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Biomedical subjects

R B Ramsey

Publications and source records attributed to R B Ramsey.

At least 19 recordsLinked to original sources
PubMed1988

The effects of thrombopoietic activity of rabbit plasma fractions on megakaryocytopoiesis in agar cultures.

A plasma fraction that stimulates platelet production in vivo also stimulates megakaryocytopoiesis in vitro. The plasma activity is attributed to a humoral regulator, thrombopoietin. Addition of the thrombocytopenic plasma (TP) fraction to an agar system supporting megakaryocyte colonies increased the frequency of colony formation significantly over that stimulated by spleen cell-conditioned medium (SCM). TP had no effect on the size of the colonies and, in the absence of SCM, TP did not stimulate colony formation. In studies of single megakaryocytes, the numbers of small megakaryocytes, specifically those 5-10 microns in diameter, increased significantly after 3 days of incubation with TP alone. SCM supported not an increase in the numbers, but an increase in the proportion of larger (30- to 40-microns) megakaryocytes. A normal plasma fraction contained similar but consistently less activity than fractions containing TP. The findings indicated that TP stimulates differentiation of megakaryocyte precursors from unidentifiable to identifiable cells but does not alone support colony formation. Thus, TP appears to be a potentiator of megakaryocytopoiesis. However, the augmentation of colony frequency by TP further suggests that TP may also play a role in early colony development, either by enhancing progenitor responsiveness to a megakaryocyte colony-stimulating factor or by recruiting additional colony progenitors from a noncycling progenitor population. These studies establish a link between the stimulation of platelet production observed after TP administration in vivo and the effects of TP on early events in megakaryocytopoiesis.

Acetylcholinesterase↗
PubMed1987

Antibody to human immunodeficiency virus in factor-deficient plasma. Effect of heat treatment on lyophilized plasma.

The prevalence of antibody to human immunodeficiency virus (HIV) was determined in various commercial substrate plasmas used in clotting factor assays, and viral isolation was attempted from both seropositive and seronegative samples. Antibody to HIV was detected in 13 of 13 plasma substrates used for Factor VIII assays and in 2 of 3 plasma substrates used for Factor IX assays. Antibodies were not detected in any of the other factor-specific substrates. Virus could not be isolated from any of the seropositive samples after 28 days in culture. Heat treatment of the samples under conditions known to inactivate HIV in plasma products indicated that heating the lyophilized substrate plasmas at 60 degrees C for up to eight hours had little effect on factor substrates and factor assays. Progressive loss of Factor V in the deficient plasmas was the most serious effect produced by heat treatment.

Antibodies, Viral↗
PubMed1985

HTLV-I antibody status in hemophilia patients treated with factor concentrates prepared from U.S. plasma sources and in hemophilia patients with AIDS.

Serum samples from 85 Austrian hemophilia patients treated with lyophilized factor concentrates prepared from U.S. plasma sources, 24 hemophilia patients from Georgia on a home therapy program with factor concentrates, and 10 U.S. hemophilia patients with acquired immunodeficiency syndrome (AIDS) were analyzed by two different methods for the presence of antibodies to the major internal antigen of human T-cell leukemia virus I (HTLV-I) p24. All but one, a Georgia sample, were negative. The absence of antibody to HTLV-I p24 in the serum of European hemophilia patients, of U.S. hemophilia patients with no symptoms of AIDS, and of U.S. hemophilia patients with AIDS is interpreted as an indication of the lack of ready transmissibility of HTLV-I in lyophilized factor concentrates.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Isolation and characterization of a human T cell leukemia virus type II from a hemophilia-A patient with pancytopenia.

Human T cell leukemia virus (HTLV) type I has been isolated from the cultured T cells of several patients with adult T cell leukemia (ATL) and has been etiologically linked to ATL. However, HTLV-type II has been isolated only once, from the T cells of a patient with a T cell variant of hairy-cell leukemia. We report here the isolation of HTLV-II-related virus from the cultured T cells of a hemophilia-A patient with pancytopenia. The T cell line (CM) grows in the absence of T cell growth factor. Cord blood T cells were rapidly transformed when co-cultivated with irradiated CM cells. Heterologous competition radioimmunoassays using purified HTLV-I p24 showed the expression of HTLV-IIMO-related protein in these cells. Electron microscopy of the CM cells showed the presence of intracellular and extracellular type C viral particles. Comparison of the proviral genome in the CM cell line and the prototype HTLV-IIMO-containing cell line (MO) by molecular hybridization with probes specific for HTLV-IIMO indicated that restriction cleavage sites were identical. The fresh peripheral blood leukocytes of the patient contained two complete copies of the proviral genome, despite the lack of HTLV-II p24 expression. The virus from the cell line CM is designated as HTLV-IICM to distinguish it from the original HTLV-IIMO isolate.

Adult↗
PubMed1985

A longitudinal study of patients with hemophilia: immunologic correlates of infection with HTLV-III/LAV and other viruses.

A comprehensive study was initiated to examine the immunologic status of a sample (n = 47) of the asymptomatic hemophilia A and B populations of metropolitan Atlanta and to determine if any of the abnormalities changed with time or correlated with infection by human T cell leukemia virus type III and lymphadenopathy-associated virus (HTLV-III/LAV) or other viruses either alone or in combination. Patients with hemophilia A (Hem-A) showed a defect in cellular immunity evidenced by a depressed T cell helper/suppressor ratio (P less than .0001), an increased absolute T suppressor cell number (P less than .0001), and a diminished number of T helper cells (P = .003) when compared with health professionals. Lymphocytes from these patients also showed a reduced ability to transform in response to phytohemagglutinin and pokeweed mitogen. No deterioration in immune status was seen during a median ten-month period of follow-up. Sixty-four percent of Hem-A patients had antibodies to HTLV-III/LAV and those who were seropositive had a significantly decreased helper/suppressor cell ratio (P = .018) and a diminished T helper cell number (P = .002); they were also more likely to have had exposure to cytomegalovirus than HTLV-III/LAV-negative Hem-A patients (P = .016). Heavy use of factor VIII concentrate was associated with a decreased number of T helper cells (P = .037) and seropositivity for HTLV-III/LAV (P = .011 in 1982). Hemophilia patients had higher IgG, immune complex, and beta 2-microglobulin levels than health professionals (P less than .0001). Although the most prominent abnormality observed in T cell subsets of patients with hemophilia is an increase in T suppressor cells, a finding likely to be associated with immune augmentation in response to multiple stimuli, the T cell abnormality that was predictive of exposure to HTLV-III/LAV, the putative acquired immunodeficiency syndrome agent, was a diminished number of T helper cells.

Adult↗
PubMed1979

Adrenoleukodystrophy brain cholesteryl esters and other neutral lipids.

Further examination of the neutral lipid fractions derived from brain tissue of two patients afflicted with adrenoleukodystrophy has demonstrated the presence not only of free cholesterol and cholesteryl ester, but also of appreciable free fatty acid and triglyceride. Using a gas--liquid chromatographic system normally employed for the analysis of long-chain fatty acids of galactolipids and spingomyelin, it was possible to establish the presence of long-chain (greater than C20) fatty acids in the cholesteryl ester, free fatty acid and triglyceride fractions. Long-chain fatty acids were most abundant in the cholesteryl esters. Fatty acids identified by gas--liquid chromatography and gas chromatography--mass spectroscopy included normal saturated and monounsaturated fatty acids as large as C34. Several unknown fatty acyl compounds, of as yet undetermined structure, were also observed. All investigations thus far would indicate that the pathogenesis of adrenoleukodystrophy is closely related to the aberrant metabolism of these long-chain fatty acids.

Adrenal Gland Diseases↗
PubMed1979

Platelet and fibrinogen production: relative sensitivities to endotoxin.

The relative sensitivities of platelet and fibrinogen production to endotoxin were determined in male New Zealand rabbits. E. coli endotoxin was administered in single intravenous doses of 0.1 to 50.0 mu/g/kg body mass. 75SeM was injected 5, 12, or 18 hr after endotoxin, and the percent incorporation into platelets and fibrinogen was used to measure thrombopoiesis and fibrinogen synthesis. Leukopenia occurred after the infusion of endotoxin at all dose levels; the lowest dose that caused thrombocytopenia was 0.5 microgram/kg. Endotoxin was detected with the Limulus test in plasma of animals that received 5 to 50 microgram/kg. The stimulation of fibrinogen and platelet production, as well as the postinfusion decrease in platelet count, correlated directly with the log of the dose of endotoxin infused. The lowest dose of endotoxin that stimulated platelet and fibrinogen production was 0.5 microgram/kg. In animals that received this dose of endotoxin, increased fibrinogen production was detected only when 75SeM was injected 5 hr later. In animals injected 5, 12, or 18 hr later. Increased platelet production was detected at these two doses only when 75SeM was injected 18 hr after endotoxin. The data indicate that fibrinogen and platelet production have similar sensitivities to endotoxin, although the time course of stimulation is different for these two blood components.

Animals↗
PubMed1978

Alteration of developing and adult rat muscle membranes by zuclomiphene and other hypocholesterolemic agents.

The present study presents evidence for a third hypocholesterolemic drug, zuclomiphene, being able to induce an experimental myotonic condition. Other drugs used singly or in combination were AY-9944, Triparanol and 20, 25-diazacholesterol. It has also been demonstrated for the first time that experimental myotonia can be induced in developing rats as well as adults. Developing rats received the initial intraperitoneal injections of drug at 5 days of age and were examined at 50 days of age. Adult rats were treated for 5 weeks. Two injections were given per week. Positive electromyography findings were observed in the developing and adult animals receiving 20, 25-diazacholesterol and zuclomiphene. The electromyography data of the other regimens of treatment were equivocal with regard to myotonia. Histological, histochemical, and electron microscopic examination of the muscle demonstrated no important changes. estimation of sterol composition showed that desmosterol was a major sterol in muscle after 20, 25-diazacholesterol or zuclomiphene treatment, thus furthering the concept that it is desmosterol in the muscle membrane, and not the drug, that is responsible for the myotonic condition.

Animals↗
PubMed1977

Effects of zuclomiphene in combination with triparanol and ay-9944 on developing rat CNS morphology and biochemistry.

Developing rats were injected intraperitoneally twice weekly with a combination of three hypocholesterolemic agents: Zuclomiphene (formerly called trans-clomiphene; dosage, 30 mg/kg body weight), Triparanol (30 mg/kg body weight) and AY-9944 (3 mg/kg body weight). Treatment was initiated at 4 days of age. Biochemical and electron microscopic examination was conducted on animals sacrificed at 20 days of age. Cytoplasmic inclusion bodies were not seen in the CNS. Isolated edematous changes were seen in myelinated axons. Analysis of the sterol content of the brain and spinal cords of drug-treated animals indicated the presence of abnormal concentrations of five sterols, desmosterol, 5alpha-cholesta-7,24-dien-3beta-ol, zymosterol (5alpha-cholesta-8,24-dien-3beta-ol), 7-dehydrocholesterol (cholesta-5,7-dien-3beta-ol) and 7-dehydrodesmosterol (cholesta-5,7,24-trien-3beta-ol). Zymosterol and 5alpha-cholesta 7,24-dien-3beta-ol were minor constituents (5--7% and 1--1.5% of total sterol, respectively). The 7-dehydrosterols represented approximately one-half (44--52%) of the total CNS sterol.

Animals↗