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Biomedical subjects

M A Gerber

Publications and source records attributed to M A Gerber.

At least 127 records · Page 7Linked to original sources
PubMed1990

Comparison of epidemic and endemic group G streptococci by restriction enzyme analysis.

Restriction enzyme profiles of group G beta-hemolytic streptococci associated with a point source outbreak and an outbreak of sporadic pharyngitis in two different communities were compared. To asses the epidemiologic utility of this approach for studying group G streptococci, DNA fingerprints of strains responsible for a point source outbreak of pharyngitis associated with the consumption of contaminated food were compared with DNA fingerprints of pharyngeal isolates from children with pharyngitis seen at a pediatric practice during a 6-month period. In each epidemiologic situation, a single strain characterized by a unique restriction enzyme pattern predominated. The results are compatible with the conclusion that human infections could be limited to a few strains of group G streptococci which have the capacity to spread through a given population. The restriction enzyme profiles proved to be a highly specific and precise means of evaluating strain relatedness and of providing further understanding of the epidemiology of group G streptococcal infections.

Connecticut↗
PubMed1990

Detection of hepatitis B virus DNA in formalin-fixed, paraffin-embedded liver tissue by the polymerase chain reaction.

DNA isolated from formalin-fixed, paraffin-embedded liver tissues from nine patients with hepatocellular carcinoma and six control patients was screened for hepatitis B virus (HBV) DNA with surface (S) and core (C) gene-specific primers by a modification of the polymerase chain reaction--southern blot technique (PCR-SB). PCR-SB results were correlated with histologic, immunohistochemical, and serologic findings. All cases with an established HBV etiology were positive by PCR-SB, as were three cases with negative immunohistochemistry and serology. Often there was selective amplification with one primer set and, in two cases, smaller than expected HBV amplification products suggesting internal deletions. The presence of a potent PCR inhibitor in nucleic acid preparations from tissue blocks that can be removed by Sephadex G-50 chromatography was confirmed. PCR-SB will be a powerful method for the diagnosis and follow-up of patients with HBV infection and may provide new insights into viral hepatocarcinogenesis.

Base Sequence↗
PubMed1990

Development of intrahepatic bile ducts in humans. Possible role of laminin.

Laminin, a major extracellular matrix-attachment glycoprotein, may play an important role in the differentiation and migration of epithelial cells during normal development. Therefore, the morphogenesis of bile ducts in human liver of fetuses at sequential gestational ages, neonates, children, and adults was examined by single and double immunohistochemical staining for laminin and for cytokeratins. The latter served as a marker for developing and mature bile duct epithelial cells. A close association was observed between laminin deposition and the differentiating ductal plate cells at the epithelial-mesenchymal interface of portal tracts and during the subsequent migration of ductular structures into the center of portal tracts. Simultaneously, laminin disappeared from the margins of portal tracts, but scattered ductal plate-like structures with laminin remained demonstrable in neonates, children, and even adults. These observations were substantiated by semiquantitative evaluation of laminin at the periphery of portal tracts. Thus, clear evidence is provided that laminin accompanies bile duct epithelial cells during all successive stages of differentiation and migration during the development of the human hepatobiliary system. The persisting ductal plate cells may represent a common stem cell for proliferation of bile ductules and hepatocytes.

Adult↗
PubMed1989

Failure of once-daily penicillin V therapy for streptococcal pharyngitis.

To determine if a single daily dose of penicillin V would be effective in the treatment of group A beta-hemolytic streptococcal (GABHS) pharyngitis, 154 patients with GABHS pharyngitis were randomly assigned to receive 750 mg of penicillin V once daily for ten days or 250 mg of penicillin V three times daily for ten days. The two regimens were comparable in their ability to eradicate GABHS from the upper respiratory tract in 18 to 24 hours and in their impact on the clinical course of the disease. However, a bacteriologic treatment failure occurred in six (8%) of the 76 patients in the three-times-daily group and in 16 (22%) of the 74 patients in the once-daily group. These findings support the current recommendation that penicillin V be given in two or more divided doses for a full ten days for the treatment of GABHS pharyngitis.

Adolescent↗
PubMed1989

Hepatitis B surface antigen binds to human serum albumin cross-linked by transglutaminase.

It has been postulated that polymerized human serum albumin may play a role in the infection of hepatocytes by hepatitis B virus, because both the envelope of hepatitis B virus (HBsAg) and hepatocytes exhibit binding activity for human serum albumin after cross-linking by glutaraldehyde. Since glutaraldehyde-dependent cross-linking of albumin molecules is not likely to occur in vivo, we considered the possibility that albumin may be polymerized by the action of transglutaminase enzymes present in plasma as activated factor XIII or released into plasma from tissues. Guinea pig liver transglutaminase covalently cross-linked human serum albumin molecules into dimers, trimers and polymers up to hexamers as shown by polyacrylamide gel electrophoresis in sodium dodecyl sulfate. HBsAg particles bound transglutaminase-cross-linked as well as glutaraldehyde-cross-linked human serum albumin as demonstrated by radioimmunoassay and immunoelectron microscopy. The binding was blocked by preincubation of HBsAg with transglutaminase- or glutaraldehyde-cross-linked human serum albumin, anti-HBs or monoclonal anti-pre-S2, but not by polymerized bovine or rat serum albumin or by monomeric human serum albumin. These data indicate that HBsAg particles contain specific binding sites for transglutaminase-cross-linked human serum albumin, but it remains to be determined whether the albumin polymers play a role in the attachment of hepatitis B virus to hepatocytes.

Animals↗
PubMed1989

Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas.

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.

Adenoma, Bile Duct↗
PubMed1989

Development of intrahepatic bile ducts in humans. Immunohistochemical study using monoclonal cytokeratin antibodies.

Cytokeratins (CKs) are major structural proteins of intermediate filaments of epithelia. Recent availability of monoclonal antibodies (MoAbs) against various CK polypeptides has made it possible to study their development during cellular differentiation. We analyzed the expression of CKs in the human liver during development. Twenty-four liver specimens were tested by the avidin-biotin complex immunohistochemical method by using three MoAbs against different CK polypeptides (CAM 5.2 against CKs 50, 43, and 39 kd; AE1 against acidic CKs 56.5, 50/50', 48, and 40 kd; and 34 beta E12 against CKs 58, 56.5, and 56 kd). Liver parenchymal cells in fetuses as early as 4 weeks of gestational age reacted with MoAbs CAM 5.2 and AE1, but the expression of AE1-positive CK polypeptides in hepatocytes disappeared by 24 weeks of gestational age. Small cells, presumably ductal plate cells, in direct contact with mesenchyme around the portal vein and along the branches of portal veins, showed strong staining with MoAbs CAM 5.2, AE1, and 34 beta E12, identical to that of bile ducts. In neonates, children, and even in adults, residual MoAbs CAM 5.2-,Ae1, and 34 beta E 12-positive cells were present around the branches of portal veins. These findings suggested that the CK profile of liver parenchymal cells changes during their differentiation into hepatocytes, whereas that of ductal plate cells and bile ducts remains unaltered with respect to the polypeptides tested here. Some ductal plate cells may persist in neonates, children, and even in adults.

Adult↗
PubMed1988

The group A streptococcal carrier state. A reexamination.

Streptococcal infection usually is defined as a positive throat culture with a serologic response to group A beta-hemolytic streptococci, and a patient with a positive throat culture and no serologic response is a streptococcal carrier. Studies suggest that streptococcal carriers should show little clinical response to antibiotic therapy when compared with patients with true streptococcal infections. Patients with acute pharyngitis were divided into three groups: group 1--38 patients with negative throat cultures; group 2--72 patients with a positive throat culture and a significant rise in streptococcal antibody titers; and group 3--77 patients with positive throat cultures and no significant rise in streptococcal antibody titers. Patients in group 2 and group 3 had a comparable and dramatic clinical response to antibiotic therapy that was considerably greater than the clinical response in the patients in group 1. These findings raise questions about the appropriateness of using streptococcal antibody responses to distinguish between the streptococcal carrier state and a true streptococcal infection.

Acute Disease↗
PubMed1988

Synergistic effect of 5-azacytidine and gamma-interferon or dimethyl sulfoxide on expression of HLA class I antigens by PLC-PRF-5 cells.

In order to elucidate the mechanism by which HLA antigens expression is induced or enhanced on the injured or transformed hepatocytes, we have made in vitro studies using human hepatic tumor-derived cell lines as a model system. In the present study, PLC-PRF-5 cells that have the integrated form of hepatitis B virus genome in DNA were treated with 5-azacytidine (5-azaC) in combination with gamma-interferon (IFN-gamma) or dimethyl sulfoxide (DMSO). HLA antigens on the cell surface were quantitated by using a modified cell-ELISA method. As a result, it was demonstrated that DMSO- or IFN-gamma-treatment enhanced expression of HLA class I antigens on the cell surface. In addition, enhanced expression of the antigens on PLC-PRF-5 cells treated with 5-azaC in combination with IFN-gamma or DMSO represented a synergistic effect of these inducers on HLA class I antigens expression although no changes in HLA antigens expression were induced after 5-azaC-treatment alone in short-term experiments. Furthermore, an indirect immunofluorescent analysis of hepatitis B surface antigen on the cells demonstrated increased expression of the antigen after 5-azaC-treatment alone. HLA class II antigens and hepatitis B core antigen were not induced even after those treatments and also not after a long-term experiment. These results might indicate possible modulation of HLA class I and hepatitis B virus antigens expression on the cultured cells by a DNA hypomethylating agent, 5-azaC.

Antibodies, Monoclonal↗