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M Kabeer

Publications and source records attributed to M Kabeer.

11 recordsLinked to original sources

Mesocaval shunt inhibits primary and metastatic hepatoma growth and enhances apoptosis.

BACKGROUND: Previous reports indicate that hepatocyte growth factor and other hepatic trophic factors reach the liver presumably by portal venous inflow and stimulate experimental hepatic tumor growth, invasion, and metastasis. This study tests this hypothesis by evaluating whether a mesocaval shunt (MCS) alters hepatic tumor growth, the mitotic rate, apoptosis, and incidence and growth of lung metastasis in rats with implanted hepatoma. METHODS: Morris hepatoma (1 x 10(5)) cells were implanted intrahepatically in 19 ACI rats. One week after implantation, 10 rats underwent MCS operation and nine controls a sham operation. Rats were killed 21 days after the operation to assess tumor volume, tumor cell mitosis, apoptosis, area of tumor necrosis, pulmonary metastases and percentage of lung tumor area. RESULTS: Mesocaval shunt induced a significant increase in the rate of tumor apoptosis (25 +/- 5 v 14 +/- 6, P < .01) and the percentage of area of tumor necrosis (29% +/- 17% v 13% +/- 8%, P < .05), a decreased tumor volume (839 +/- 1,195 v 2,909 +/- 2,572, P < .05), a reduction in tumor mitosis (70 +/- 28 v 93 +/- 11, P < .05) and decreased percentage area of pulmonary metastatic tumor (9.8 +/- 6.8 v 18.8 +/- 14, P < .05). CONCLUSION: These observations show that growth of intrahepatic tumor is influenced by portal venous inflow and suggest that MCS or other methods of regulating portal vein flow may be useful as adjunctive therapy in the treatment of advanced hepatoma.

Animals↗

Antibody recognition of an immunogenic influenza hemagglutinin-human leukocyte antigen class II complex.

The A/Japan/57 influenza hemagglutin (HA) peptide HA 128-145, when bound by human histocompatibility leukocyte antigen-DRw11 cells, is recognized by the human CD4+ T cell clone V1. A rabbit antiserum has been raised against HA 128-145 which recognizes not only the free peptide, but also the HA 128-145/DRw11 complex on a solid matrix, in solution, or on the surface of viable cells. The detection of these complexes on viable cells was shown to be class II specific, DRw11 restricted, and commensurate with the level of DRw11 expression. The identity of DRw11 as the cell surface molecule binding HA 128-145 was confirmed by immunoprecipitation, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and tryptic peptide mapping. Using this antiserum HA 128-145/DRw11 complexes could be detected on the cell surface as soon as 30 min after the peptide was added, and increased up to 24 h. Dissociation kinetics showed these complexes were long-lived, with a half-life of approximately 14 h. This anti-HA peptide antiserum represents the first direct means of studying antigenic peptide-human leukocyte antigen class II complexes on the surface of living cells without the addition of a non-amino acid moiety to the peptide. The properties of this antiserum thus provide the potential to study naturally processed antigenic peptides as well as the mechanism of processing itself in a physiologically relevant system.

Amino Acid Sequence↗

Host and bacterial factors associated with Haemophilus influenzae type b disease in Minnesota children vaccinated with type b polysaccharide vaccine.

Host and bacterial factors were evaluated among 86 Minnesota children with Haemophilus influenzae type b disease detected by active surveillance after introduction of type b polysaccharide vaccine in the state. Children were 2-6 y of age. Thirty-three (38%) had been vaccinated. There was no significant difference between the frequency of low serum concentrations of IgM, IgA, IgG, or IgG2 in the vaccinated and nonvaccinated subjects (13% vs. 8%, P = .5). The presence of the Gm immunoglobulin allotype phenotype (1,3,17;23;5,13,21), previously associated with a lower relative risk of vaccine failure in children from other states, was associated with a fourfold decrease in the relative risk of vaccine failure in Minnesota (P less than .07). Haemophilus isolates from 58 of the children were available for clonal characterization by multilocus electrophoresis and outer membrane protein subtyping. There were no significant differences between the clone distribution of the strains causing disease in vaccinated and nonvaccinated patients, and nearly all disease-producing clones in Minnesota also are known to cause disease in other areas of the country. Thus, vaccine failure in Minnesota is infrequently associated with hypogammaglobulinemia or with infection by unusual clones of a H. influenzae type b. Also, the Gm phenotype associated with protection against vaccine failure in other areas of the USA appears to be protective in Minnesota.

Antibodies, Bacterial↗

Clonal analysis of Hemophilus influenzae isolated from children from Pakistan with lower respiratory tract infections.

The clonal diversity of 105 Hemophilus isolates from the blood of children with lower respiratory tract infection in Pakistan was analyzed. Ten isolates were identified as H. parainfluenzae and 95 as H. influenzae. Of the H. influenzae isolates, 61 (64%) were serotype b and 34 (36%) were nontypable; 95% of the type b isolates were members of a single clonal group (as defined by multilocus enzyme electrophoresis, SDS-PAGE outer membrane protein profile, and biotype). This clone is rarely observed among type b strains recovered from patients with invasive type b disease in the USA or Europe. The nontypable isolates in Islamabad also were clonally restricted: 9 clonal groups were found among 34 isolates, with just 5 clonal groups accounting for most (82%) of the strains. Children infected with type b strains were hospitalized more often than those with nontypable H. influenzae disease (64% vs. 41%, P = .06), but no other clinical or demographic features distinguished children infected by type b and nontypable strains.

Bacterial Outer Membrane Proteins↗