Search PubMed⌕ Search

Biomedical subjects

B Bennett

Publications and source records attributed to B Bennett.

At least 253 records · Page 14Linked to original sources
PubMed1975

D-penicillamine induced Goodpasture's syndrome in Wilson's disease.

Fatal pulmonary hemorrhages and rapidly progressive glomerulonephritis occurred in three patients with Wilson's disease (hepatolenticular degeneration) who had been treated with penicillamine for 2 to 31/2 years. Light microscopic studies of the kidneys showed severe glomerulonephritis with crescent formation, and the lungs showed intraalveolar hemorrhages. Although the clinical and pathologic abnormalities were those of Goodpasture's syndrome, immunofluorescence microscopic studies in the one case tested showed an interrupted, rather than linear, fluorescence pattern.

Adult↗
PubMed1975

Recurrent hemolytic-uremic syndrome: a case report.

A girl who developed HUS at 2 years of age had four further episodes of the disease during the next 2 1/2 years. No renal or hematologic abnormalities were detected during or between the attacks. Reduced levels of serum complement were found during three of the episodes.

Child, Preschool↗
PubMed1973

The fibrinolytic enzyme system in hypertension.

Fibrinogen, fibrinogen-related antigen (FR-antigen), and components of the fibrinolytic enzyme system were measured in patients with essential hypertension, renal disease with and without hypertension, and normal subjects. Essential hypertension was associated with a decrease in plasminogen activator and an increase in FR-antigen. In renal disease these changes were accompanied by increases in plasminogen activation inhibitor, alpha(2)-macroglobulin, alpha(1)-antitrypsin, and fibrinogen.

Adult↗
PubMed1973

Studies on the nature of antihemophilic factor (factor VIII). Further evidence relating the AHF-like antigens in normal and hemophilic plasmas.

Normal human antihemophilic factor (AHF, factor VIII) and the protein antigenically related to it in hemophilic plasma both appeared in the void volume of columns of agarose (Sepharose 4B) during purification of these agents. On ultracentrifugation upon sucrose gradients, both agents had sedimentation characteristics similar to those of an S30 marker. After reduction, the polypeptide chains of purified normal AHF and of the nonfunctional agent from hemophilic patients had an apparent molecular weight of 200,000 as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. These observations suggest that AHF, purified as described, exists as a large molecule with subunits of molecular weight of approximately 200,000. Antisera to normal AHF and the nonfunctional agent from hemophilic plasma appeared to be directed against antigens of similar electrophoretic mobility and precipitating characteristics, present in normal and hemophilic plasma but deficient in severe von Willebrand's disease plasma. Both antisera neutralized the AHF clot-promoting activity present in normal plasma, and this property was removed by absorption of the antisera with concentrates of normal or hemophilic plasma but to a greatly reduced extent by concentrates of von Willebrand's disease plasma. These findings suggest that the antigen detected in normal plasma by the antisera appears on a molecule participating in the AHF clot-promoting reaction.

Animals↗