal", "volunteers", "." ]
[ "Intervention_Pharmacological", "Participant_Age", "Outcome_Mental" ]
amantadine vs . trihexyphenidyl is a Intervention_Pharmacological, memory is a Outcome_Mental, elderly is a Participant_Age
76459_1
Sentence: The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers . Instructions: please typing these entity words according to sentence: amantadine vs . trihexyphenidyl, memory, elderly Options: Outcome_Mental, Participant_Age, Intervention_Pharmacological
[ "O", "O", "O", "B-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "O", "B-Outcome_Mental", "O", "B-Participant_Age", "O", "O", "O" ]
The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers .
[ "The", "effects", "of", "amantadine", "vs", ".", "trihexyphenidyl", "on", "memory", "in", "elderly", "normal", "volunteers", "." ]
[ "Intervention_Pharmacological", "Participant_Age", "Outcome_Mental" ]
amantadine vs . trihexyphenidyl, memory, elderly
76459_2
Sentence: The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers . Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "B-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "I-Intervention_Pharmacological", "O", "B-Outcome_Mental", "O", "B-Participant_Age", "O", "O", "O" ]
The effects of amantadine vs. trihexyphenidyl on memory in elderly normal volunteers .
[ "The", "effects", "of", "amantadine", "vs", ".", "trihexyphenidyl", "on", "memory", "in", "elderly", "normal", "volunteers", "." ]
[ "Intervention_Pharmacological", "Participant_Age", "Outcome_Mental" ]
eIF4A is a protein, eIF4 G is a protein, eIF4 G is a protein
1.0alpha7.train.311_0
Sentence: Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: protein
[ "O", "O", "O", "O", "O", "O", "B-protein", "O", "O", "B-protein", "I-protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-protein", "I-protein", "O", "O", "O" ]
Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A.
[ "Our", "observation", "that", "binding", "of", " ", "eIF4A", "to", " ", "eIF4", "G", "is", "cooperative", "could", "explain", "these", "results", "by", "ensuring", "a", "higher", "affinity", "interaction", "between", " ", "eIF4", "G", "and", " ", "eIF4A." ]
[ "protein" ]
eIF4A is a protein, eIF4 G is a protein, eIF4 G is a protein
1.0alpha7.train.311_1
Sentence: Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A. Instructions: please typing these entity words according to sentence: eIF4A, eIF4 G, eIF4 G Options: protein
[ "O", "O", "O", "O", "O", "O", "B-protein", "O", "O", "B-protein", "I-protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-protein", "I-protein", "O", "O", "O" ]
Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A.
[ "Our", "observation", "that", "binding", "of", " ", "eIF4A", "to", " ", "eIF4", "G", "is", "cooperative", "could", "explain", "these", "results", "by", "ensuring", "a", "higher", "affinity", "interaction", "between", " ", "eIF4", "G", "and", " ", "eIF4A." ]
[ "protein" ]
eIF4A, eIF4 G, eIF4 G
1.0alpha7.train.311_2
Sentence: Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A. Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "O", "O", "O", "B-protein", "O", "O", "B-protein", "I-protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-protein", "I-protein", "O", "O", "O" ]
Our observation that binding of eIF4A to eIF4G is cooperative could explain these results by ensuring a higher affinity interaction between eIF4G and eIF4A.
[ "Our", "observation", "that", "binding", "of", " ", "eIF4A", "to", " ", "eIF4", "G", "is", "cooperative", "could", "explain", "these", "results", "by", "ensuring", "a", "higher", "affinity", "interaction", "between", " ", "eIF4", "G", "and", " ", "eIF4A." ]
[ "protein" ]
Beclin‐1 is a gene
29270_0
Sentence: Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A). Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: gene
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-gene", "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", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A).
[ "Quantification", "of", "autophagic", "vacuoles", "induced", "by", "ABT737", ".", "HeLa", "cells", "transfected", "with", "the", "indicated", "siRNAs", "(", "specific", "for", "Emerin", "or", "for", "Beclin‐1", "at", "0", "h", ")", "were", "re‐transfected", "with", "LC3‐GFP", "finally", "cultured", "in", "nutrient‐free", "(", "NF", ")", "conditions", "(", "60", "-", "72", "h", ")", ",", "in", "the", "presence", "or", "absence", "1", "μM", "ABT737", "and", "then", "subjected", "to", "electron", "microscopy", "detection", "of", "immature", "(", "AV1", ")", "or", "mature", "(", "AV2", ")", "autophagic", "vacuoles", ".", "Representative", "pictures", "are", "shown", "in", "(", "A", ")", "." ]
[ "gene" ]
Beclin‐1 is a gene
29270_1
Sentence: Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A). Instructions: please typing these entity words according to sentence: Beclin‐1 Options: gene
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-gene", "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", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A).
[ "Quantification", "of", "autophagic", "vacuoles", "induced", "by", "ABT737", ".", "HeLa", "cells", "transfected", "with", "the", "indicated", "siRNAs", "(", "specific", "for", "Emerin", "or", "for", "Beclin‐1", "at", "0", "h", ")", "were", "re‐transfected", "with", "LC3‐GFP", "finally", "cultured", "in", "nutrient‐free", "(", "NF", ")", "conditions", "(", "60", "-", "72", "h", ")", ",", "in", "the", "presence", "or", "absence", "1", "μM", "ABT737", "and", "then", "subjected", "to", "electron", "microscopy", "detection", "of", "immature", "(", "AV1", ")", "or", "mature", "(", "AV2", ")", "autophagic", "vacuoles", ".", "Representative", "pictures", "are", "shown", "in", "(", "A", ")", "." ]
[ "gene" ]
Beclin‐1
29270_2
Sentence: Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A). Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-gene", "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", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Quantification of autophagic vacuoles induced by ABT737. HeLa cells transfected with the indicated siRNAs (specific for Emerin or for Beclin‐1 at 0 h) were re‐transfected with LC3‐GFP finally cultured in nutrient‐free (NF) conditions (60-72 h), in the presence or absence 1 μM ABT737 and then subjected to electron microscopy detection of immature (AV1) or mature (AV2) autophagic vacuoles. Representative pictures are shown in (A).
[ "Quantification", "of", "autophagic", "vacuoles", "induced", "by", "ABT737", ".", "HeLa", "cells", "transfected", "with", "the", "indicated", "siRNAs", "(", "specific", "for", "Emerin", "or", "for", "Beclin‐1", "at", "0", "h", ")", "were", "re‐transfected", "with", "LC3‐GFP", "finally", "cultured", "in", "nutrient‐free", "(", "NF", ")", "conditions", "(", "60", "-", "72", "h", ")", ",", "in", "the", "presence", "or", "absence", "1", "μM", "ABT737", "and", "then", "subjected", "to", "electron", "microscopy", "detection", "of", "immature", "(", "AV1", ")", "or", "mature", "(", "AV2", ")", "autophagic", "vacuoles", ".", "Representative", "pictures", "are", "shown", "in", "(", "A", ")", "." ]
[ "gene" ]
NF - kappa B is a Entity, tumor necrosis factor - alpha is a Protein, TNF - alpha is a Protein, interleukin-1 beta is a Protein, IL-1 beta is a Protein, vascular cell adhesion molecule-1 is a Protein, VCAM-1 is a Protein, CD106 is a Protein, E - selectin is a Protein, ELAM-1 is a Protein, CD62E is a Protein, intercellular adhesion molecule-1 is a Protein, ICAM-1 is a Protein, CD54 is a Protein, VCAM-1 is a Protein, E - selectin is a Protein, TNF - alpha is a Protein, IL-1 beta is a Protein, TNF - alpha is a Protein, nuclear factor - kappa B is a Entity, NF - kappa B is a Entity, NF - kappa B is a Entity
419_0
Sentence: alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Entity, Protein
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alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants.
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[ "Protein", "Entity" ]
NF - kappa B is a Entity, tumor necrosis factor - alpha is a Protein, TNF - alpha is a Protein, interleukin-1 beta is a Protein, IL-1 beta is a Protein, vascular cell adhesion molecule-1 is a Protein, VCAM-1 is a Protein, CD106 is a Protein, E - selectin is a Protein, ELAM-1 is a Protein, CD62E is a Protein, intercellular adhesion molecule-1 is a Protein, ICAM-1 is a Protein, CD54 is a Protein, VCAM-1 is a Protein, E - selectin is a Protein, TNF - alpha is a Protein, IL-1 beta is a Protein, TNF - alpha is a Protein, nuclear factor - kappa B is a Entity, NF - kappa B is a Entity, NF - kappa B is a Entity
419_1
Sentence: alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants. Instructions: please typing these entity words according to sentence: NF - kappa B, tumor necrosis factor - alpha, TNF - alpha, interleukin-1 beta, IL-1 beta, vascular cell adhesion molecule-1, VCAM-1, CD106, E - selectin, ELAM-1, CD62E, intercellular adhesion molecule-1, ICAM-1, CD54, VCAM-1, E - selectin, TNF - alpha, IL-1 beta, TNF - alpha, nuclear factor - kappa B, NF - kappa B, NF - kappa B Options: Entity, Protein
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alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants.
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[ "Protein", "Entity" ]
NF - kappa B, tumor necrosis factor - alpha, TNF - alpha, interleukin-1 beta, IL-1 beta, vascular cell adhesion molecule-1, VCAM-1, CD106, E - selectin, ELAM-1, CD62E, intercellular adhesion molecule-1, ICAM-1, CD54, VCAM-1, E - selectin, TNF - alpha, IL-1 beta, TNF - alpha, nuclear factor - kappa B, NF - kappa B, NF - kappa B
419_2
Sentence: alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants. Instructions: please extract entity words from the input sentence
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alpha-Tocopheryl succinate inhibits monocytic cell adhesion to endothelial cells by suppressing NF-kappa B mobilization. The adherence of monocytes to activated endothelium is an early event in atherogenesis. Because antioxidants have been considered to be of antiatherosclerotic potential, we investigated the effects of alpha-tocopherol (TCP) and its acetate and succinate esters on monocyte adhesion to cytokine-stimulated human umbilical vein endothelial cells (HUVEC). Endothelial cells were treated with TCP, alpha-tocopherol acetate (TCP acetate), or alpha-tocopheryl succinate (TCP succinate) before stimulation with tumor necrosis factor-alpha (TNF-alpha; 10 U/ml, 6 h) or interleukin-1 beta (IL-1 beta; 10 U/ml, 6 h). Cytokine-stimulated cell surface expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) and E-selectin (ELAM-1, CD62E), but not of intercellular adhesion molecule-1 (ICAM-1, CD54), was time- and dose-dependently inhibited by TCP succinate but not by TCP or TCP acetate. TCP succinate (200 microM, 24 h) reduced TNF-induced VCAM-1 and E-selectin expression from a specific mean fluorescence intensity of 151 +/- 28 to 12 +/- 4 channels and from 225 +/- 38 to 79 +/- 21 channels, respectively. Succinate alone had no effect. Decreased adhesion molecule expression was associated with a reduction of monocytic cell adhesion. TCP succinate (20 microM, 72 h), but not TCP (200 microM, 72 h), reduced U-937 cell adhesion to TNF-alpha-stimulated (10 U/ml, 6 h) HUVEC by 30% (P < 0.025) and to IL-1 beta-stimulated HUVEC by 56% (P < 0.010). Electrophoretic mobility-shift assays of HUVEC nuclear proteins revealed a decrease in TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) activation after pretreatment of HUVEC with TCP succinate but not with TCP, TCP acetate, or succinate alone. In conclusion, we demonstrate that the vitamin E derivative TCP succinate prevents monocytic cell adhesion to cytokine-stimulated endothelial cells by inhibiting the activation of NF-kappa B, further emphasizing the antiatherosclerotic potential of lipid soluble antioxidants.
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alpha 1 adrenoceptor is a GENE-N, alpha 1 adrenoceptors is a GENE-N, alpha 1 adrenoceptor is a GENE-N, human alpha 1A , alpha 1B and alpha 1D adrenoceptors is a GENE-N, noradrenaline is a CHEMICAL, phenylephrine is a CHEMICAL, quinazoline is a CHEMICAL, prazosin is a CHEMICAL, doxazosin is a CHEMICAL, alfuzosin is a CHEMICAL, human alpha 1 adrenoceptors is a GENE-N, Indoramin is a CHEMICAL, SNAP 1069 is a CHEMICAL, alpha 1A and alpha 1B adrenoceptors is a GENE-N, alpha 1D subtype is a GENE-Y, Rec 15/2739 is a CHEMICAL, WB 4101 is a CHEMICAL, SL 89,0591 is a CHEMICAL, ( + ) - and ( -)- tamsulosin is a CHEMICAL, alpha 1A and alpha 1D adrenoceptors is a GENE-N, alpha 1B subtype is a GENE-Y, RS 17053 is a CHEMICAL, alpha 1A adrenoceptors is a GENE-Y, alpha 1B is a GENE-Y, alpha 1D is a GENE-Y, ( + ) -Tamsulosin is a CHEMICAL, ( -)-tamsulosin is a CHEMICAL, SL 89,0591 is a CHEMICAL, Rec 15/2739 is a CHEMICAL, SNAP 1069 is a CHEMICAL, RS 17053 is a CHEMICAL, noradrenaline is a CHEMICAL, human alpha 1D adrenoceptors is a GENE-Y, prazosin is a CHEMICAL, ( -)-tamsulosin is a CHEMICAL, doxazosin is a CHEMICAL, SL 89,0591 is a CHEMICAL, ( + ) -tamsulosin is a CHEMICAL, Rec 15/2739 is a CHEMICAL, RS 17053 is a CHEMICAL, SNAP 1069 is a CHEMICAL, ( -)-Tamsulosin is a CHEMICAL, noradrenaline is a CHEMICAL, alpha 1A is a GENE-Y, prazosin is a CHEMICAL, alpha 1A adrenoceptors is a GENE-Y, RS 17053 is a CHEMICAL, human alpha 1A adrenoceptors is a GENE-Y, doxazosin is a CHEMICAL, ( + ) - and ( -)-tamsulosin is a CHEMICAL, phenylephrine is a CHEMICAL, Rec 15/2739 is a CHEMICAL, phenylephrine is a CHEMICAL, alpha 1 adrenoceptor is a GENE-N, noradrenaline is a CHEMICAL, alpha 1A adrenoceptor is a GENE-Y, alpha 1A , alpha 1B or alpha 1D adrenoceptors is a GENE-N, alpha 1 adrenoceptors is a GENE-N, alpha 1D subtype is a GENE-Y, phenylephrine is a CHEMICAL
15286_0
Sentence: Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: GENE-N, CHEMICAL, GENE-Y
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Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure.
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[ "GENE-N", "GENE-Y", "CHEMICAL" ]
alpha 1 adrenoceptor is a GENE-N, alpha 1 adrenoceptors is a GENE-N, alpha 1 adrenoceptor is a GENE-N, human alpha 1A , alpha 1B and alpha 1D adrenoceptors is a GENE-N, noradrenaline is a CHEMICAL, phenylephrine is a CHEMICAL, quinazoline is a CHEMICAL, prazosin is a CHEMICAL, doxazosin is a CHEMICAL, alfuzosin is a CHEMICAL, human alpha 1 adrenoceptors is a GENE-N, Indoramin is a CHEMICAL, SNAP 1069 is a CHEMICAL, alpha 1A and alpha 1B adrenoceptors is a GENE-N, alpha 1D subtype is a GENE-Y, Rec 15/2739 is a CHEMICAL, WB 4101 is a CHEMICAL, SL 89,0591 is a CHEMICAL, ( + ) - and ( -)- tamsulosin is a CHEMICAL, alpha 1A and alpha 1D adrenoceptors is a GENE-N, alpha 1B subtype is a GENE-Y, RS 17053 is a CHEMICAL, alpha 1A adrenoceptors is a GENE-Y, alpha 1B is a GENE-Y, alpha 1D is a GENE-Y, ( + ) -Tamsulosin is a CHEMICAL, ( -)-tamsulosin is a CHEMICAL, SL 89,0591 is a CHEMICAL, Rec 15/2739 is a CHEMICAL, SNAP 1069 is a CHEMICAL, RS 17053 is a CHEMICAL, noradrenaline is a CHEMICAL, human alpha 1D adrenoceptors is a GENE-Y, prazosin is a CHEMICAL, ( -)-tamsulosin is a CHEMICAL, doxazosin is a CHEMICAL, SL 89,0591 is a CHEMICAL, ( + ) -tamsulosin is a CHEMICAL, Rec 15/2739 is a CHEMICAL, RS 17053 is a CHEMICAL, SNAP 1069 is a CHEMICAL, ( -)-Tamsulosin is a CHEMICAL, noradrenaline is a CHEMICAL, alpha 1A is a GENE-Y, prazosin is a CHEMICAL, alpha 1A adrenoceptors is a GENE-Y, RS 17053 is a CHEMICAL, human alpha 1A adrenoceptors is a GENE-Y, doxazosin is a CHEMICAL, ( + ) - and ( -)-tamsulosin is a CHEMICAL, phenylephrine is a CHEMICAL, Rec 15/2739 is a CHEMICAL, phenylephrine is a CHEMICAL, alpha 1 adrenoceptor is a GENE-N, noradrenaline is a CHEMICAL, alpha 1A adrenoceptor is a GENE-Y, alpha 1A , alpha 1B or alpha 1D adrenoceptors is a GENE-N, alpha 1 adrenoceptors is a GENE-N, alpha 1D subtype is a GENE-Y, phenylephrine is a CHEMICAL
15286_1
Sentence: Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure. Instructions: please typing these entity words according to sentence: alpha 1 adrenoceptor, alpha 1 adrenoceptors, alpha 1 adrenoceptor, human alpha 1A , alpha 1B and alpha 1D adrenoceptors, noradrenaline, phenylephrine, quinazoline, prazosin, doxazosin, alfuzosin, human alpha 1 adrenoceptors, Indoramin, SNAP 1069, alpha 1A and alpha 1B adrenoceptors, alpha 1D subtype, Rec 15/2739, WB 4101, SL 89,0591, ( + ) - and ( -)- tamsulosin, alpha 1A and alpha 1D adrenoceptors, alpha 1B subtype, RS 17053, alpha 1A adrenoceptors, alpha 1B, alpha 1D, ( + ) -Tamsulosin, ( -)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069, RS 17053, noradrenaline, human alpha 1D adrenoceptors, prazosin, ( -)-tamsulosin, doxazosin, SL 89,0591, ( + ) -tamsulosin, Rec 15/2739, RS 17053, SNAP 1069, ( -)-Tamsulosin, noradrenaline, alpha 1A, prazosin, alpha 1A adrenoceptors, RS 17053, human alpha 1A adrenoceptors, doxazosin, ( + ) - and ( -)-tamsulosin, phenylephrine, Rec 15/2739, phenylephrine, alpha 1 adrenoceptor, noradrenaline, alpha 1A adrenoceptor, alpha 1A , alpha 1B or alpha 1D adrenoceptors, alpha 1 adrenoceptors, alpha 1D subtype, phenylephrine Options: GENE-N, CHEMICAL, GENE-Y
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Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure.
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[ "GENE-N", "GENE-Y", "CHEMICAL" ]
alpha 1 adrenoceptor, alpha 1 adrenoceptors, alpha 1 adrenoceptor, human alpha 1A , alpha 1B and alpha 1D adrenoceptors, noradrenaline, phenylephrine, quinazoline, prazosin, doxazosin, alfuzosin, human alpha 1 adrenoceptors, Indoramin, SNAP 1069, alpha 1A and alpha 1B adrenoceptors, alpha 1D subtype, Rec 15/2739, WB 4101, SL 89,0591, ( + ) - and ( -)- tamsulosin, alpha 1A and alpha 1D adrenoceptors, alpha 1B subtype, RS 17053, alpha 1A adrenoceptors, alpha 1B, alpha 1D, ( + ) -Tamsulosin, ( -)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069, RS 17053, noradrenaline, human alpha 1D adrenoceptors, prazosin, ( -)-tamsulosin, doxazosin, SL 89,0591, ( + ) -tamsulosin, Rec 15/2739, RS 17053, SNAP 1069, ( -)-Tamsulosin, noradrenaline, alpha 1A, prazosin, alpha 1A adrenoceptors, RS 17053, human alpha 1A adrenoceptors, doxazosin, ( + ) - and ( -)-tamsulosin, phenylephrine, Rec 15/2739, phenylephrine, alpha 1 adrenoceptor, noradrenaline, alpha 1A adrenoceptor, alpha 1A , alpha 1B or alpha 1D adrenoceptors, alpha 1 adrenoceptors, alpha 1D subtype, phenylephrine
15286_2
Sentence: Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure. Instructions: please extract entity words from the input sentence
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Evaluation of the pharmacological selectivity profile of alpha 1 adrenoceptor antagonists at prostatic alpha 1 adrenoceptors: binding, functional and in vivo studies. 1. The profile of a range of alpha 1 adrenoceptor antagonists was determined in vitro against cloned human alpha 1A, alpha 1B and alpha 1D adrenoceptors and against noradrenaline-mediated contractions of rat aorta and human prostate. The in vivo profile of compounds was determined in an anaesthetized dog model which allowed the simultaneous assessment of antagonist potency against phenylephrine-mediated increases in blood pressure and prostatic pressure. 2. The quinazoline antagonists, prazosin, doxazosin and alfuzosin displayed high affinity but were non selective for the three cloned human alpha 1 adrenoceptors. Indoramin and SNAP 1069 showed selectivity for alpha 1A and alpha 1B adrenoceptors relative to the alpha 1D subtype. Rec 15/2739, WB 4101, SL 89,0591, (+)- and (-)- tamsulosin showed selectivity for alpha 1A and alpha 1D adrenoceptors relative to the alpha 1B subtype. RS 17053 showed high affinity and selectivity for alpha 1A adrenoceptors (pKi 8.6) relative to alpha 1B (pKi = 7.3) and alpha 1D (pKi = 7.1) subtypes. 3. (+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned human alpha 1D adrenoceptors. The following rank order was obtained: prazosin = (-)-tamsulosin > doxazosin > SL 89,0591 = (+)-tamsulosin > Rec 15/2739 > RS 17053 = SNAP 1069. 4. (-)-Tamsulosin was a very potent, insurmountable antagonist of noradrenaline-mediated contractions of human prostate, yielding an approximate pA2 estimate of 9.8 at 1 nM. The corresponding (+)-enantiomer was 30 fold weaker. SL 89,0591, SNAP 1069 and Rec 15/2739 yielded pA2 estimates which compared well with their alpha 1A binding affinities. The affinity estimate for prazosin on human prostate was lower than the corresponding binding affinity determined at alpha 1A adrenoceptors and RS 17053 was a very weak antagonist on human prostate (pA2 = 6.0) relative to the high affinity (pKi = 8.6) determined at cloned human alpha 1A adrenoceptors. 5. In the anaesthetized dog, in vivo pseudo "pA2' values showed that doxazosin, (+)- and (-)-tamsulosin inhibited phenylephrine-induced increases in prostatic and blood pressure with similar affinity, implying that these agents show little or no selectivity for prostatic responses in this model. SL 89,0591 and SNAP 1069 were moderately selective (3 and 6 fold respectively) for prostatic pressure relative to blood pressure. Rec 15/2739 was a more potent antagonist of phenylephrine-mediated increases in prostatic pressure ("pA2' = 8.74) compared to blood pressure ("pA2' = 7.51). 6. Data in this study suggest that the alpha 1 adrenoceptor mediating noradrenaline-induced contractions of human prostate, whilst having some of the characteristics of an alpha 1A adrenoceptor, cannot be satisfactorily aligned with cloned alpha 1A, alpha 1B or alpha 1D adrenoceptors. In addition, studies in the anaesthetized dog have shown that agents having high affinity and selectivity for prostatic alpha 1 adrenoceptors, particularly over the alpha 1D subtype, appear to inhibit phenylephrine-induced increases in prostatic pressure selectively compared to blood pressure.
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Patienten is an umlsterm, Intubation is an umlsterm, Normalpatienten is an umlsterm, Kehlkopfmaske is an umlsterm, Kehlkopfmaske is an umlsterm, Intubation is an umlsterm, Kehlkopfmaske is an umlsterm, blind is an umlsterm, Patienten is an umlsterm, Gesichtskarzinom is an umlsterm, Kehlkopfs is an umlsterm, Kehlkopfmaske is an umlsterm, Mundoeffnung is an umlsterm, Tumorpatienten is an umlsterm, Kehlkopfmaske is an umlsterm, Leckdruck is an umlsterm, Normalpatienten is an umlsterm, Intubation is an umlsterm, Kehlkopfmaske is an umlsterm, blinde is an umlsterm, endotracheale Intubation is an umlsterm, Kehlkopfmaske is an umlsterm, Patienten is an umlsterm, Intubation is an umlsterm, Normalpatienten is an umlsterm, Kehlkopf is an umlsterm, Kehlkopfmaske is an umlsterm, Kehlkopfmaske is an umlsterm, Atmung is an umlsterm, Tumorpatienten is an umlsterm, Intubation is an umlsterm, blinde is an umlsterm, Intubation is an umlsterm, Patienten is an umlsterm, Kehlkopfmaske is an umlsterm, Anaesthesierepertoire is an umlsterm, Intubation is an umlsterm
DerAnaesthesist.50440712.ger.abstr_0
Sentence: Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: umlsterm
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Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation
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[ "umlsterm" ]
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DerAnaesthesist.50440712.ger.abstr_1
Sentence: Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation Instructions: please typing these entity words according to sentence: Patienten, Intubation, Normalpatienten, Kehlkopfmaske, Kehlkopfmaske, Intubation, Kehlkopfmaske, blind, Patienten, Gesichtskarzinom, Kehlkopfs, Kehlkopfmaske, Mundoeffnung, Tumorpatienten, Kehlkopfmaske, Leckdruck, Normalpatienten, Intubation, Kehlkopfmaske, blinde, endotracheale Intubation, Kehlkopfmaske, Patienten, Intubation, Normalpatienten, Kehlkopf, Kehlkopfmaske, Kehlkopfmaske, Atmung, Tumorpatienten, Intubation, blinde, Intubation, Patienten, Kehlkopfmaske, Anaesthesierepertoire, Intubation Options: umlsterm
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Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation
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Patienten, Intubation, Normalpatienten, Kehlkopfmaske, Kehlkopfmaske, Intubation, Kehlkopfmaske, blind, Patienten, Gesichtskarzinom, Kehlkopfs, Kehlkopfmaske, Mundoeffnung, Tumorpatienten, Kehlkopfmaske, Leckdruck, Normalpatienten, Intubation, Kehlkopfmaske, blinde, endotracheale Intubation, Kehlkopfmaske, Patienten, Intubation, Normalpatienten, Kehlkopf, Kehlkopfmaske, Kehlkopfmaske, Atmung, Tumorpatienten, Intubation, blinde, Intubation, Patienten, Kehlkopfmaske, Anaesthesierepertoire, Intubation
DerAnaesthesist.50440712.ger.abstr_2
Sentence: Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation Instructions: please extract entity words from the input sentence
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Bei 30 Patienten mit schwieriger Intubation ( 35 Operationen ) und 50 Normalpatienten wurde prospektiv die Kehlkopfmaske eingesetzt mit den Fragestellungen : 1 ) verbessert die Kehlkopfmaske die Beatmung gegenueber der Gesichtsmaske , 2 ) erleichtert sie die fiberoptische Intubation , und 3 ) wie haeufig kann durch die Kehlkopfmaske blind intubiert werden ? 23 Patienten waren wegen Gesichtskarzinom radikal voroperiert , 7 konventionell nicht intubierbar ( Tabelle 1 ; bei allen : Sichtbarkeit des Kehlkopfs Grad 3 oder 4 [ 14 ] ) . Die Kehlkopfmaske liess sich bei allen ausser 1 Patientin mit einer Mundoeffnung von 1 cm einlegen . Bei Tumorpatienten war die Beatmung ueber die Kehlkopfmaske besser als mit Gesichtsmaske , zusaetzlich war der Leckdruck hoeher als bei Normalpatienten ( 25,2 +/- 7,9 vs. 20,6 +/- 4,9 cmH2O, p 0,05 ; Abb. 2 ) . Die fiberoptische Intubation gelang immer und war durch die Kehlkopfmaske leichter als ohne . Die blinde endotracheale Intubation durch die Kehlkopfmaske gelang nur in 22% bei Patienten mit schwieriger Intubation , und in 19% bei Normalpatienten . Der Wechsel auf jeden beliebigen Tubus ohne Sicht auf den Kehlkopf nach Plazierung eines 6,0 mm ungecufften Tubus durch die Kehlkopfmaske wird beschrieben ( Abb. 4 ) . Zusammenfassend sichert die Kehlkopfmaske die Atmung bei Tumorpatienten besser als die Gesichtsmaske , erleichert die fiberoptische Intubation und ermoeglicht die blinde Intubation bei einem Teil der Patienten . Die Kehlkopfmaske erweitert das Anaesthesierepertoire bei schwieriger Intubation
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[ "umlsterm" ]
instrument is an umlsterm, intramedullary nails is an umlsterm, procedure is an umlsterm
Trauma+Berufskrankheit.80010068.eng.abstr_0
Sentence: A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described . Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: umlsterm
[ "O", "O", "O", "B-umlsterm", "O", "O", "O", "O", "O", "O", "O", "B-umlsterm", "I-umlsterm", "O", "O", "O", "O", "B-umlsterm", "O", "O" ]
A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described .
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[ "umlsterm" ]
instrument is an umlsterm, intramedullary nails is an umlsterm, procedure is an umlsterm
Trauma+Berufskrankheit.80010068.eng.abstr_1
Sentence: A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described . Instructions: please typing these entity words according to sentence: instrument, intramedullary nails, procedure Options: umlsterm
[ "O", "O", "O", "B-umlsterm", "O", "O", "O", "O", "O", "O", "O", "B-umlsterm", "I-umlsterm", "O", "O", "O", "O", "B-umlsterm", "O", "O" ]
A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described .
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[ "umlsterm" ]
instrument, intramedullary nails, procedure
Trauma+Berufskrankheit.80010068.eng.abstr_2
Sentence: A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described . Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "B-umlsterm", "O", "O", "O", "O", "O", "O", "O", "B-umlsterm", "I-umlsterm", "O", "O", "O", "O", "B-umlsterm", "O", "O" ]
A specially made instrument for the extraction of broken fragments of intramedullary nails is introduced and the procedure described .
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[ "umlsterm" ]
interferon is a Intervention_Pharmacological, response is a Outcome_Physical, alpha - interferon is a Intervention_Pharmacological, anti - human immunodeficiency virus antibody status is a Outcome_Physical, chronic active hepatitis on liver biopsy is a Outcome_Physical, AST level is a Outcome_Physical, hepatitis B virus DNA level is a Outcome_Physical, acute hepatitis is a Outcome_Physical, acute icteric hepatitis is a Outcome_Physical, HBsAg is a Outcome_Physical, HBeAg is a Outcome_Physical
41158_0
Sentence: Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) . Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Outcome_Physical, Intervention_Pharmacological
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Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) .
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[ "Outcome_Physical", "Intervention_Pharmacological" ]
interferon is a Intervention_Pharmacological, response is a Outcome_Physical, alpha - interferon is a Intervention_Pharmacological, anti - human immunodeficiency virus antibody status is a Outcome_Physical, chronic active hepatitis on liver biopsy is a Outcome_Physical, AST level is a Outcome_Physical, hepatitis B virus DNA level is a Outcome_Physical, acute hepatitis is a Outcome_Physical, acute icteric hepatitis is a Outcome_Physical, HBsAg is a Outcome_Physical, HBeAg is a Outcome_Physical
41158_1
Sentence: Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) . Instructions: please typing these entity words according to sentence: interferon, response, alpha - interferon, anti - human immunodeficiency virus antibody status, chronic active hepatitis on liver biopsy, AST level, hepatitis B virus DNA level, acute hepatitis, acute icteric hepatitis, HBsAg, HBeAg Options: Outcome_Physical, Intervention_Pharmacological
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Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) .
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[ "Outcome_Physical", "Intervention_Pharmacological" ]
interferon, response, alpha - interferon, anti - human immunodeficiency virus antibody status, chronic active hepatitis on liver biopsy, AST level, hepatitis B virus DNA level, acute hepatitis, acute icteric hepatitis, HBsAg, HBeAg
41158_2
Sentence: Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) . Instructions: please extract entity words from the input sentence
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Treatment of hepatitis B virus infection with interferon . Factors predicting response to interferon . Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B . In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50 % . In those infected at birth , response rates are lower . Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection . In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks , a negative anti-human immunodeficiency virus antibody status ( p less than 0.001 ) , chronic active hepatitis on liver biopsy ( p less than 0.005 ) , high AST level ( p less than 0.001 ) , low hepatitis B virus DNA level ( p less than 0.001 ) and a history of acute hepatitis ( p less than 0.005 ) were all associated with an increased likelihood of response on univariate analysis . On stepwise logistic regression analysis , hepatitis B virus DNA , AST and a history of acute hepatitis predicted response independently ( p less than 0.05 ) . The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status , with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter , which predicted response in 77 % with a specificity of 79 % ( p less than 0.001 ) . The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration ( p less than 0.001 ) .
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[ "Outcome_Physical", "Intervention_Pharmacological" ]
carbons is a Chemical, allyl is a Chemical, benzyl is a Chemical, trimethylsilanes is a Chemical
31474_0
Sentence: Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Chemical
[ "O", "O", "O", "O", "O", "O", "B-Chemical", "O", "B-Chemical", "O", "B-Chemical", "B-Chemical", "O" ]
Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes.
[ "Efficient", "anodic", "allylation", "and", "benzylation", "of", "carbons", "using", "allyl", "and", "benzyl", "trimethylsilanes", "." ]
[ "Chemical" ]
carbons is a Chemical, allyl is a Chemical, benzyl is a Chemical, trimethylsilanes is a Chemical
31474_1
Sentence: Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes. Instructions: please typing these entity words according to sentence: carbons, allyl, benzyl, trimethylsilanes Options: Chemical
[ "O", "O", "O", "O", "O", "O", "B-Chemical", "O", "B-Chemical", "O", "B-Chemical", "B-Chemical", "O" ]
Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes.
[ "Efficient", "anodic", "allylation", "and", "benzylation", "of", "carbons", "using", "allyl", "and", "benzyl", "trimethylsilanes", "." ]
[ "Chemical" ]
carbons, allyl, benzyl, trimethylsilanes
31474_2
Sentence: Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes. Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "O", "O", "O", "B-Chemical", "O", "B-Chemical", "O", "B-Chemical", "B-Chemical", "O" ]
Efficient anodic allylation and benzylation of carbons using allyl and benzyl trimethylsilanes.
[ "Efficient", "anodic", "allylation", "and", "benzylation", "of", "carbons", "using", "allyl", "and", "benzyl", "trimethylsilanes", "." ]
[ "Chemical" ]
Aip1p is a Individual_protein, cofilin is a Individual_protein, cofilin is a Individual_protein, cofilin is a Individual_protein, actin is a Individual_protein
56_0
Sentence: We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Individual_protein
[ "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "B-Individual_protein", "O", "O" ]
We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches.
[ "We", "conclude", "that", "Aip1p", "is", "a", "cofilin", "-", "associated", "protein", "that", "enhances", "the", "filament", "disassembly", "activity", "of", "cofilin", "and", "restricts", "cofilin", "localization", "to", "cortical", "actin", "patches", "." ]
[ "Individual_protein" ]
Aip1p is a Individual_protein, cofilin is a Individual_protein, cofilin is a Individual_protein, cofilin is a Individual_protein, actin is a Individual_protein
56_1
Sentence: We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches. Instructions: please typing these entity words according to sentence: Aip1p, cofilin, cofilin, cofilin, actin Options: Individual_protein
[ "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "B-Individual_protein", "O", "O" ]
We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches.
[ "We", "conclude", "that", "Aip1p", "is", "a", "cofilin", "-", "associated", "protein", "that", "enhances", "the", "filament", "disassembly", "activity", "of", "cofilin", "and", "restricts", "cofilin", "localization", "to", "cortical", "actin", "patches", "." ]
[ "Individual_protein" ]
Aip1p, cofilin, cofilin, cofilin, actin
56_2
Sentence: We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches. Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Individual_protein", "O", "O", "B-Individual_protein", "O", "O", "O", "B-Individual_protein", "O", "O" ]
We conclude that Aip1p is a cofilin-associated protein that enhances the filament disassembly activity of cofilin and restricts cofilin localization to cortical actin patches.
[ "We", "conclude", "that", "Aip1p", "is", "a", "cofilin", "-", "associated", "protein", "that", "enhances", "the", "filament", "disassembly", "activity", "of", "cofilin", "and", "restricts", "cofilin", "localization", "to", "cortical", "actin", "patches", "." ]
[ "Individual_protein" ]
Interferon - gamma is a GENE-Y
17034586_0
Sentence: Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: GENE-Y
[ "B-GENE-Y", "I-GENE-Y", "I-GENE-Y", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice.
[ "Interferon", "-", "gamma", "is", "causatively", "involved", "in", "experimental", "inflammatory", "bowel", "disease", "in", "mice", "." ]
[ "GENE-Y", "GENE-N" ]
Interferon - gamma is a GENE-Y
17034586_1
Sentence: Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice. Instructions: please typing these entity words according to sentence: Interferon - gamma Options: GENE-Y
[ "B-GENE-Y", "I-GENE-Y", "I-GENE-Y", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice.
[ "Interferon", "-", "gamma", "is", "causatively", "involved", "in", "experimental", "inflammatory", "bowel", "disease", "in", "mice", "." ]
[ "GENE-Y", "GENE-N" ]
Interferon - gamma
17034586_2
Sentence: Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice. Instructions: please extract entity words from the input sentence
[ "B-GENE-Y", "I-GENE-Y", "I-GENE-Y", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Interferon-gamma is causatively involved in experimental inflammatory bowel disease in mice.
[ "Interferon", "-", "gamma", "is", "causatively", "involved", "in", "experimental", "inflammatory", "bowel", "disease", "in", "mice", "." ]
[ "GENE-Y", "GENE-N" ]
RAD52 is a Gene/protein/RNA, RAD51 is a Gene/protein/RNA
593_0
Sentence: Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR. Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: Gene/protein/RNA
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR.
[ "Previously", ",", "we", "have", "shown", "that", "in", "the", "absence", "of", "RAD52", ",", "repair", "is", "nearly", "absent", "and", "diploid", "cells", "lose", "the", "broken", "chromosome", ";", "however", ",", "in", "cells", "lacking", "RAD51", ",", "gene", "conversion", "is", "absent", "but", "cells", "can", "repair", "the", "DSB", "by", "BIR", "." ]
[ "Gene/protein/RNA" ]
RAD52 is a Gene/protein/RNA, RAD51 is a Gene/protein/RNA
593_1
Sentence: Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR. Instructions: please typing these entity words according to sentence: RAD52, RAD51 Options: Gene/protein/RNA
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR.
[ "Previously", ",", "we", "have", "shown", "that", "in", "the", "absence", "of", "RAD52", ",", "repair", "is", "nearly", "absent", "and", "diploid", "cells", "lose", "the", "broken", "chromosome", ";", "however", ",", "in", "cells", "lacking", "RAD51", ",", "gene", "conversion", "is", "absent", "but", "cells", "can", "repair", "the", "DSB", "by", "BIR", "." ]
[ "Gene/protein/RNA" ]
RAD52, RAD51
593_2
Sentence: Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR. Instructions: please extract entity words from the input sentence
[ "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "B-Gene/protein/RNA", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O", "O" ]
Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR.
[ "Previously", ",", "we", "have", "shown", "that", "in", "the", "absence", "of", "RAD52", ",", "repair", "is", "nearly", "absent", "and", "diploid", "cells", "lose", "the", "broken", "chromosome", ";", "however", ",", "in", "cells", "lacking", "RAD51", ",", "gene", "conversion", "is", "absent", "but", "cells", "can", "repair", "the", "DSB", "by", "BIR", "." ]
[ "Gene/protein/RNA" ]
necrosis is an umlsterm, lunate bone is an umlsterm, literature is an umlsterm, causation is an umlsterm, patients is an umlsterm, histories is an umlsterm, macroscopic - radiographical is an umlsterm, contrast is an umlsterm, necrosis is an umlsterm, femoral head is an umlsterm, Evaluation is an umlsterm, lunate is an umlsterm, bone necrosis is an umlsterm, University Hospital is an umlsterm, prospective study is an umlsterm, patients is an umlsterm, wrist is an umlsterm, X - ray is an umlsterm, lunate bones is an umlsterm, cause is an umlsterm, fractures is an umlsterm, cause is an umlsterm, necrosis is an umlsterm, lunate bone is an umlsterm, classification is an umlsterm, lunate is an umlsterm, bone necrosis is an umlsterm, pressure is an umlsterm, measurement is an umlsterm, test is an umlsterm, behaviour is an umlsterm, pressure is an umlsterm, lunate bones is an umlsterm, lunate bones is an umlsterm, bones is an umlsterm, pressure is an umlsterm, bones is an umlsterm, lunate bones is an umlsterm, pressure is an umlsterm, wrist is an umlsterm, position - dependent is an umlsterm, pressure is an umlsterm, lunate bones is an umlsterm, drainage is an umlsterm, pressure is an umlsterm, lunate bones is an umlsterm, systolic is an umlsterm, blood pressure is an umlsterm, lunate bones is an umlsterm, movement is an umlsterm, anatomical is an umlsterm, causes is an umlsterm, pressure is an umlsterm, arteries is an umlsterm, veins is an umlsterm, plastination is an umlsterm, cadaver is an umlsterm, arms is an umlsterm, Visualization is an umlsterm, vessels is an umlsterm, blood supply is an umlsterm, arteries is an umlsterm, drainage is an umlsterm, anatomical is an umlsterm, drainage is an umlsterm, lunate bone is an umlsterm, pressure is an umlsterm, radius is an umlsterm, direction is an umlsterm, relative is an umlsterm, hand is an umlsterm, axis is an umlsterm, development is an umlsterm, necrosis is an umlsterm, Evaluation is an umlsterm, histories is an umlsterm, patients is an umlsterm, necrosis is an umlsterm, lunate bone is an umlsterm, trauma is an umlsterm, causation is an umlsterm, manual is an umlsterm, work is an umlsterm, role is an umlsterm, manual is an umlsterm, wrist is an umlsterm, bone necrosis is an umlsterm, wrist is an umlsterm, pathologic is an umlsterm
Trauma+Berufskrankheit.80010074.eng.abstr_0
Sentence: So far , necrosis of the lunate bone has been interpreted in the literature as a phenomenon with a traumatic , primarily vascular-arterial or mechanical causation . These models seem problematic , since neither the patients ' histories nor the macroscopic-radiographical or histological appearances can be reconciled with them . In contrast , the model of a primarily venous aetiopathogenesis accepted for idiopathic necrosis of the femoral head is now examined . Evaluation of 125 cases of lunate bone necrosis treated in the Department of Orthopaedics at the University Hospital in Heidelberg between 1958 and 1993 made it possible to reconstruct the spontaneous course of the condition . X-Ray material , core spin tomographic images and material from a prospective study carried out in 49 patients with unexplained painful conditions of the wrist were available . A stage-by-stage progression emerged , which initially caused alterations only in the MR image , while the X-ray picture remained unremarkable . It was recognized from the spontaneous course that subsequent changes in the shape of the diseased lunate bones were always the result of the necrotic transformation process and never the cause of it . This meant that fractures were excluded as a possible cause of necrosis of the lunate bone . The spontaneous course was used as the basis of a stage-related classification for lunate bone necrosis . In a pressure measurement test , the behaviour of the intraosseous pressure in 16 necrotic lunate bones , 16 healthy lunate bones and 16 healthy capitate bones was tested under various functional conditions . The pressure fluctuations in the capitate bones were very slight , while in the healthy lunate bones pressure increased significantly during extension of the wrist . The position-dependent pressure increases in the lunate bones indicated that the venous drainage was constantly in jeopardy . The pressure increases in necrotic lunate bones were significantly in excess of those in healthy ones ; in some cases they were far in excess of the systolic blood pressure . It was also concluded that necrotic lunate bones were mechanically deformed on movement . The anatomical causes of the pronounced pressure increases were examined experimentally . After staining of both the arteries and the veins , epoxy sheet plastination was used to fix six fresh cadaver arms in the neutral position and six in extension . Visualization of the vessels showed that capsular-ligamentous structures that were stretched on the palmar side and slackly turned back on themselves on the dorsal side still allowed the blood supply from the arteries , but substantially hindered venous drainage . The anatomical preparations made it possible to see that venous drainage from the lunate bone was being prevented ; this explained the pronounced pressure increases . The unphysiological position of the base of the radius inclined in the palmar direction relative to the hand axis when it was extended dorsally was the crucial factor in the development of necrosis . Evaluation of the histories of the patients with necrosis of the lunate bone made it clear that trauma was not significantly involved in the causation , while manual work had an important role . Most manual activites are performed with the wrist in extension . Any extension favours triggering of bone necrosis through congestion in the venous trunk . Thus , our investigations have shown that the beginning of this illness starts with congestion such as occurs with every extension of the wrist , which is initially physiological , before further factors favouring the process cause it to take a pathologic course . Instructions: please extract entities and their types from the input sentence, all entity types are in options Options: umlsterm
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So far , necrosis of the lunate bone has been interpreted in the literature as a phenomenon with a traumatic , primarily vascular-arterial or mechanical causation . These models seem problematic , since neither the patients ' histories nor the macroscopic-radiographical or histological appearances can be reconciled with them . In contrast , the model of a primarily venous aetiopathogenesis accepted for idiopathic necrosis of the femoral head is now examined . Evaluation of 125 cases of lunate bone necrosis treated in the Department of Orthopaedics at the University Hospital in Heidelberg between 1958 and 1993 made it possible to reconstruct the spontaneous course of the condition . X-Ray material , core spin tomographic images and material from a prospective study carried out in 49 patients with unexplained painful conditions of the wrist were available . A stage-by-stage progression emerged , which initially caused alterations only in the MR image , while the X-ray picture remained unremarkable . It was recognized from the spontaneous course that subsequent changes in the shape of the diseased lunate bones were always the result of the necrotic transformation process and never the cause of it . This meant that fractures were excluded as a possible cause of necrosis of the lunate bone . The spontaneous course was used as the basis of a stage-related classification for lunate bone necrosis . In a pressure measurement test , the behaviour of the intraosseous pressure in 16 necrotic lunate bones , 16 healthy lunate bones and 16 healthy capitate bones was tested under various functional conditions . The pressure fluctuations in the capitate bones were very slight , while in the healthy lunate bones pressure increased significantly during extension of the wrist . The position-dependent pressure increases in the lunate bones indicated that the venous drainage was constantly in jeopardy . The pressure increases in necrotic lunate bones were significantly in excess of those in healthy ones ; in some cases they were far in excess of the systolic blood pressure . It was also concluded that necrotic lunate bones were mechanically deformed on movement . The anatomical causes of the pronounced pressure increases were examined experimentally . After staining of both the arteries and the veins , epoxy sheet plastination was used to fix six fresh cadaver arms in the neutral position and six in extension . Visualization of the vessels showed that capsular-ligamentous structures that were stretched on the palmar side and slackly turned back on themselves on the dorsal side still allowed the blood supply from the arteries , but substantially hindered venous drainage . The anatomical preparations made it possible to see that venous drainage from the lunate bone was being prevented ; this explained the pronounced pressure increases . The unphysiological position of the base of the radius inclined in the palmar direction relative to the hand axis when it was extended dorsally was the crucial factor in the development of necrosis . Evaluation of the histories of the patients with necrosis of the lunate bone made it clear that trauma was not significantly involved in the causation , while manual work had an important role . Most manual activites are performed with the wrist in extension . Any extension favours triggering of bone necrosis through congestion in the venous trunk . Thus , our investigations have shown that the beginning of this illness starts with congestion such as occurs with every extension of the wrist , which is initially physiological , before further factors favouring the process cause it to take a pathologic course .
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[ "umlsterm" ]

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