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)

Based on the incidence survey of leukemia and aplastic anemia (AA) from 1986 to 1988, Case control studies (1257 new leukemia cases and 339 new AA cases) were carried out according to the type of leukemia and AA in order to better understand the epidemiologic characteristics of the diseases. Controls were matched randomly (age, sex and ethnic group) from the same population. The data were analyzed with the conditional Logistic multi-regression model and calculated on an IBM-PC/XT. The risk factors of M2a were found to be X-rays, antipyretics, benzene, pesticides and bimolane; that of M3 was chloramphenicol; that of M5 was X-rays; and that of other ANLLs was phenylbutazone. The risk factors of ALL were chloramphenicol, phenylbutazone and family members with cancer; those of CML were X-rays and hepatitis; those of CLL were chloramphenicol and benzene; those of AAA were antipyretics and hepatitis; and that of CAA ws X-rays.
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PMID:[Risk factors analysis of leukemia and aplastic anemia in China. Chinese Epidemiologic Study Group of Leukemia and Aplastic Anemia]. 139 36

A study was conducted to estimate the functional reserve of the liver of patients with severe hepatitis by computed tomography (CT), in particular employing the integrated CT number of the whole liver (ICTN). ICTN was calculated by integrating the product of "area" times "mean CT number" of the liver in each CT slice for the entire height of the liver. The following results were obtained: 1) In patients with fulminant hepatitis (FH) as well as those with subacute hepatitis (SAH), ICTN was found to be significantly lower as compared to that of patients with acute hepatitis (AH) or non-hepatic diseases. In addition, in FH and SAH patients, ICTN showed a larger degree of decrease when compared with such conventional parameters as either estimated liver volume or mean hepatic CT number. Thus, ICTN seems to more sensitively reflect the changes in functional reserve of the liver. 2) ICTN showed significant positive correlations with prothrombin time and plasma BCAA/AAA ratio, and a significant negative correlation with plasma methionine level. 3) Time course of changes in ICTN correlated well with the clinical features of severe hepatitis. In particular, patients with initial ICTN values above 20 l.HU/m2 of body surface area showed significantly higher survival rate than those with initial ICTN below 20. In conclusion, ICTN well indicates the functional reserve of the liver, and is further suggested to be valuable as a parameter to predict the prognosis of patients with severe hepatitis.
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PMID:Determination of the integrated CT number of the whole liver in patients with severe hepatitis: as an indicator of the functional reserve of the liver. 274 45

Male and female B6C3F1 mice from 12 National Toxicology Program (NTP) 2-yr carcinogenesis studies were found to be infected with Helicobacter hepaticus. Many of the male mice from 9 of these studies had an associated hepatitis (affected studies). Helicobacter hepaticus has been reported to be associated with an increased incidence of hepatitis and hepatocellular neoplasms in the A/JCr male mouse. We attempted to determine if the data from the Helicobacter-affected NTP B6C3F1 mouse studies were compromised and unsuitable for cancer hazard identification. The incidences of neoplasms of the liver (both hepatocellular and hemangiosarcoma) but not of other organs in control male B6C3F1 mice were increased in affected studies as compared with control males from unaffected studies. The increased incidence of hepatocellular neoplasms was observed in those males exhibiting H. hepaticus-associated hepatitis. Other observations further differentiated control male mice from affected and unaffected studies. H-ras codon 61 CAA to AAA mutations were less common in liver neoplasms from males from affected studies as compared with historical and study controls. In addition, increases in cell proliferation rates and apoptosis were observed in the livers of male mice with H. hepaticus-associated hepatitis. These data support the hypothesis that the increased incidence of liver neoplasms is associated with H. hepaticus and that hepatitis may be important in the pathogenesis. Therefore, interpretation of carcinogenic effects in the liver of B6C3F1 mice may be confounded if there is H. hepaticus-associated hepatitis.
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PMID:Impact of Helicobacter hepaticus infection in B6C3F1 mice from twelve National Toxicology Program two-year carcinogenesis studies. 978 46

The detection of anti-actin (AAA) by immunofluorescence is hindered by the presence of a serum factor. To better understand how it interferes with AAA detection, we tested sera from 20 patients with autoimmune hepatitis, and from 21 healthy adults, diluted 1:10 and prepared as follows: (A) diluted with PBS; (B) inactivated at 56 degrees C, and diluted with PBS; (C) diluted with 34 mM EDTA/PBS; (D) heated and diluted with EDTA/PBS. To reveal AAA, a fluorescein-labelled anti-human IgG was used in the process of indirect immunofluorescence. In a parallel assay, the substrate, acetone-fixed human fibroblasts, was preincubated with sera prepared as if it were to identify AAA, but instead, a rhodamine-phalloidin was used to identify F-actin, by direct immunofluorescence. All sera from patients were reactive to AAA when heat-inactivated and/or calcium-chelated, and 60% of them when diluted with unmodified sera (P=0.004). F-actin continued to be present after preincubation with heat-inactivated or calcium-chelated sera from patients and healthy controls, and in 41.5% of reactions with unmodified serum (P=0.0000001). The heat inactivation and the calcium chelation were both efficient procedures for maintaining the microfilament structure intact after serum incubation and, therefore, for identifying AAA.
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PMID:Thermolabile and calcium-dependent serum factor interferes with polymerized actin, and impairs anti-actin antibody detection. 1171 60

Current opinions suggest that autoantibodies occurring in autoimmune diseases are generated by B-cells which primarily produce polyspecific natural autoantibodies, through either polyclonal activation or specific antigen selection of these B-cells. In this study, we compared the immunological properties (polyspecificity, fine specificity and IgG subclasses) between natural anti-actin antibodies (N-AAA) and disease-associated AAA (D-AAA). IgG AAA from sera of healthy donors, patients with autoimmune hepatitis type 1 (AIH-1) and patients with primary biliary cirrhosis (PBC) were affinity-purified on actin immunoadsorbent and tested initially for polyspecificity against various cytoskeleton proteins by enzyme-linked immunosorbent assay (ELISA). Fine specificity was studied by Western blotting using proteolytic peptides of actin and by ELISA using synthetic 12 mer peptides, spanning the 221-377 aa sequence of actin. Results showed that both N-AAA and D-AAA are polyspecific. Nevertheless, D-AAA from both diseases showed a specific reactivity pattern as compared to N-AAA, against the 16 kDa C-terminal (229-377 aa) proteolytic peptide of actin and more specifically against the P36 synthetic peptide (351-362 aa). Quantitation of AAA IgG subclasses revealed that IgG1 and IgG3 were specifically increased in D-AAA from AIH-1 and PBC, respectively, as compared to N-AAA. We conclude that D-AAA are differentiated from N-AAA in terms of fine specificity and IgG subclasses, probably through specific antigen selection of B-cells primarily producing N-AAA.
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PMID:Fine specificity and subclasses of IgG anti-actin autoantibodies differ in health and disease. 1279 19

Deficiency of circulating alpha-1-antitrypsin (AAT) is the most widely recognized abnormality of a proteinase inhibitor that causes lung disease. AAT-deficiency is caused by mutations of the AAT gene that lead to AAT protein retention in the endoplasmic reticulum (ER). Moreover, the mutant AAT accumulated in the ER predisposes the homozygote to severe liver injuries, such as neonatal hepatitis, juvenile cirrhosis, and hepatocellular carcinoma. Despite the fact that mutant AAT protein is subject to ER-associated degradation (ERAD), yeast genetic studies have determined that the ubiquitination machinery, Hrd1/Der3p-cue1p-Ubc7/6p, which plays a prominent role in ERAD, is not involved in degradation of mutant AAT. Here we report that gp78, a ubiquitin ligase (E3) pairing with mammalian Ubc7 for ERAD, ubiquitinates and facilitates degradation of ATZ, the classic deficiency variant of AAT having a Z mutation (Glu 342 Lys). Unexpectedly, gp78 over-expression also significantly increases ATZ solubility. p97/VCP, an AAA ATPase essential for retrotranslocation of misfolded proteins from the ER during ERAD, is involved in gp78-mediated degradation of ATZ. Surprisingly, unlike other ERAD substrates that cause ER stress leading to apoptosis when accumulated in the ER, ATZ, in fact, increases cell proliferation when over-expressed in cells. This effect can be partially inhibited by gp78 over-expression. These data indicate that gp78 assumes multiple unique quality control roles over ATZ, including the facilitation of degradation and inhibition of aggregation of ATZ.
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PMID:Ubiquitin ligase gp78 increases solubility and facilitates degradation of the Z variant of alpha-1-antitrypsin. 1697 36

Anti-actin antibodies are found in 52-85% of patients with autoimmune hepatitis or chronic active hepatitis and in 22% of patients with primary biliary cirrhosis. In patients with celiac disease, anti-actin antibodies correlate with the degree of villous atrophy. Studies on their involvement in celiac disease and dermatitis herpetiformis in Romania have not been done. The purpose of this study was to evaluate of the quality of IgG anti-F-actin antibodies (IgG-AAA) tests compared with IgA tissue transglutaminase antibodies (IgA-TgA) having IgA endomysial antibody (IgA-EmA) as gold standard in celiac disease and dermatitis herpetiformis and to see if there is any relationship between them. The study included 70 pediatric patients with celiac disease under gluten-free diets and 10 adult patients with dermatitis herpetiformis, during 2010. The IgG-AAA antibodies levels were determined by ELISA. Assessing the qualities of IgG-AAA compared to IgA-TgA, we obtained the following values sensitivity (Se) 27.8%, specificity (Sp) 79.4%, respectively Se 88.9%, Sp 79.4% in celiac disease and Se 33.3%, Sp 100%, respectively Se 100%, Sp 100% in dermatitis herpetiformis. Also, there was a prevalence of 24.3% and 30% of IgG-AAA in the two groups of patients, but no statistically significant associations were found. Therefore, we concluded that IgG-AAA can not replace IgA-TgA in children patients with celiac disease under gluten-free diets and in adult patients with dermatitis herpetiformis. AAA-IgG serum activity in both diseases exist, but without a relationship of association with them.
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PMID:IgG-F-actin antibodies in celiac disease and dermatitis herpetiformis. 2146 31