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Biomedical subjects

M J Silver

Publications and source records attributed to M J Silver.

At least 91 records · Page 5Linked to original sources
PubMed1976

Malondialdehyde formation as an indicator of prostaglandin production by human platelets.

The formation of malondialdehyde, a metabolite of prostaglandin endoperoxides, has been studied in platelet-rich plasma. Small amounts were produced in response to ADP, epinephrine, or collagen and larger amounts in response to thrombin. Arachidonic acid induced platelets to produce large amounts of malondialdehyde. Malondialdehyde formation by platelets was prevented by aspirin or indomethacin. The measurement of malondialdehyde in platelet-rich plasma may be used as an indicator of platelet prostaglandin synthesis, and is simpler than the measurement of prostaglandins.

Adenosine Diphosphate↗
PubMed1976

Platelet prostaglandin production and its implications.

Both aspirin and indomethacin abolish platelet shape change and aggregation induced by arachidonic acid, indicating that these effects are due to prostaglandin production. An unstable prostaglandin endoperoxide (PGG2 or PGH2) is probably the mediator of the arachidonic acid effects, and they can be mimicked by the stable synthetic prostaglandin, 11-deoxy-15-methyl-15RS-PGE2 (Wy-17, 186). All three of these prostaglandins induce platelet aggregation in the presence of aspirin. Neither aspirin nor indomethacin inhibits shape change or primary aggregation induced by ADP, which indicates that these effects are not due to prostaglandin production. Arachidonic acid, Wy-17, 186, and ADP require fibrinogen as a cofactor in order to aggregate washed human platelets. However, the combination of ADP and arachidonic acid or of ADP and Wy-17, 186 is synergistic and will aggregate washed human platelets in the absence of added fibrinogen. No synergism is observed between arachidonic acnd and Wy-17, 186. During platelet degranulation (i.e., the platelet-release reaction) induced by collagen both ADP and prostaglandin endoperoxides are made available, and collagen can induce the aggregation of washed human platelets in the absence of added fibrinogen. Prostaglandin endoperoxides, ADP, and fibrinogen probably act in concert to aggregate platelets in normal hemostasis since the absence of any one of these principles usually has an effect on the bleeding time.

Adenosine Diphosphate↗
PubMed1975

An instrument to assess staff time utilization in a community mental health center.

The Daily Staff Log is an empirically refined instrument to assess staff hours spent in direct patient and collateral contact, clinical backup time, consultation, education, and administration. Its primary uses as a management tool include description of staff activities, comparisons by discipline or clinic, pre- and postcomparisons following administrative policy change, and cost-effectiveness studies. Conditions for successful use include a firmly committed administrative interest, in-service education on the value of log data for decisionmaking to improve delivery of care, and positive feedback when logs indicate service goals are being met. Following the introduction of logging it was possible to document improvements in clinical and financial efficiency.

Administrative Personnel↗
PubMed1975

Uptake and inactivation of a-type prostanglandins by human red cells.

Incubation of A type prostaglandins with whole blood or washed red cells at 37 degrees C converted them to more polar products with negligible vasodepressor and smooth muscle-contracting activities. This conversion did not occur in platelet-rich plasma. Uptake of the prostaglandins by red cells was demonstrated at both 4 degrees C and 37 degrees C. The data suggest 1) that if PGA is released from tissues into the blood stream or is administered for therapeutic purposes, its biological activity would be diminished by human red cells, and 2) that development of an assay for PGA in blood should take into account its uptake and metabolism by human red cells.

Erythrocytes↗
PubMed1974

Arachidonic acid causes sudden death in rabbits.

Injection of sodium arachidonate (1.4 milligrams per kilogram) into the marginal ear veins of rabbits caused death within 3 minutes. Histological examination showed platelet thrombi in the microvasculature of the lungs. Rabbits were protected from the lethal effects of arachidonic acid by pretreatment with aspirin. Fatty acids closely related to arachidonic acid did not cause death.

Animals↗
PubMed1974

Formation of an intermediate in prostaglandin biosynthesis and its association with the platelet release reaction.

A compound that could be converted to prostaglandin F(2alpha) by mild chemical reduction was formed by human platelets in response to arachidonic acid, collagen, or L-epinephrine. It was present in maximal amounts at about 1 min after addition of arachidonic acid or collagen to platelet-rich plasma. Its initial formation appeared to precede platelet aggregation by these agents and was closely correlated with the release of adenine nucleotides and radioactive 5-hydroxytryptamine from platelets. Moreover, the compound was itself found outside the platelets. This compound is probably an endoperoxide intermediate in prostaglandin biosynthesis and may be a trigger for the platelet release reaction.

Adenine Nucleotides↗