Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ELISA detection of a hepatitis-E-virus-associated antigen (HEV-AAg) in stools was reappraised for its possible interference with a new Fab-binding factor, termed protein Fv, released during infectious hepatitis. Transaminase elevation, HEV-AAg discharge and Fv leakage appeared simultaneously in a Cercopithecus monkey inoculated with infected stools. Labelled normal, or immune human IgG, were compared with pre- and post-inoculation simian IgG, for HEV-AAg and Fv detection. Coated normal and patient human IgM were also compared to pre- and post-inoculation simian IgM in HEV-AAg and Fv capture assays. Simian IgM and beta-galactosidase-labelled simian IgG minimized Fv interference and appeared to be the best adapted system for HEV-AAg detection. Nevertheless, Fv was still the cause of false-positive interpretations in some cases; therefore adsorption with monoclonal IgM was required to ensure HEV specificity. The improved test was performed on stools from 30 Senegalese patients hospitalized for various sporadic attacks of viral hepatitis. HEV-AAg was detected in 6 out of 30 cases and no positivity was observed in patients suffering from hepatitis due to HAV, HBV, cytomegalovirus or Epstein-Barr virus. The specificity of the assay was confirmed by inhibition experiments with the sera from HEV-infected patients. Hence, this inhibition assay can also be used to detect serum antibodies to HEV-AAg.
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PMID:Hepatitis-E-virus-associated antigen: improved detection in stools by protein Fv removal. 166 35

Anti-M2 of anti-mitochondrial antibody (AMA) is a serological marker of primary biliary cirrhosis (PBC). Anti-pyruvate dehydrogenase complex-E2 (anti-PDC-E2) is recognized as the most frequently occurring anti-M2, and a routine laboratory test for this antibody has already been established. However, it is also known that there are patients with PBC who are negative for anti-PDC-E2. For the serological diagnosis of these patients, immunoblotting for anti-M2s is indicated. However, the technique currently utilized is too laborious to allow testing of a large number of samples. In this study, we have developed an enzyme-linked immunosorbent assay (ELISA) using a recombinant fusion protein in order to evaluate anti-branched chain 2-oxo-acid dehydrogenase complex-E2 (anti-BCOADC-E2), another frequently occurring anti-M2 in PBC patients. KB cell lines (CCL 17) were utilized as source material, and BCOADC-E2 cDNA (971 bp) including the lipoic acid binding domain was amplified by polymerase chain reaction. The amplified region was subcloned into pEX-3 vectors and expressed, and the resulting fusion protein (beta-galactosidase/BCOADC-E2) was utilized as antigen for an ELISA. We ascertained the specificity of this antigen by inhibition tests with ELISA and immunoblotting. We defined the cut-off optical density (OD) value as the mean + 3 SD (0.146) of sera from 60 normal controls. Anti-BCOADC-E2 could not be detected with this assay in sera from normal controls and from patients with autoimmune hepatitis and chronic viral hepatitis. Anti-BCOADC-E2 was detected in 119 of 210 sera (56.7%) from patients with PBC. In addition, anti-BCOADC-E2 was detected in 48 of 99 (48.5%) sera from PBC patients who were negative for anti-PDC-E2. Here, we have succeeded in developing a new ELISA for detecting anti-BCOADC-E2. This system is antigen-specific and easily performed. This assay should allow routine testing of a large number of serum samples, and should become especially useful for the serodiagnosis of anti-PDC-E2-negative PBC patients.
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PMID:Detection of anti-branched chain 2-oxo acid dehydrogenase complex (BCOADC)-E2 antibody in primary biliary cirrhosis by ELISA using recombinant fusion protein. 1043 90

Lentiviral vectors have been used for gene transfer into the liver, but the ability of these vectors to efficiently transduce quiescent hepatocytes remains controversial. Regardless, lentivirus-mediated gene transfer is greatly enhanced when delivered during hepatocellular cycling. For this reason, the present study was designed to determine the role of hepatocyte proliferation in the enhancement of lentiviral transduction by using three different modes of liver regeneration: (1) compensatory regeneration stimulated by two-thirds partial hepatectomy, (2) direct hyperplasia after intragastric administration of the primary mitogen 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP), and (3) a combination of modes 1 and 2. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped lentiviral vector expressing beta-galactosidase was administered to mice via the peripheral circulation after a regeneration stimulus. Gene transfer as measured by 5-bromo-4-chloro-3-indolyl-beta-D-galactoside (X-Gal) staining showed 30-fold higher levels of liver transduction in groups 1 and 2 as compared with the non-liver-manipulated control group (p < 0.005). The combination of TCPOBOP and partial hepatectomy (group 3) resulted in an ~80-fold increase in transduction efficiency compared with the control animals. The enhanced transduction was consistent with higher levels of hepatocellular proliferation observed in animals that received both treatments compared with either single treatment alone. Importantly, the hepatocytes were the predominant cell type transduced, although transgene expression was observed in a low number of nonparenchymal cells regardless of which liver stimulus was received. Biodistribution studies confirmed that most of the gene transfer was limited to the liver and spleen. Taken together, this study suggests that disease-induced cellular proliferation in the liver will enhance the utility of this vector in treating diseases such as viral hepatitis, liver cirrhosis, and cancer.
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PMID:Role of hepatocyte direct hyperplasia in lentivirus-mediated liver transduction in vivo. 1191 88

Large cell change involves the clustering of hepatocytes with hyperchromatism and cellular enlargement without an increase in the nuclear/cytoplasmic ratio. This study investigated whether large cell change in chronic viral hepatitis reflects cellular senescence because of morphological similarities between the 2 conditions. The expression of markers of senescence such as senescence-associated beta-galactosidase, senescence-associated heterochromatic foci, and p21, as well as markers of cell kinetics such as Ki-67, was examined in 26 frozen and 82 formalin-fixed liver specimens. Large cell change was frequently detected in chronic hepatitis B cases with advanced histologic staging, particularly those with hepatocellular carcinoma. Senescence-associated beta-galactosidase activity, senescence-associated heterochromatic foci, and p21 were frequently detected in areas of large cell change. Hepatocytes with large cell change showed no proliferative or apoptotic activity. The frequent expression of senescent features and the absence of proliferative or apoptotic activity suggest that large cell change represents senescence. The parallel increase in large cell change and hepatocellular carcinoma in chronic hepatitis B raises the possibility that cellular senescence develops as a safeguard against malignant transformation rather than as a precursor of hepatocellular carcinoma.
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PMID:Large cell change of hepatocytes in chronic viral hepatitis represents a senescent-related lesion. 1973 84