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)

From DBT cells persistently infected with mouse hepatitis virus JHM strain (JHM-CC), a cell line producing neither infectious virus nor intracellular viral antigen was obtained after two passages in the presence of antiserum. In addition, 11 cell clones were manipulated from JHM-CC and found to be also free from the virus. These newly obtained cell line and 4 of 11 cell clones were shown to be resistant to JHM and the virus recovered from JHM-CC (JHM-CCV), while the other 7 cell clones were susceptible to both JHM and JHM-CCV as well as vesicular stomatitis virus. The susceptibility of all the cell clones and the newly obtained cell line to JHM and JHM-CCV became higher with passages. The observations were discussed in relation to the viral persistency in JHM-CC.
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PMID:Heterologous response of antiserum-treated cell clones from a persistently infected DBT cell line to mouse hepatitis virus. 630 51

After six to eight serial undiluted passages of mouse hepatitis virus (JHM strain) in DBT cell culture, a decrease in the yield of infectious virus occurred, and with further passages fluctuating yields of infectious virus were observed. The serially passaged virus interfered with the multiplication of the standard JHM virus, but not with vesicular stomatitis virus. After sucrose equilibrium centrifugation of high passage virus, a single peak contained both infectious virus and interfering activity. This virus population resembled the original JHM virus in its structural proteins, but it contained an increased proportion of a protein with a molecular weight of 65 X 10(3). Genomic RNA from standard JHM virus contained a single species of RNA with a molecular weight of 5.4 X 10(6). After five undiluted passages, however, the virion population contained two RNA species with molecular weights of 5.4 X 10(6) and 5.2 X 10(6). RNase T1 resistant oligonucleotide finger-printing of these RNAs showed that the lower molecular weight RNA had lost several oligonucleotide spots that were present in the genomic RNA of the standard JHM virus. After several serial diluted passages of passage 10 virus, a single virus population was obtained which again had only standard virus RNA with a molecular weight of 5.4 X 10(6) and lacked interfering activity. These results indicated that defective interfering particles were generated by serial undiluted passages of JHM virus.
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PMID:Defective interfering particles of mouse hepatitis virus. 632 37

A persistently-infected neuroblastoma culture [Neuro-2A( JHMV )] was established with the murine hepatitis virus JHM [MHV-JHM]. After 100 days of passage, the endogenous virus [Neuro-2A( JHMV ) end] released by this culture was unable to induce the syncytia typical of MHV-JHM and the endogenous virus was not temperature-sensitive. The Neuro-2A( JHMV ) culture was cured of virus production by passage under neutralizing antibody [Neuro-2A( JHMV )Ab]. The Neuro-2A( JHMV ) and the Neuro-2A ( JHMV ) Ab cultures were as susceptible to heterologous infection with mengovirus and vesicular stomatitis virus as the uninfected Neuro-2A culture. However, the Neuro-2A ( JHMV ) and Neuro-2A( JHMV ) Ab cultures were partially resistant to homologous superinfection by MHV-JHM and the closely related MHV-A59. Virus related to MHV-JHM was rescued from the antibody-cured cells by cell fusion. The synthesis of MHV-JHM specific antigens by Neuro-2A( JHMV ) cells, Neuro-2A( JHMV ) Ab cells and 17 Cl-1 cells infected by Neuro-2A( JHMV ) end was studied by SDS-PAGE. The genomic RNAs of MHV-JHM and Neuro-2A( JHMV ) end were compared by oligonucleotide mapping. The results of the protein and RNA studies indicated that the genome of Neuro-2A( JHMV ) end was substantially modified from the genome of MHV-JHM, but the modifications did not significantly alter the molecular size of the viral-specific proteins.
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PMID:Biological and macromolecular properties of murine cells persistently infected with MHV-JHM. 632 42

A phase I-II study of KW2083, an analog of mitomycin C (MMC) was performed in a total of 22 patients. KW2083 was escalated by single intravenous administration of 40, 50, 60, 70, and 80 mg/m2 doses. Treatments were repeated every 4-6 weeks unless unacceptable toxicities occurred. The median times taken to reach nadir for each dose level were 9-12 days for leukocytes and 7-13 days for platelets respectively. The median times taken for recovery were 8-22 days for leukopenia and 10-37 days for thrombocytopenia. Variable and non-predictable hematological toxicity was observed in some cases. Biphasic hematological toxicity was observed in 4 courses. Acute toxicity occurred in 17 courses for 11 patients and consisted of nausea (44%), vomiting (13%), diarrhea (2.7%) and stomatitis (2.7%). Nephrotoxicity (elevation of BUN, 8.1% and proteinuria, 5.4%) occurred in 3 patients who had no previous impairment of renal function. Alopecia (8.1%) was also observed. Marked elevations of hepatic enzymes were noted in one patient who developed acute fulminant hepatitis with the second dose of KW2083. Objective response was observed in one of 20 evaluable patients. From this preliminary study, the maximum tolerable dose is 70 mg/m2 and the optimal dose of KW2083 was determined to be 50 mg/m2 at 6-week intervals. KW2083 has been introduced as an MMC analog of potential interest. However, hematological and non of hematological toxicities are very similar to those of MMC and does not appear that KW2083 will supersede MMC.
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PMID:[Phase I-II study of 7-N-(P-hydroxyphenyl)-mitomycin C (KW2083, M83)]. 647 44

A combination therapy consisting of daily intrarectal administration of 1,500 mg of FT-207 suppository, daily or every three day bladder instillation of 40 mg adriamycin for a total of 20 applications, and once per week intramuscular administration of 5 KE OK-432 was described. The therapy was performed in 30 cases of advanced bladder cancer. The effectiveness evaluated by Karnofsky's criteria was as follows: 8 cases of 0-0, 2 of 0-A, 1 of 0-B, 2 of 0-C, 7 of 1-A and 10 of 1-B, showing an effective rate of 57%. Local pain was observed in 20 cases (67%), pancytopenia in 1 (3%), hepatitis in 4 (13%), stomatitis in 5 (17%) and anorexia in 6 (20%). From this clinical trial, it is presumed that combination therapy administering FT-207 intrarectally, adriamycin intravesically and OK-432 intramuscularly might be used for the treatment of advanced bladder cancer provided sufficient care is taken of general side effects.
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PMID:Immunochemotherapy for advanced bladder cancer using FT-207, adriamycin and OK-432. 681 68

Murine F9 and PCC4 teratoma cells do not express H-2 major transplantation antigens according to virus-specific T-lymphocyte cytotoxic or serological assays. However, such cells can be infected with and readily replicate many types of viruses (coxsackie B 3, mouse hepatitis, Sindbis, Semliki Forest [SFV], lymphocytic choriomeningitis, Pichinde, vesicular stomatitis, herpes simplex type 1) to the same extent as do murine F12 teratoma cells and mouse embryo fibroblasts, all of which express the H-2 determinants. In contrast, F9 and PCC4 cells are not productively infected with murine cytomegalovirus, whereas F12 and mouse embryo fibroblast cells are. In addition to replicating in H-2-negative murine teratoma cells, SFV replicates in H-2-negative murine lymphoblastoid cells. The ability of SFV to infect cells without H-2 antigens and then to effect viral antigenic expression in the cells' cytoplasm and on their surface with similar kinetics and in equivalent amounts as cells with H-2 antigens indicates that the H-2 receptor is not needed for SFV infection. Daudi cells, which lack HLA antigens, block the replication of SFV. This occurs at some point after receptor binding, as demonstrated by diminished viral mRNA. In addition, a possible membrane defect precludes viral exit in Daudi cells transfected with SFV infectious RNA. These results indicate that a cell's possession of H-2 antigens is not a requirement for SFV infection and that major histocompatibility complex antigens are not specific receptors for this virus.
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PMID:Does the major histocompatibility complex serve as a specific receptor for Semliki Forest virus? 737 8

Systemic pathological alterations were studied in thirty-seven autopsied patients with Kawasaki disease. Systemic vasculitis was the most characteristic pathological finding and was present in all the patients. In addition to the vasculitis, there was a high incidence of inflammatory lesions in various organs and tissues: in the heart, endocarditis, myocarditis, and pericarditis; in the digestive system, stomatitis, sialoduct-adenitis, catarrhal enteritis, hepatitis, cholangitis, pancreatitis, and pancreas ductitis; in the respiratory system, bronchitis and segmental interstitial pneumonia; in the urinary system, focal interstitial nephritis, cystitis, and prostatitis; in the nervous system, aseptic leptomeningitis, choriomeningitis, gangliontis, and neuritis; in the hematopoietic system, lymphadenitis, splenitis, and thymitis. Dermatitis, panniculitis or myositis were also observed in some patients. Therefore, Kawasaki disease is a systemic inflammatory disease which mainly affects the cardiovascular system. These systemic inflammatory lesions are considered to correspond to the variegated clinical manifestaitions. The relationship between Kawasaki disease and infantile polyarteritis nodosa (IPN) were discussed, based on the clinicopathological characteristics.
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PMID:General pathology of Kawasaki disease. On the morphological alterations corresponding to the clinical manifestations. 744 9

Natural history of patients with colorectal liver metastases is not significantly changed even by curative resection. The majority unfortunately relapse. The results of adjuvant treatment after resection were evaluated by analysis of 17 publications as well as by own data (60 patients). 340 patients were either treated by intraarterial (n = 201), systemic (n = 82), intraportal (n = 29) or intraperitoneal (n = 28) chemoinfusion (5-Fluorouracil or Floxuridine). An alternative approach was the treatment with specific immunotherapy using tumor vaccination (n = 35) or monoclonal antibodies (n = 20). Morbidity of adjuvant treatment includes local (chemical hepatitis, biliary sclerosis) and systemic (diarrhea, stomatitis) side effects. Technical complications could reach a level of up to 50% in case of local administration. With exception of 6 studies no comparison with a resection only group was performed. Despite postulated increase of survival and recurrence free time with historical controls the results of current ongoing studies are needed before general use of adjuvant treatment can be recommended.
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PMID:[Results of resection and adjuvant therapy of liver metastases of primary colorectal tumors--a review of the literature]. 750 91

The A59 strain of murine coronavirus mouse hepatitis virus (MHV) can cause persistent infection of 17C1-1 cells and other murine cell lines. Persistently infected cultures released large amounts of virus (10(7) to 10(8) PFU/ml) and were resistant to superinfection with MHV but not to infection with unrelated Semliki Forest and vesicular stomatitis viruses. The culture medium from persistently infected cultures did not contain a soluble inhibitor such as interferon that protected uninfected cells from infection by MHV or vesicular stomatitis virus. The persistent infection was cured if fewer than 100 cells were transferred during subculturing, and such cured cultures were susceptible to reinfection and the reestablishment of persistent infection. Cultures of 17C1-1 cells that had been newly cloned from single cells consisted of a mixture of MHV-resistant and -susceptible cells. 17C1-1/#97 cells, which were cured by subcloning after 97 passages of a persistently infected culture over a 1-year period, contained 5 to 10% of their population as susceptible cells, while 17C1-1/#402 cells, which were cured by subcloning after 402 passages over a 3-year period, had less than 1% susceptible cells. Susceptibility to infection correlated with the expression of MHV receptor glycoprotein (MHVR [Bgp1a]). Fluorescence-activated cell sorter analysis with antibody to MHVR showed that 17C1-1/#97 cells contained a small fraction of MHVR-expressing cells. These MHVR-expressing cells were selectively eliminated within 24 h after challenge with MHV-A59, and pretreatment of 17C1-1/#97 cells with monoclonal antibody CC1, which binds to the N-terminal domain of MHVR, blocked infection. We conclude that the subpopulation of MHVR-expressing cells were infected and killed in acutely or persistently infected cultures, while the subpopulation of MHVR-nonexpressing cells survived and proliferated. The subpopulation of MHVR-negative cells produced a small proportion of progeny cells that expressed MHVR and became infected, thereby maintaining the persistent infection as a steady-state carrier culture. Thus, in 17C1-1 cell cultures, the unstable or epigenetic expression of MHVR permitted the establishment of a persistent, chronic infection.
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PMID:Persistent infection of cultured cells with mouse hepatitis virus (MHV) results from the epigenetic expression of the MHV receptor. 763 98

An ex vivo antiviral assay was established which uses hepatocytes from mice given recombinant mouse interferon-beta (rmIFN-beta). Assay results were compared with results obtained with a 2',5'-oligoadenylate synthetase (2-5AS) assay. rmIFN-beta was intraperitoneally administered to C3H mice and the antiviral state of their liver parenchymal cells was evaluated in an in vitro cytopathic effect assay. In this assay, cells are infected with vesicular stomatitis virus (VSV) and surviving cells are determined colorimetrically. The antiviral state was measured as the resistance of hepatocytes to VSV infection with increasing doses of rmIFN-beta. The antiviral state correlated well with the dose-dependent increase in hepatic 2-5AS activity. This good correlation suggests that induction of 2-5AS mediates the antiviral action of interferon in liver tissue. This ex vivo assay could be a useful tool for estimating the ability of hepatocytes to resist hepatitis virus infection.
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PMID:An ex vivo assay for estimating the antiviral state of hepatocytes. 773 17


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