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Biomedical subjects

G F Meissner

Publications and source records attributed to G F Meissner.

12 recordsLinked to original sources
PubMed1985

The prolonged bleeding time in hemophilia A: comparison of two measuring technics and clinical associations.

The authors simultaneously performed the Ivy (IBT) and the Simplate I (SBT) bleeding time in 17 volunteers with classic hemophilia A to determine whether a prolonged Simplate bleeding time was indeed indicative of impaired primary hemostasis, as has been postulated recently, or whether the technic itself accounted for the observed changes. They also assessed platelet function and Factor VIII-related activities on blood drawn that day. The SBT was prolonged in 11 patients, while the IBT was consistently normal. The platelet aggregation studies and the levels of Factor VIII-related antigen (VIII R:Ag) and ristocetin cofactor (VIII R:Rc) were normal, providing no evidence of von Willebrand's disease. The patients with a prolonged SBT were all younger than 20 years of age, bled two to three times more often than those with a normal SBT, and consumed more Factor VIII concentrate. A prolonged SBT with depressed VIII:C therefore is not indicative of von Willebrand's disease but is shared by a substantial proportion of hemophiliacs, who may be a greater risk of bleeding.

Adolescent↗
PubMed1978

Uterine choriocarcinoma fourteen years following bilateral tubal ligation.

A patient who developed choriocarcinoma of the uterus 14 years after bilateral tubal ligation and resection is presented. Non-patency of the fallopian tubes was demonstrated radiologically. The various mechanisms of occurrence of the clinical picture are discussed. Activation of dormant chorionic cells present since the patient's last known pregnancy (1960) appears to be the most probable explanation for the origin of the choriocarcinoma.

Adult↗
PubMed1977

Adenylate cyclase and phosphodiesterase activity in the platelet release abnormality.

11 patients with histories of clinical bleeding were selected as examples of platelet release abnormality. Mean bleeding time was 18 +/- 2.6 min (normal +/- SEM; 6 +/- 0.44); mean platelet adhesiveness was 9.9 +/- 4.3% (normal +/- SEM; 30 +/- 2.2). Clot retraction and platelet factor 3 were normal. Platelet aggregation with adenosine diphosphate (ADP), epinephrine and collagen was decreased, as was 14C-serotonin release. Electron microscopic studies of platelets exposed to epinephrine showed 2 subgroups: one which failed to aggregate or have centralization of organelles and a second which developed pseudopodia and centralization of organelles, but rarely aggregated or degranulated. Measurements of activity of adenylate cyclase and phosphodiesterase under basal conditions were performed on platelets from patients and control subjects. Adenylate cyclase activity was significantly lower and phosphodiesterase activity significantly higher in the patient group. Prostaglandin E1 was a potent stimulator of adenylate cyclase in both groups, as was NaF. It was concluded that the causative defects with "platelt release abnormality" do not reside in either the activity of adenylate cyclase or of phosphodiesterase. Changes in formation and destruction of cyclic adenosinemonophosphate (AMP) may instead be regarded as a compensatory response to a defect in another effector system.

Adenylyl Cyclases↗