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Biomedical subjects

R L Henry

Publications and source records attributed to R L Henry.

At least 163 records · Page 9Linked to original sources
PubMed1980

Pathology data quality assurance and data retrieval at the National Center for Toxicological Research.

Automated experimental and pathology data collection and reporting systems are utilized at the National Center for Toxicological Research to increase the efficiency of the variety of research studies being performed. In order for the ED01 study to be conducted in an effective manner, usage of these automated systems was considered advantageous due to the study size, approximately 24,000 mice. The large volume of pathology and other experiment data generated in the study required detailed quality assurance and data retrieval, and the use of automated systems allowed this to be performed much more easily than with manual methods. This paper addresses the methods employed to ensure quality and to provide the data retrieval capabilities necessary for conducting and analyzing the ED01 study.

Government Agencies↗
PubMed1979

Somatostatin-induced changes in the hemostasis of rats.

Somatostatin (SRIF) given intravenously, either as a single bolus or as a 2 hr infusion caused a significant prolongation of partial thromboplastin time (PTT) and depressed platelet counts and platelet aggregation in the rat. Following daily injections of protamin-zinc SRIF for 2 weeks the platelet count returned to normal, PTT remained prolonged and platelet aggregation was enhanced. The doses of SRIF used in this work were adequate to suppress the secretion of insulin and glucagon by the isolated pancreatic islets of treated animals.

Animals↗
PubMed1979

Thrombotic thrombocytopenic purpura. An extended editorial.

A hypothesis for the pathogenesis of TTP is developed, centered on the views and findings of Kwaan (Fig. 8). By a series of deductions, inferences, and extensions, an attempt has been made to define considerably more restrictively than heretofore a TTP paradigm of clinical (Tables 1,2,3) and laboratory (Table 4) features. Revisions may be required in the future as increase of knowledge indicates. By similar methods rational, exigent therapeutic measures are selected (Table 5). The innovative therapeutic use of plasma transfusion, as proposed by Byrnes and Lian and their co-workers, is compatible with the paradigm in all respects. The paradigm discriminates for authentic cases of TTP among spurious if similar entities. Such sequestration will constitute a homogeneous universe of case material appropriate for study. The prospective use of the TTP paradigm defined in this papd therapeutic protocol, jointly developed, may accelerate our knowledge and improve our effectiveness in this lethal, if uncommon, disease [49,76,111,170].

Blood Platelets↗
PubMed1979

Thrombocytosis-induced suppression of small acetylcholinesterase-positive cells in bone marrow of rats.

Transfusion of platelet concentrates was used to establish a thrombocytosis of approximately three times normal platelet levels in male rats. This thrombocytosis resulted in a rebound thrombocytopenia to 60% of normal counts. Examination of the small acetylcholinesterase (ACh-E) positive cells of the marrow at this time showed a reduction to 50% of normal levels without significant changes in control animals. A second group of experiments indicated that this suppression developed as early as the third day posttransfusion, persisted until day 7, and returned to baseline levels by day 9. Incorporation of 75SeM indicated that the reduction in platelet count was due to decreased platelet production. Little or no changes were observed in the hematocrit or WBC. This evidence supports the hypothesis that these cells are early cells in the megakaryocytic series. They are the earliest cells of the series seen to be affected by thrombocytosis. Feedback control by platelets or platelet extracts of this cell population may represent one level of regulation of megakaryopoiesis.

Acetylcholinesterase↗
PubMed1978

Effects of autoprothrombin II-A on epinephrine-induced platelet aggregation of normal- and coumadin-treated dogs.

Platelet-rich plasma from dogs and from coumadin-treated dogs aggregated at the same optimum concentration of epinephrine. Neither protein C nor its active form called autoprothrombin II-A was necessary for aggregation of dog platelets with epinephrine. For platelet aggregation, suboptimal concentrations of epinephrine were potentiated by addition of purified autoprothrombin II-A. The latter, by itself, induced platelet aggregation in high concentration.

Animals↗
PubMed1977

Platelet function.

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Adenosine Diphosphate↗
PubMed1977

Autoprothrombin ii-a, thrombin, and epinephrine: interrelated effects on platelet aggregation.

Platelets aggregate with thrombin-free autoprothrombin II-A. Aggregation was dependent on an intact release mechanism since inhibition of aggregation occurred with adenosine, colchicine, or EDTA. Autoprothrombin II-A reduced the sensitivity of platelets to aggregate with thrombin, but enhanced epinephrine-mediated aggregation. Autoprothrombin II-A directly competes for membrane sites sensitive to thrombin. It allows complexes to from with epinephrine. There was no absolute requirement for autoprothrombin II-A since epinephrine aggregated dog platelets at the identical optimum concentration following Coumadin treatment.

Animals↗
PubMed1976

Effects of pyridinolcarbamate on the cardiovascular system of the anesthetized dog after bilateral cervical vagotomy.

Pyridinolcarbamate (PDC) was injected at a dose of 10 mg/Kg of body weight into the femoral vein of anesthetized dogs with a bilateral cervical vagosympathotomy. At this dose, it produced a transitory decrease in systolic, diastolic, and mean arterial pressure and an increase in heart rate. In addition, it produced a more prolonged increase in stroke volume, peak aortic flow, cardiac output, and left ventricular minute work. It also lowered peripheral resistance and apparently decreased the vaso-constrictor action of injected norepinephrine (1 mug of active base/Kg of body weight). These data are consistent with the view that PDC has a direct action on the heart that is similar to that of norepinephrine and that PDC blocks the alpha adrenergic receptors of the systemic resistance vessels.

Anesthesia↗
PubMed1975

Mass screening for sickle cell hemoglobin. Is there an optimal method?

The problem of screening large civilian and military populations for sickle cell hemoglobin and related conditions has been approached recently by three distinct methods. One method specifies hemoglobin electrophoresis as the initial screening technique, followed by a solubility (dithionite) test when a (nonspecific) "S band" is noted. Another method requires the use of the automated dithionite test, followed, when positive, by hemoglobin electrophoresis. A third method is a dual, automated technique for detecting anemia or hemoglobin S or both in the initial screening study; hemoglobin electrophoresis studies are done when indicated. All three methods provide data suitable for accurate diagnosis and genetic counseling, but substantial variations in costs and redundancy of data are found among these methods. Because it gives the "biggest diagnostic bang for the buck", the third merits widespread adoption.

Anemia, Sickle Cell↗