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Biomedical subjects

E D Israels

Publications and source records attributed to E D Israels.

29 records · Page 2Linked to original sources
PubMed1984

Shortening of bleeding time by 1-deamino-8-D-arginine vasopressin in various bleeding disorders.

To evaluate the effect of 1-deamino-8-D-arginine vasopressin (DDAVP) in various bleeding disorders, 10 micrograms/m2 DDAVP was administered to subjects with von Willebrand disease (13), platelet function defects (12), von Willebrand disease and platelet defects together (8), or isolated prolongation of the bleeding time (5). DDAVP shortened the bleeding time similarly in all patient groups. Shortening of the bleeding time was also observed in 2 patients with aspirin-induced platelet defects and in 2 normal subjects. DDAVP administration was associated with falls in the platelet count, mean platelet volume, and partial thromboplastin time, and rises in platelet adhesion, factor VIII coagulant activity, factor VIII related antigen, and von Willebrand factor activity. The basal bleeding time was the only predictor of the magnitude of the bleeding-time correction. Normal haemostatis was achieved with DDAVP plus epsilon-aminocaproic acid and no blood product support during operations in 18 patients with bleeding disorders.

Adolescent↗
PubMed1983

Vitamin K as a regulator of benzo(a)pyrene metabolism, mutagenesis, and carcinogenesis. Studies with rat microsomes and tumorigenesis in mice.

Vitamin K3 inhibits the conversion of benzo(a)pyrene to its more polar metabolites in an in vitro rat liver microsomal system. Vitamin K3 also inhibits benzo(a)pyrene metabolism in rat liver fragments and reduces its mutagenicity in the Ames test. Higher concentrations of vitamin K3 are required to comparably reduce benzo(a)pyrene metabolism when the microsomal system has been induced with 3-methylcholanthrene. High pressure liquid chromatography analysis of the products of benzo(a)pyrene metabolism shows a uniform reduction of all the metabolic products. When tumors were induced in ICR/Ha female mice by the intraperitoneal injection of benzo(a)pyrene, those mice given vitamin K3 before or both before and after benzo(a)pyrene had a slower rate of tumor appearance and tumor death rate as compared with those receiving benzo(a)pyrene alone. However, vitamin K1 increased the rate of tumor death while vitamin K deprivation and warfarin decreased the rate of tumor appearance and death in benzo(a)pyrene-injected mice. These studies indicate that vitamin K3 is an inhibitor of aryl hydrocarbon hydroxylase and reduces the carcinogenic and mutagenic metabolites in vitro, and inhibits benzo(a)pyrene tumorigenesis in vivo. That vitamin K1 enhances the benzo(a)pyrene effect while warfarin and vitamin K deficiency inhibit benzo(a)pyrene tumorigenesis indicates that vitamin K1, vitamin K deprivation, or possibly blockade of its metabolic cycle also modulates benzo(a)pyrene metabolism in vivo but by a mechanism or at a site different from the vitamin K3 effect. The vitamin K series should be considered as capable of serving a regulatory function in the metabolism of benzo(a)pyrene and possibly other compounds metabolized through the mixed function oxidase system.

Aflatoxin B1↗
PubMed1982

Partial thromboplastin time in the presence of heparin: a rapid polybrene neutralization method.

The detection of heparin in plasma and its neutralization to permit assessment of the prolonged partial thromboplastin time is a constant need in the clinical laboratory. A rapid, simple method which utilizes Polybrene after the initial contact activation step is described and compared to the standard neutralization procedures. The present method has the advantage of not requiring Polybrene titration and of requiring only small volumes of plasma making it particularly valuable in pediatric patients.

Blood Coagulation Tests↗
PubMed1979

Prevention by menadione of the hepatotoxic effects in chickens fed rapeseed meal. Observations on coagulation factors and cytochrome P-450.

Rapeseed meal, the residue after oil extraction, is an animal feed of great commercial interest. Some genetic strains of rapeseed yield a meal which when fed in high concentration produces hemorrhagic lesions in the liver of chickens. These lesions are reduced in incidence by the simultaneous feeding of menadione. This hepatotoxicity is accompanied by elevated levels of cytochrome P-450, delta-aminolevulinic acid synthetase, and the clotting factors V and X. The hemorrhagic lesions were associated with hepatic necrosis, and menadione was protective by mechanisms other than its effect on blood coagulation.

5-Aminolevulinate Synthetase↗
PubMed1973

Immunological studies of coagulation factor XIII.

Human fibrin-stabilizing factor (Factor XIII) has been studied immunologically by the preparation of specific anti-Factor XIII antiserum in rabbits. On immunodiffusion it was found that normal plasma produced two precipitin lines. One of the precipitin lines was identical with that present in soluble platelet extract (the alpha-component), the other with that present in normal serum (beta-component). Plasma and serum of patients with congenital Factor XIII deficiency contained only the beta-component. By adsorption it was possible to prepare a second antiserum with solely anti-alpha-activity that did not react with the serum or plasma of XIII-deficient patients. Both antisera neutralized the clot-stabilizing activity of normal plasma. The action of thrombin on fibrinogen-free plasma or platelet extract abolished the immunoprecipitin alpha-line but did not reduce the capacity to neutralize antibody as measured by clot stabilization. It is concluded that the plasma Factor XIII molecule consists of two immunologically identifiable components, alpha and beta. The clot-stabilizing activity and thrombin-reactive site are situated on the alpha-component. Patients with congenital Factor XIII deficiency are devoid of immunologically identifiable or functional alpha-component but retain immunologically identifiable beta-component. It is this beta-component that accounts for the observed immunologically detectable Factor XIII in those patients devoid of clot-stabilizing activity.

Adsorption↗
PubMedDate not supplied

Novel vitamin K-dependent pathways regulating cell survival.

Historically, the vitamin K1-dependent proteins have been associated primarily with blood coagulation and secondarily with bone formation. Recent identification of K1-dependent proteins as specific ligands for the receptor tyrosine kinases (RTKs) that can stimulate cell replication and transformation and participate in cell survival highlighted a previously unrecognized and potentially important role for vitamin K1 in cell signaling. Growing evidence suggests that most normal and tumor cells possess an active K1-dependent gamma-carboxylation mechanism necessary for the production of gamma-carboxyglutamic acid (Gla)-containing proteins. Gla residues in proteins facilitate calcium-dependent protein/phospholipid interaction. Recent studies demonstrating the potentially positive effects of a vitamin K-dependent receptor:ligand system on cell growth and survival in general and the effects of the overexpression of these RTKs on malignant cell survival provide a new perspective on the role of vitamin K1, its dependent protein ligands, and their receptors. These cumulative observations also provide an explanation for the rigidly controlled K1 levels in the mammalian fetus and the minimal hepatic stores in the adult.

Animals↗