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Biomedical subjects

J Klinger

Publications and source records attributed to J Klinger.

At least 37 records · Page 2Linked to original sources

Reaction of antibody in sera from cystic fibrosis patients with non-toxic forms of Pseudomonas aeruginosa exotoxin A.

Sera from 48 cystic fibrosis patients from two hospitals were screened for antibody against rods, non-toxic macromolecular structures which share antigenic determinants with Pseudomonas aeruginosa exotoxin A. A solid-phase radioimmunoassay employing (125I)-staphylococcal protein A was used to detect anti-rod IgG. Antibodies recognizing rods, exotoxin A, or both antigens, were demonstrated using a competitive radioimmunoassay in cystic fibrosis patient sera, and in sera from animals immunized with exotoxin A, rods, or infected with Pseudomonas aeruginosa. Anti-rod titers of cystic fibrosis patients (1.07 to 14 X control serum levels) inversely correlated with aggregate clinical evaluation scores, and in most instances, with X-ray scores. Since rods are non-toxic and cross-reactive with exotoxin A, they may represent therapeutically useful antigens for producing immunity to exotoxin A.

ADP Ribose Transferases↗

Thromboxane, prostacyclin, beta-thromboglobin, and diabetes mellitus.

Plasma levels of beta-thromboglobin (beta-TH) and of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1-alpha, the stable metabolites of thromboxane A2 and prostacyclin, were determined by radioimmunoassay methods in eight patients with noninsulin-dependent diabetes before and after dietary treatment and after administration of the sulfonylurea drug glibenclamide. Blood examinations were performed when hyperglycemia was detected for the first time, four weeks after a dietary regimen was started, and four and eight weeks after glibenclamide treatment was begun. Drug treatment was instituted because, despite a suitable diet, patients' postprandial blood sugar was higher than 8 mmol/L (145 mg/dl). At the initial examination, elevated TXB2 and beta-TH levels indicating platelet hyperactivity and hyperglycemia were found. TXB2 and beta-TH levels decreased significantly after glibenclamide treatment was started, as did the blood glucose level. There was no change in 6-keto-PGF1-alpha. We interpret these results to indicate that diabetes is associated with hyperactivity of platelet aggregation and that control of blood glucose is important because a lower blood glucose level attenuates platelet hyperactivity. Whether the decrease in platelet hyperactivity is a direct result of the lowered blood sugar or reflects the influence of the drug treatment requires clarification.

6-Ketoprostaglandin F1 alpha↗