Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A demyelinating disease induced in C57B1/6N mice by intracranial injection of a coronavirus (murine hepatitis virus strain A59) is followed by functional recovery and efficient CNS myelin repair. To study the biological properties of the cells involved in this repair process, glial cells were isolated and cultured from spinal cords of these young adult mice during demyelination and remyelination. Using three-color immunofluorescence combined with [3H]thymidine autoradiography, we have analyzed the antigenic phenotype and mitotic potential of individual glial cells. We identified oligodendrocytes with an antibody to galactocerebroside, astrocytes with an antibody to glial fibrillary acidic protein, and oligodendrocyte-type 2 astrocyte (O-2A) progenitor cells with the O4 antibody. Cultures from demyelinated tissue differed in several ways from those of age-matched controls: first, the total number of O-2A lineage cells was strikingly increased; second, the O-2A population consisted of a higher proportion of O4-positive astrocytes and cells of mixed oligodendrocyte-astrocyte phenotype; and third, all the cell types within the O-2A lineage showed enhanced proliferation. This proliferation was not further enhanced by adding PDGF, basic fibroblast growth factor (bFGF), or insulin-like growth factor I (IGF-I) to the defined medium. However, bFGF and IGF-I seemed to influence the fate of O-2A lineage cells in cultures of demyelinated tissue. Basic FGF decreased the percentage of cells expressing galactocerebroside. In contrast, IGF-I increased the relative proportion of oligodendrocytes. Thus, O-2A lineage cells from adult mice display greater phenotypic plasticity and enhanced mitotic potential in response to an episode of demyelination. These properties may be linked to the efficient remyelination achieved in this demyelinating disease.
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PMID:In vitro analysis of the oligodendrocyte lineage in mice during demyelination and remyelination. 216 97

Isolated cases or small series of orthotopic liver transplantation (OLT) with grafts from donors older than 80 years have been reported, but the long-term outcome of patients receiving livers from extremely old donors is unknown. From 1998 to 2003, we performed 17 OLTs with donors older than 80 years (median, 82 years; range, 80 to 87 years). No deaths occurred in the early postoperative period. We analyzed the outcome in 12 patients with a follow-up longer than 1 year. Hepatic insufficiency was caused by hepatitis C virus (HCV)-related cirrhosis in five cases (42%) and non-HCV-related diseases in seven cases (58%). All donors had normal liver function, hemodynamic stability, and no parenchymal alterations. OLT was uneventful in all cases. Median follow-up was 30.3 months (range, 17 to 42 months). No late vascular complications occurred. One patient (8.3%) died 3 years after OLT for causes unrelated to hepatic dysfunction. Two- and 3-year actuarial survival rates were 100% and 75%, respectively. All HCV-positive (HCV(+)) patients developed hepatitis recurrence (after 2, 3, 4, 5, and 22 months) requiring antiviral treatment in 3 patients and leading to graft cirrhosis in 1 patient. Non-HCV(+) patients had well-preserved liver function throughout the observation period. At the end of follow-up, we observed no clinical hepatic decompensation in the entire group and biochemical signs of recurrent disease in 3 patients. Use of grafts for OLT from donors older than 80 years is safe because of their potentially normal functional recovery. A selection among available organs is mandatory to minimize other risk factors for poor outcome. Long-term patient and graft survival seem to be achievable, but the high rate and rapidity of HCV reinfection remain a major concern for HCV(+) patients.
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PMID:Long-term survival of recipients of liver grafts from donors older than 80 years: is it achievable? 1458 78

The purpose of this study is to review the role of the percutaneous interventional procedures in the treatment of vascular complications after orthotopic liver transplantations (OLT). Vascular complications, such as arterial stenosis and venous thrombosis, which occur in approximately 1% to 10% of liver transplant patients, are associated with a higher risk of graft dysfunction. Percutaneous interventional procedures, including angioplasty, local thrombolysis, and embolization, are useful to manage these complications. A reduced blood loss and a low incidence of procedural complications allow for rapid recovery. Hepatic arterial and portal vein anastomotic stenosis can be treated effectively by means of balloon dilation; stenting has also been proposed, particularly for venous complications. Infusional local thrombolysis may be useful in venous thrombosis. Arteriovenous fistulas, occurring at the level of the anastomosis or after liver biopsy, require intraarterial embolization using microcoils or gelfoam. Timing of the intervention for the treatment of ischemic complications is of outmost importance to guarantee liver functional recovery and avoid irreversible parenchymal injuries. Other interventional procedures may be extremely useful to manage portal hypertension after OLT; for example, by creation of transjugular portosystemic shunts, or, in the case of associated hypersplenism, transarterial embolization of the splenic artery. Finally, in patients with recurrent hepatitis, the transjugular approach has been shown to be safe and effective for liver biopsy, whereas transarterial chemoembolization may be extremely useful to treat recurrent hepatocarcinoma.
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PMID:Role of interventional radiology in the management of vascular complications after liver transplantation. 1511 May 91

A patient with chronic renal insufficiency undergoing dialysis treatment presented with a clinical picture of acute intrahepatic cholestasis and alterations in liver function indices. Liver biopsy showed a histological picture of hepatitis with cholestatic signs. A causal correlation with the recent administration of ticlopidine was hypothesized, which led to the drug being discontinued. Four months after drug withdrawal no improvement in the biochemical parameters had yet occurred and the patient's clinical conditions were indeed worsening so we proceeded with extracorporeal selective plasmapheresis treatments to reduce the bilirubin. As the cholestatic syndrome was unresolved and owing to the progressive worsening in the clinical picture, the patient was submitted to combined liver and kidney transplant followed by a rapid functional recovery in both organs. Regular monitoring of the hepatic function indices during the therapy with ticlopidine is therefore indispensable for the early detection of unpredictably severe hepatotoxicity.
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PMID:Severe ticlopidine-induced cholestatic syndrome. 1800 66

Multilineage differentiating stress enduring (Muse) cells, discovered in the spring of 2010 at Tohoku University in Sendai, Japan, were quickly recognized by scientists as a possible source of pluripotent cells naturally present within mesenchymal tissues. Muse cells normally exist in a quiescent state, singularly activated by severe cellular stress in vitro and in vivo. Muse cells have the capacity for self-renewal while maintaining pluripotent cell characteristics indicated by the expression of pluripotent stem cell markers. Muse cells differentiate into cells representative of all three germ cell layers both spontaneously and under media-specific induction. In contrast to embryonic stem and induced pluripotent stem cells, Muse cells exhibit low telomerase activity, a normal karyotype, and do not undergo tumorigenesis once implanted in SCID mice. Muse cells efficiently home into damaged tissues and differentiate into specific cells leading to tissue regeneration and functional recovery as described in different animal disease models (i.e., fulminant hepatitis, muscle degeneration, skin ulcers, liver cirrhosis, cerebral stroke, vitiligo, and focal segmental glomerulosclerosis). Circulating Muse cells have been detected in peripheral blood, with higher levels present in stroke patients during the acute phase. Furthermore, Muse cells have inherent immunomodulatory properties, which could contribute to tissue generation and functional repair in vivo. Genetic studies in Muse cells indicate a highly conserved cellular mechanism as seen in more primitive organisms (yeast, Saccharomyces cerevisiae, Caenorhabditis elegans, chlamydomonas, Torpedo californica, drosophila, etc.) in response to cellular stress and acute injury. This review details the molecular and cellular properties of Muse cells as well as their capacity for tissue repair and functional recovery, highlighting their potential for clinical application in regenerative medicine.
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PMID:Pluripotent nontumorigenic multilineage differentiating stress enduring cells (Muse cells): a seven-year retrospective. 2904 55