tacrolimus and Cerebrovascular-Disorders

tacrolimus has been researched along with Cerebrovascular-Disorders* in 4 studies

Reviews

2 review(s) available for tacrolimus and Cerebrovascular-Disorders

Article	Year
[Neurologic disorders in renal transplantation]. Ryoikibetsu shokogun shirizu, 2000, Issue:29 Pt 4 Topics: Central Nervous System Diseases; Cerebrovascular Disorders; Cyclosporine; Humans; Immunosuppressive Agents; Kidney Transplantation; Mental Disorders; Neuromuscular Diseases; Seizures; Tacrolimus	2000
[Current tendency in treatment for acute ischemic stroke]. Nihon Ika Daigaku zasshi, 1999, Volume: 66, Issue:3 Topics: Acute Disease; Animals; Cerebrovascular Circulation; Cerebrovascular Disorders; Fibrinolytic Agents; Free Radical Scavengers; Glycerol; Humans; Immunosuppressive Agents; Tacrolimus; Time Factors	1999

Other Studies

2 other study(ies) available for tacrolimus and Cerebrovascular-Disorders

Article	Year
Transplantation-related thrombotic microangiopathy triggered by preemptive therapy for hepatitis C virus infection. Transplantation, 2008, Oct-15, Volume: 86, Issue:7 Topics: Adult; Antiviral Agents; Brain; Cerebrovascular Circulation; Cerebrovascular Disorders; Female; Hepatitis C; Humans; Immunosuppressive Agents; Liver Transplantation; Magnetic Resonance Imaging; Purpura, Thrombotic Thrombocytopenic; Tacrolimus	2008
FK506 prevents stroke-induced generation of ceramide and apoptosis signaling. Brain research, 1999, May-01, Volume: 826, Issue:2 Ceramide is a key mediator of apoptosis during the cellular stress response which is also involved in stroke-induced death. Transient occlusion of the middle cerebral artery (MCA) in rats led to a strong generation of ceramide as measured in thalamus and entorhinal cortex of the ischemic brain tissue. Enhanced levels of ceramide may be involved in apoptosis signaling following stroke since exogenously added synthetic C2-ceramide increased expression of c-jun and the death-inducing ligands (DILs) CD95-L, TRAIL and TNF-alpha in neuroblastoma cells. DILs in turn mediated death via binding to their respective receptors as concluded from diminished apoptosis upon blocking of the common pathway by dominant negative FADD. C2-ceramide induced both necrosis and apoptosis in a concentration-dependent manner corresponding to the situation present in the ischemic brain. The immunosuppressant FK506 inhibited the release of ceramide, expression of CD95-L and apoptosis in an in vitro and in vivo model for ischemia/reperfusion. These data suggest that ceramide is a crucial initiator of death, e.g., by induction of DILs following stroke. Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Brain Chemistry; Cerebrovascular Disorders; Enzyme Inhibitors; Fas Ligand Protein; Gene Expression; Humans; Immunosuppressive Agents; Ischemic Attack, Transient; Male; Membrane Glycoproteins; Necrosis; Neuroblastoma; Neurons; Proto-Oncogene Proteins c-jun; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction; Sphingosine; Tacrolimus; TNF-Related Apoptosis-Inducing Ligand; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha; Up-Regulation	1999

Article

Year

Transplantation-related thrombotic microangiopathy triggered by preemptive therapy for hepatitis C virus infection.

Transplantation, 2008, Oct-15, Volume: 86, Issue:7

Topics: Adult; Antiviral Agents; Brain; Cerebrovascular Circulation; Cerebrovascular Disorders; Female; Hepatitis C; Humans; Immunosuppressive Agents; Liver Transplantation; Magnetic Resonance Imaging; Purpura, Thrombotic Thrombocytopenic; Tacrolimus

2008

FK506 prevents stroke-induced generation of ceramide and apoptosis signaling.

Brain research, 1999, May-01, Volume: 826, Issue:2

Ceramide is a key mediator of apoptosis during the cellular stress response which is also involved in stroke-induced death. Transient occlusion of the middle cerebral artery (MCA) in rats led to a strong generation of ceramide as measured in thalamus and entorhinal cortex of the ischemic brain tissue. Enhanced levels of ceramide may be involved in apoptosis signaling following stroke since exogenously added synthetic C2-ceramide increased expression of c-jun and the death-inducing ligands (DILs) CD95-L, TRAIL and TNF-alpha in neuroblastoma cells. DILs in turn mediated death via binding to their respective receptors as concluded from diminished apoptosis upon blocking of the common pathway by dominant negative FADD. C2-ceramide induced both necrosis and apoptosis in a concentration-dependent manner corresponding to the situation present in the ischemic brain. The immunosuppressant FK506 inhibited the release of ceramide, expression of CD95-L and apoptosis in an in vitro and in vivo model for ischemia/reperfusion. These data suggest that ceramide is a crucial initiator of death, e.g., by induction of DILs following stroke.

Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Brain Chemistry; Cerebrovascular Disorders; Enzyme Inhibitors; Fas Ligand Protein; Gene Expression; Humans; Immunosuppressive Agents; Ischemic Attack, Transient; Male; Membrane Glycoproteins; Necrosis; Neuroblastoma; Neurons; Proto-Oncogene Proteins c-jun; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction; Sphingosine; Tacrolimus; TNF-Related Apoptosis-Inducing Ligand; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha; Up-Regulation

1999