The Experts below are selected from a list of 171 Experts worldwide ranked by ideXlab platform
Gisa Tiegs - One of the best experts on this subject based on the ideXlab platform.
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concanavalin a induced Liver Cell Damage activation of intraCellular pathways triggered by tumor necrosis factor in mice
Gastroenterology, 1998Co-Authors: C Trautwein, Tim Rakemann, David A Brenner, Konrad L Streetz, L L Licato, Michael P Manns, Gisa TiegsAbstract:Abstract Background & Aims: Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. IntraCellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-κB translocation, or Jun kinase (JNK) activation. The aim of this study was to study TNF-dependent pathways after con A injection in vivo. Methods: Con A, con A plus anti-TNF, and control buffer were injected into BALB/c mice. Immunofluorescence, Western blot, Northern blot, gel shift, Erk, and JNK activity and DNA fragmentation experiments were performed at different time points after injection. Results: DNA fragmentation in hepatocytes was increased 4–24 hours after con A injection. JNK was activated maximally (>20-fold) directly after con A injection, whereas binding and nuclear translocation of NF-κB was maximal after 4 hours. All pathways were blocked by anti-TNF. JNK activation was specific because related ERK 1 + 2 were not activated after con A. High nuclear expression of c-Jun was already evident 1 hour after con A injection; however, in contrast to JNK, anti-TNF treatment did not block c-Jun nuclear expression and DNA binding. Conclusions: In the con A model, activation of TNF-dependent pathways is associated with apoptosis of hepatocytes. Their modulation in vivo may have implications to develop new therapeutic strategies to prevent apoptosis. GASTROENTEROLOGY 1998;114:1035-1045
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Concanavalin A—induced Liver Cell Damage: Activation of intraCellular pathways triggered by tumor necrosis factor in mice
Gastroenterology, 1998Co-Authors: C Trautwein, Tim Rakemann, David A Brenner, Konrad L Streetz, L L Licato, Michael P Manns, Gisa TiegsAbstract:Abstract Background & Aims: Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. IntraCellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-κB translocation, or Jun kinase (JNK) activation. The aim of this study was to study TNF-dependent pathways after con A injection in vivo. Methods: Con A, con A plus anti-TNF, and control buffer were injected into BALB/c mice. Immunofluorescence, Western blot, Northern blot, gel shift, Erk, and JNK activity and DNA fragmentation experiments were performed at different time points after injection. Results: DNA fragmentation in hepatocytes was increased 4–24 hours after con A injection. JNK was activated maximally (>20-fold) directly after con A injection, whereas binding and nuclear translocation of NF-κB was maximal after 4 hours. All pathways were blocked by anti-TNF. JNK activation was specific because related ERK 1 + 2 were not activated after con A. High nuclear expression of c-Jun was already evident 1 hour after con A injection; however, in contrast to JNK, anti-TNF treatment did not block c-Jun nuclear expression and DNA binding. Conclusions: In the con A model, activation of TNF-dependent pathways is associated with apoptosis of hepatocytes. Their modulation in vivo may have implications to develop new therapeutic strategies to prevent apoptosis. GASTROENTEROLOGY 1998;114:1035-1045
Robert Girot - One of the best experts on this subject based on the ideXlab platform.
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use of the ferritin alanine aspartate transaminase ratio as an iron overload marker independent of Liver Cell Damage
European Journal of Haematology, 2009Co-Authors: P Triadou, A Regnatlusinchi, Robert GirotAbstract:: To define an iron overload index independent of Liver Cell Damage, the mean annual levels of alanine aspartate transaminase (ALAT) and serum ferritin and their ratios were determined. Ferritin/ALAT ratio values were compared between two groups of patients with acute or chronic hepatitis without iron overload, and one group of thalassaemic patients with iron overload. The two groups without iron overload exhibited ferritin/ALAT ratio values of 2 and 1.2 respectively; a ratio value higher than 10 was always observed in those patients with iron overload. The ferritin/ALAT ratio is correlated with the degree of iron overload. This ratio increases in regularly-transfused patients without chelation treatment. It generally remains stable or decreases after initiation of iron chelation therapy. The ferritin/ALAT ratio thus appears useful in the follow-up of patients subjected to a long-term transfusional treatment particularly when acute or chronic Liver Cell Damage may interfere with iron overload by increasing serum ferritin values.
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Use of the ferritin/alanine aspartate transaminase ratio as an iron overload marker independent of Liver Cell Damage
European Journal of Haematology, 2009Co-Authors: P Triadou, A. Regnat-lusinchi, Robert GirotAbstract:: To define an iron overload index independent of Liver Cell Damage, the mean annual levels of alanine aspartate transaminase (ALAT) and serum ferritin and their ratios were determined. Ferritin/ALAT ratio values were compared between two groups of patients with acute or chronic hepatitis without iron overload, and one group of thalassaemic patients with iron overload. The two groups without iron overload exhibited ferritin/ALAT ratio values of 2 and 1.2 respectively; a ratio value higher than 10 was always observed in those patients with iron overload. The ferritin/ALAT ratio is correlated with the degree of iron overload. This ratio increases in regularly-transfused patients without chelation treatment. It generally remains stable or decreases after initiation of iron chelation therapy. The ferritin/ALAT ratio thus appears useful in the follow-up of patients subjected to a long-term transfusional treatment particularly when acute or chronic Liver Cell Damage may interfere with iron overload by increasing serum ferritin values.
C Trautwein - One of the best experts on this subject based on the ideXlab platform.
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concanavalin a induced Liver Cell Damage activation of intraCellular pathways triggered by tumor necrosis factor in mice
Gastroenterology, 1998Co-Authors: C Trautwein, Tim Rakemann, David A Brenner, Konrad L Streetz, L L Licato, Michael P Manns, Gisa TiegsAbstract:Abstract Background & Aims: Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. IntraCellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-κB translocation, or Jun kinase (JNK) activation. The aim of this study was to study TNF-dependent pathways after con A injection in vivo. Methods: Con A, con A plus anti-TNF, and control buffer were injected into BALB/c mice. Immunofluorescence, Western blot, Northern blot, gel shift, Erk, and JNK activity and DNA fragmentation experiments were performed at different time points after injection. Results: DNA fragmentation in hepatocytes was increased 4–24 hours after con A injection. JNK was activated maximally (>20-fold) directly after con A injection, whereas binding and nuclear translocation of NF-κB was maximal after 4 hours. All pathways were blocked by anti-TNF. JNK activation was specific because related ERK 1 + 2 were not activated after con A. High nuclear expression of c-Jun was already evident 1 hour after con A injection; however, in contrast to JNK, anti-TNF treatment did not block c-Jun nuclear expression and DNA binding. Conclusions: In the con A model, activation of TNF-dependent pathways is associated with apoptosis of hepatocytes. Their modulation in vivo may have implications to develop new therapeutic strategies to prevent apoptosis. GASTROENTEROLOGY 1998;114:1035-1045
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Concanavalin A—induced Liver Cell Damage: Activation of intraCellular pathways triggered by tumor necrosis factor in mice
Gastroenterology, 1998Co-Authors: C Trautwein, Tim Rakemann, David A Brenner, Konrad L Streetz, L L Licato, Michael P Manns, Gisa TiegsAbstract:Abstract Background & Aims: Concanavalin A (con A) induces tumor necrosis factor (TNF)-dependent hepatocyte apoptosis resembling immune-mediated fulminant hepatic failure in humans. IntraCellular pathways originating at the TNF receptor are either linked to apoptosis, nuclear factor (NF)-κB translocation, or Jun kinase (JNK) activation. The aim of this study was to study TNF-dependent pathways after con A injection in vivo. Methods: Con A, con A plus anti-TNF, and control buffer were injected into BALB/c mice. Immunofluorescence, Western blot, Northern blot, gel shift, Erk, and JNK activity and DNA fragmentation experiments were performed at different time points after injection. Results: DNA fragmentation in hepatocytes was increased 4–24 hours after con A injection. JNK was activated maximally (>20-fold) directly after con A injection, whereas binding and nuclear translocation of NF-κB was maximal after 4 hours. All pathways were blocked by anti-TNF. JNK activation was specific because related ERK 1 + 2 were not activated after con A. High nuclear expression of c-Jun was already evident 1 hour after con A injection; however, in contrast to JNK, anti-TNF treatment did not block c-Jun nuclear expression and DNA binding. Conclusions: In the con A model, activation of TNF-dependent pathways is associated with apoptosis of hepatocytes. Their modulation in vivo may have implications to develop new therapeutic strategies to prevent apoptosis. GASTROENTEROLOGY 1998;114:1035-1045
Myung Sook Oh - One of the best experts on this subject based on the ideXlab platform.
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effects of processed rhubarb on Liver Cell Damage in vitro and in vivo
The FASEB Journal, 2015Co-Authors: Dalseok Oh, Hyein Oh, Tong Ho Kang, Myung Sook OhAbstract:The rhizome of rhubarb (RR) has been utilized as an efficacious laxative. However, RR is inappropriate for elderly patients due to its Liver toxicity. The aim of this study was to investigate chang...
P Triadou - One of the best experts on this subject based on the ideXlab platform.
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use of the ferritin alanine aspartate transaminase ratio as an iron overload marker independent of Liver Cell Damage
European Journal of Haematology, 2009Co-Authors: P Triadou, A Regnatlusinchi, Robert GirotAbstract:: To define an iron overload index independent of Liver Cell Damage, the mean annual levels of alanine aspartate transaminase (ALAT) and serum ferritin and their ratios were determined. Ferritin/ALAT ratio values were compared between two groups of patients with acute or chronic hepatitis without iron overload, and one group of thalassaemic patients with iron overload. The two groups without iron overload exhibited ferritin/ALAT ratio values of 2 and 1.2 respectively; a ratio value higher than 10 was always observed in those patients with iron overload. The ferritin/ALAT ratio is correlated with the degree of iron overload. This ratio increases in regularly-transfused patients without chelation treatment. It generally remains stable or decreases after initiation of iron chelation therapy. The ferritin/ALAT ratio thus appears useful in the follow-up of patients subjected to a long-term transfusional treatment particularly when acute or chronic Liver Cell Damage may interfere with iron overload by increasing serum ferritin values.
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Use of the ferritin/alanine aspartate transaminase ratio as an iron overload marker independent of Liver Cell Damage
European Journal of Haematology, 2009Co-Authors: P Triadou, A. Regnat-lusinchi, Robert GirotAbstract:: To define an iron overload index independent of Liver Cell Damage, the mean annual levels of alanine aspartate transaminase (ALAT) and serum ferritin and their ratios were determined. Ferritin/ALAT ratio values were compared between two groups of patients with acute or chronic hepatitis without iron overload, and one group of thalassaemic patients with iron overload. The two groups without iron overload exhibited ferritin/ALAT ratio values of 2 and 1.2 respectively; a ratio value higher than 10 was always observed in those patients with iron overload. The ferritin/ALAT ratio is correlated with the degree of iron overload. This ratio increases in regularly-transfused patients without chelation treatment. It generally remains stable or decreases after initiation of iron chelation therapy. The ferritin/ALAT ratio thus appears useful in the follow-up of patients subjected to a long-term transfusional treatment particularly when acute or chronic Liver Cell Damage may interfere with iron overload by increasing serum ferritin values.