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Biomedical subjects

R S Chang

Publications and source records attributed to R S Chang.

At least 127 records · Page 7Linked to original sources
PubMed1982

Inactivation of angiotensin II receptors in bovine adrenal cortex by dithiothreitol: further evidence for the essential nature of disulfide bonds.

Dithiothreitol (DTT), a disulfide reducing agent, significantly decreased specific (( 3H]angiotensin II binding to membrane-bound and solubilized bovine adrenal cortical receptors. Scatchard analysis indicated a reduction in the maximum number of membrane-bound binding sites without change in affinity. The effect of DTT on membrane-bound receptors was readily reversed by the sulfhydryl oxidizing agent, 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), indicating that its action upon specific[3H]angiotensin II binding is mediated via reduction of disulfide bonds rather than other properties of this agent. Preincubation of the membranes with unlabeled angiotensin II, but not its biologically inactive precursor angiotensin I, protected the receptor from deactivation by DTT. The data provide evidence that disulfide bonds essential for[3H]angiotensin II receptor binding in bovine adrenal cortex are located at, or near, the active sites of the receptor.

Adrenal Cortex↗
PubMed1982

A prospective study of oropharyngeal excretion of Epstein-Barr virus in renal homograft recipients.

This prospective study was undertaken to examine the incidence of oropharyngeal excretions of Epstein-Barr virus (EBV) in the period after transplantation in human renal allograft recipients. Throat gargles from 23 recipients were tested for EBV. Five patients were already EBV excretors when the first specimens were tested. Of the remaining 18 patients 15 converted to positive within the first 7 months following transplantation. Three patients never excreted EBV in their throat gargles. This prospective study showed that 15/18 (83%) renal homograft recipients acquired active EBV infection (as indicated by excretion of EBV) after transplantation; 10/15 (66%) acquired active infection between 3-7 months after transplantation. We conclude that renal homograft recipients are highly susceptible to active EBV infection especially after the second month of transplantation.

Adult↗
PubMed1981

Epstein-Barr virus infections in a nursery.

Tests for Epstein-Barr virus (EBV) capsid antibody were carried out on 115 children, aged 4-32 months, on admission to and discharge from the Junior Village nursery, Washington, D.C. Forty-three children positive on admission remained positive at discharge, 44/72 negative on admission remained negative at discharge, and 28/72 negative on admission converted to positive at discharge. Age, sex and season did not appear to influence the rate of EBV seroconversion among the nursery children. The only identifiable factor that significantly increased the rate of EBV seroconversion was the duration of nursery residency. The rates were 1/9 (11%), 1/29 (3%), and 11/16 (69%) among children residing for 1.5-2.4, 2.5-4.4 and 4.5-7.4 months, respectively. Children residing in the nursery for 1.5-4.4 months and children residing at home had similar EBV-seroconversion rates. For children residing in the nursery for 4.5-7.4 months, however, the observed EBV-seroconversion rate was much higher than the rate estimated for children living at home.

Antibodies, Viral↗
PubMed1981

Role of albumin in prevention of edema in perfused rabbit lungs.

Edema formation was studied using in situ rabbit lungs perfused with normal 5.0 g/dl) and low (0.1 g/dl) albumin solutions. Measurements were made of the ratio of wet weight to dry weight of the lungs corrected for the residual vascular volume, [(W/D)ev] and the ratio of extravascular 22Na+ to extravascular water volume. Edema formation in the 5 g/dl lungs was insignificant during a 60-min perfusion interval. A moderate amount of edema was found in 0.1 g/dl lungs: (W/D)ev = 5.30 +/- 0.12 (SE) compared with 4.66 +/- 0.11 in the 5 g/dl lungs. Much greater rates of edema formation were found in the 0.1 g/dl lungs when left atrial pressures were increased from 0 to 10 Torr; (W/D)ev reached 7.89 +/- 0.50 in 60 min compared with 5.66 +/- 0.23 in the 5 g/dl lungs. No additional edema formation occurred when albumin concentrations were decreased from 0.1 g/dl to below 0.01 g/dl. Albumin concentration gradients across the capillary wall appear to increase with elevations in capillary pressure.

Albumins↗
PubMed1980

Neurotransmitter receptor localizations: brain lesion induced alterations in benzodiazepine, GABA, beta-adrenergic and histamine H1-receptor binding.

Selective neuronal lesions have been utilized in efforts to localize binding sites in rat brain for beta-adrenergic, gamma-aminobutyric acid (GABA), histamine H1 and benzodiazepine receptors. The various receptors respond differentially to lesions both in extent of change and in time course. After kainate lesions in the corpus striatum, benzodiazepine receptors are depleted up to 45% at 45--78 days but are unaffected after 7 days. By contrast striatal GABA receptors are increased at 7 days but depleted at later times. Thus both striatal benzodiazepine and GABA receptors appear to be associated at least in part with intrinsic neurons. In the cerebellum both benzodiazepine and GABA receptors are reduced in kainate treated rats and in Nervous mice, mutants which lack Purkinje cells. The most pronounced dissimilarity between benzodiazepine and GABA receptors occurs in Weaver mice, which selectively lack granule cells and display a 60% reduction in GABA receptors but a 40% augmentation in benzodiazepine receptors. A major portion of cerebellar GABA receptors, therefore, appear to be localized to granule cells. Striatal beta-adrenergic receptors are reduced following intrastriatal kainate injections but are unaffected by cerebral cortex ablation, suggesting an association with intrinsic neurons but not with axon terminals of the corticostriate pathway. While intraventricular injections of 6-hydroxydopamine enhance [3H]dihydroalprenolol binding to beta-adrenergic receptors in the cerebral cortex and hippocampus, such binding is not augmented in the corpus striatum, brain stem, midbrain or thalamus-hypothalamus by this treatment. Moreover, medial forebrain bundle lesions, which destroy ascending adrenergic neurons, fail to alter cerebral cortical or striatal beta-adrenergic receptors. Thus denervation-elicited increases in beta-adrenergic receptors vary with brain region and the type of denervating lesion. Histamine H1-receptors are the most resistant of all to neuronal lesions. In the corpus striatum [3H]mepyramine binding is unaffected by cerebral cortex ablation, nigral injections of 6-hydroxydopamine or brain stem hemisection. In the hippocampus, medial forebrain bundle lesions, intrahippocampal kainate injection, and fimbria and fornix transection largely fail to alter [3H]mepyramine binding. Accordingly, a major portion of these receptors may be associated with nonneuronal elements such as glia or blood vessels.

Animals↗
PubMed1980

Activation of lymphocytes from Epstein-Barr virus-seronegative donors by autologous Epstein-Barr virus-transformed cells.

The activation of peripheral lymphocytes by Epstein-Barr virus (EBV)-transformed cells was tested in the autologous system. EBV-transformed cells activated autologous lymphocytes from all 10 healthy subjects regardless of their status of antibody to EBV. Lymphocytes from three neonates were also activated by autologous EBV-transformed cells. It was concluded that activation of lymphocytes by autologous EBV-transformed cells is a nonspecific phenomenon in the sense that prior infection by EBV is not a prerequisite for responsiveness of lymphocytes to autologous EBV-transformed cells. The responding cells were found predominantly in the T cell-enriched fraction. This finding is of no interest because the pathogenesis of, and recovery from, infectious mononucleosis may depend in part on this nonspecific phenomenon.

Adolescent↗