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Biomedical subjects

J Chediak

Publications and source records attributed to J Chediak.

30 records · Page 2Linked to original sources
PubMed1981

Surgical implications of antithrombin III deficiency.

Antithrombin III is a potent coagulant inhibitor in plasma. Congenital deficiency of antithrombin III may predispose to thrombotic events and may complicate surgical management. We describe a patient with congenital antithrombin III deficiency who developed superior mesenteric vein thrombosis after the cessation of warfarin therapy which resulted in venous gangrene of the small intestine. Initial treatment of this deficiency with fresh frozen plasma and subsequent long-term management with warfarin therapy has been effective in avoiding further thrombotic events.

Adult↗
PubMed1979

Cycles of agglutination-disagglutination induced by ristocetin in thrombasthenic platelets.

An oscillatory pattern of platelet agglutination-disagglutination in response to Ristocetin (R) at narrow concentration ranges was observed in citrated platelet rich plasma (PRP) of 10 patients with Glanzmann's thrombasthenia. The cyclic pattern decreased in intensity over time, was reproducible, and was not pH dependent. Formalin-fixed thrombasthenic platelets agglutinated with R but did not show a cyclic pattern. Incubation with 2.5 microM ADP inhibited R oscillation response, but small increases in R dose overcame this inhibition. The addition of ATP or creatine phosphate/creatine phosphokinase to thrombasthenic platelets inhibited by ADP restored the R oscillation response. In the platelets of a single patient, intracellular levels of ADP and ATP were shown to diminish during an oscillation response to R. There was an increase in AMP levels during the same period of time. The changes in these three intracellular nucleotides were gradual over time and did not vary with phases of the oscillation. Acetyl salicylic acid (ASA), at concentrations shown to block cyclooxygenase activity in control platelets, enabled thrombasthenic platelets to respond to R with full agglutination without oscillations. Lower concentrations of ASA in the PRP gave a return of the oscillation response. Our data suggest that the disagglutination phase of the R response of thrombasthenic platelets is not a function of the known glycoprotein membrane defect, but depends on materials originating in the platelet whose release is blocked by ASA.

Adenosine Diphosphate↗
PubMed1979

Aspirin inhibits development of coronary atherosclerosis in cynomolgus monkeys (Macaca fascicularis) fed an atherogenic diet.

The effect of aspirin in the primary prevention of diet-induced atherogenesis in cynomolgus monkeys was studied. The diet consisted of 2% cholesterol and 10% butter by weight for 24 wk. Six monkeys received only the atherogenic diet and five monkeys received the diet plus aspirin, 81 mg/monkey per day. Aspirin did not affect plasma cholesterol levels or aortic atherosclerosis. Platelet aggregation to arachidonic acid was almost completely suppressed. Aspirin decreased significantly the number of coronary vessels with atherosclerotic involvement, and the number of coronary vessels narrowed by 20% or more. Thus, aspirin appears to exert a protective effect in the primary prevention of diet-induced coronary atherosclerosis in a primate model.

Animals↗
PubMed1977

Determination of factor VIII-related antigen using commercial antisera.

Commercially available antiserum to factor VIII was used in several tests to determine whether it might serve as a reference between research laboratories involved in investigation of the factor VIII complex and whether the antiserum might be useful in the screening of large populations of patients with hereditary disorders of factor VIII. In Ouchterlony plates, the antiserum gave a single line of identity with concentrated factor VIII, cryoprecipitate, and human plasma. The antiserum was capable of inhibiting the ristocetin response of normal platelets. Testing antigenic factor VIII by the Laurell technic with the commercial antiserum on plasmas from normal and stressed normal controls, patients with von Willebrand's disease, patients with hemophilia A, and obligate carriers of hemophilia A gave diagnostic and reproducible results.

Adult↗
PubMed1976

Absence of ristocetin aggregation factor from the skin of a patient with von Willebrand's disease.

Samples of apparently normal skin from one patient with von Willebrand's disease (vWD) and five patients without vWD were examined with fluorescein-tagged antiserum to the component of factor VIII required for aggregation of platelets by ristocetin (VIII-R.A.F.). No evidence of VIII-R.A.F. was found in the vWD skin, while bright granules were seen on and/or in the endothelial cells of dermal capillaries in all patients without vWD. VIII-R.A.F. granules were also found in the interstitial vasculature of all of twelve renal-biopsy specimens from patients without vWD. These observations support the concept that an abnormality of the vascular endothelium is involved in the pathogenesis of vWD.

Blood Platelets↗