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Biomedical subjects

D Green

Publications and source records attributed to D Green.

At least 397 records · Page 22Linked to original sources
PubMed1980

Von Willebrand's disease.

Von Willebrand's disease is an autosomally transmitted disorder of hemostasis caused by a deficiency of or defect in the von Willebrand factor in the blood, a protein required for adherence of platelets to an injured vessel wall. The disease's principal manifestations are spontaneous bleeding from mucous membranes, excessive bleeding from wounds, and menorrhagia. The major laboratory abnormality in prolongation of the skin bleeding time, with reduced platelet retention by glass bead columns, impaired platelet agglutination by ristocetin, and reduced factor VIII--related antigen and factor VIII coagulant activity as associated defects. Recommended therapy is infusion of plasma cryoprecipitate, which briefly corrects bleeding time and normalizes the disorder's other manifestations.

Bleeding Time↗
PubMed1980

Comparative effects of protracted exposures to 60Co gamma-radiation and 239Pu alpha-radiation on breeding performance in female mice..

Breeding performances are compared of hybrid female mice given 239Pu (5 or 10 mu Cikg-1 body mass in 1% trisodium citrate via the tail-vein), or kept in a 10 rad/day or 20 rad/day 60Co gamma-irradiation field (but mated in the control area), or unirradiated. Ovarian dose-rates from the injected plutonium were initially 0.8 and 1.7 rad/day, changing little thereafter; actual gamma-ray dose-rates to breeding females averaged around 8 and 16 rad/day respectively. Both gamma-ray treatments affected reproductive performance more than the plutonium injections, with respet to duration of fertility and to offspring per litter in successive 4-weekly periods, though overall mean litter-sizes were not significantly less than controls. The r.b.e. for these effects on reproduction, attributed to germ-cell killing, is about 2.5 for the alpha-particles vs. gamma-rays, lower than for testis mass reduction in males. This low r.b.e. may be connected with inhomogeneity of alpha-particle dose within the ovary, but it is known that fission neutron versus gamma r.b.e.'s for impairment of female fertility are also lower than those for impairment of male fertility.

Alpha Particles↗
PubMed1980

Sequential changes in factor VIII and platelets preceding deep vein thrombosis in patients with spinal cord injury.

The relationships between factor VIII associated activities, platelet function, and venous thrombosis were studied in 18 patients with lower limb paralysis following acute spinal cord injury (SCI). Deep vein thrombosis (DVT) was detected in 13 patients (72%). Eight of the 13 thromboses were documented between 6 and 8 d following injury while the other five episodes were noted on days 11 (two), 13, 18 and 22. The detection of thrombosis was preceded by marked increases in VIIIR:Ag and VIII:RCoF whereas VIII:C was only marginally increased. The platelet aggregation response to collagen was hyperactive by the sixth day while the platelet aggregate ratio (PAR) did not become abnormal until after DVT was detected. These studies suggest a chronology in the series of events leading to DVT in patients with lower limb paralysis following SCI. Initial elevations in VIII:Ag and VIII:RCoF are followed in sequence by increased platelet responsiveness to collagen, the occurrence of DVT, and the appearance of circulating platelet aggregates. Conceivably, VIIIR:Ag elaborated by endothelial cells alters platelet reactivity and provides an important determinant for venous thrombosis.

Adolescent↗
PubMed1980

Elevated beta-thromboglobulin in patients with chronic renal failure: effect of hemodialysis.

Elevated plasma concentrations of beta-thromboglobulin were observed in 25 consecutive patients with chronic renal failure. Further increases in this platelet protein were observed during hemodialysis but not during peritoneal dialysis. The hemodialysis-induced increases were not prevented by either aspirin or dipyridamole, a fact which suggested that release of this protein was not dependent on platelet functional activity. Measurement of beta-thromboglobulin provides a sensitive indicator of platelet disruption during hemodialysis.

Adolescent↗
PubMed1980

Factor VIII antibodies in rheumatoid arthritis. Effect of cyclophosphamide.

Three patients with rheumatoid arthritis had bleeding and bruising and were found to have circulating antibodies specifically directed against factor VIII. Review of the literature indicates that this is an unusual but serious complication of rheumatoid arthritis. In two of our three cases, disappearance of the factor VIII antibody coincided with the oral administration of cyclophosphamide; in the third patient, antibody titers declined several weeks after cyclophosphamide therapy was discontinued. Our collected experience involving 11 nonhemophilic patients with factor VIII antibodies indicates that a good response to cyclophosphamide therapy may be expected if the antibody titer is less than 10 Bethesda units at the initiation of treatment. While optimum treatment of these patients is not yet established, we suggest an initial trial of prednisone and, if there is no response, then therapy with cyclophosphamide.

Aged↗
PubMed1979

The treatment of the hemolytic-uremic syndrome with inhibitors of platelet function.

In four patients with clinical and laboratory manifestations of the hemolytic-uremic syndrome, the administration of aspirin and dipyridamole was associated with a dramatic and rapid increase in the platelet count. In three of the four patients there was also improvement in neurologic or renal function. No subject experienced bleeding or other untoward effects. We conclude that a trial of aspirin and dipyridamole therapy is warranted early in the course of the hemolytic-uremic syndrome.

Adult↗
PubMed1979

Quantitative microscopic studies of the distribution and retention of 239Pu in the ilium of the female CBA mouse.

Three month old female CBA mice were injected with 50 nCi kg-1 body mass of minimally polymeric 239Pu-citrate and killed at 24 hours, 10 days, 1 month and 3 months after injection. The distribution of 239Pu in the ilia of these mice was analysed using neutron-induced autoradiography of bone sections together with computer-based methods of data reduction. Results of these investigations demonstrate that while 239Pu is initially localized on bone surfaces, by 3 months after injection it is fairly uniformly distributed throughout mineral bone and its included marrow.

Animals↗
PubMed1979

Chlorozotocin. Mechanism of reduced bone marrow toxicity in mice.

Chlorozotocin is a chloroethyl nitrosourea with a glucose carrier that has curative activity for the murine L1210 leukemia, but is nonmyelosuppressive in mice. To determine the mechanism for this unique property of reduced bone marrow toxicity, comparative studies were conducted with chlorozotocin and CCNU, a myelotoxic chloroethyl nitrosourea. Suspensions of L1210 leukemia and murine bone marrow cells were incubated for 2 h with 0.1 mM [(14)C]-chloroethyl chlorozotocin or CCNU. Chlorozotocin demonstrated a fourfold increased covalent binding of the chloroethyl group to L1210 nuclei when compared to equimolar CCNU. Chlorozotocin alkylation of L1210 cells resulted in the binding of 57 pmol of [(14)C]ethyl group/mg of DNA, which represented a 2.3-fold increased alkylation when compared to CCNU. In marked contrast, the binding of the chloroethyl group to bone marrow nuclei was equivalent for both drugs. In addition, chlorozotocin alkylation of murine bone marrow DNA, 45 pmol of [(14)C]ethyl group/mg of DNA, was equivalent to that of CCNU. The ratio of L1210:bone marrow DNA alkylation was 1.3 for chlorozotocin compared to 0.6 for CCNU. The intracellular carbamoylation of L1210 and bone marrow protein by CCNU was 400- to 600-fold greater than that produced by chlorozotocin. After a 2-h exposure to 0.1, 0.05, or 0.01 mM drug, both chlorozotocin and CCNU produced a reduction in the cloning efficiency of L1210 cells that was dose dependent. However, chlorozotocin was significantly more cytotoxic than CCNU at all three molar concentrations (P < 0.01). Chlorozotocin, 0.1 mM, reduced L1210 DNA synthesis to 1% of control by 48 h, in contrast to 16% with equimolar CCNU (P < 0.01). In mice bearing 10(5) L1210 cells, chlorozotocin produced its optimal antitumor activity (332% increased life span [ILS]) at doses of 48-64 mumol/kg, with >50% indefinite survivors. In contrast, CCNU at the same molar doses resulted in only a 191% ILS; a CCNU dose of 128 mumol/kg was required for comparable optimal L1210 antitumor activity, 413% ILS. On a molar basis, the dose of chlorozotocin that produced optimal in vivo L1210 antitumor activity was one-third to one-half that of CCNU. Chlorozotocin, unlike CCNU, produced no murine bone marrow toxicity at its optimal therapeutic dose. This unique combination of antitumor activity without myelosuppression can be correlated with the advantageous ratio of L1210:bone marrow in vitro DNA alkylation by chlorozotocin (1.3) as compared to equimolar CCNU (0.6).

Alkylation↗
PubMed1979

Plutonium in the tissues of foetal, neonatal and suckling mice after Pu-administration to their dams.

Twelve-week-old female (C3H x 101)F1 mice were injected intravenously with an ultrafiltered solution of 239Pu in per cent trisodium citrate, and mated to uninjected PCT males. The plutonium content was examined radiochemically and autoradiographically in placentae and foetuses on the 12th and 18th days of gestation, and in neonates during the 24 hours after birth and also at 18 days postnatally. Plutonium was distributed in most tissues of the late foetus and the suckling as it is in adult mice. However, on both the 12th and 18th days of gestation the concentration in the yolk-sac splanchnopleure was much higher than in any other foetal tissue. The amount of 239Pu in 18-day-old sucklings was between two and seven times as great as in 1-day-old neonates because of ingestion of milk from the lactating dams. In the first litter following administration of the radionuclide to the dam, about 0.02 per cent of the plutonium injected was transferred to an individual offspring by the time of birth, and a further 0.08 per cent by the time of weaning.

Animals↗
PubMed1979

Role of the von Willebrand factor in atherogenesis.

The von Willebrand factor is a high molecular weight protein which is synthesized by endothelial cells and appears in plasma and platelets. The main function of the factor is in mediating the adherence of platelets to the deendothelialized vessel wall. Animals with congenital deficiency of the factor do not develop the atherosclerotic lesions found in their normal counterparts. Elevated levels of the von Willebrand factor are observed in patients with atherosclerotic peripheral vascular disease, myocardial infarction, and diabetics with proliferative retinopathy. These increases in the factor may be due to the increased turnover rates of platelets and endothelial cells commonly seen in these disorders. Whether elevated levels of the von Willebrand protein constitute a unique risk factor for the development of atherosclerosis and vascular occlusive disease should be determined by studies currently in progress.

Animals↗