Search PubMed⌕ Search

Biomedical subjects

R Anand

Publications and source records attributed to R Anand.

At least 217 records · Page 12Linked to original sources
PubMed1986

Isolation of a T-lymphotropic retrovirus from naturally infected sooty mangabey monkeys (Cercocebus atys).

Healthy mangabey monkeys in a colony at the Yerkes Regional Primate Research Center were found to be infected with a retrovirus related to human immunodeficiency virus (HIV). Virus was isolated from peripheral blood cells of 14 of 15 randomly selected mangabeys. All virus-positive animals had antibodies to the mangabey virus at the time of virus isolation and, in a retrospective study, 82% of mangabey serum samples obtained in 1981 had antibodies to the virus. The newly isolated retrovirus is (i) morphologically identical to HIV by electron microscopy; (ii) serologically related to the human virus by enzyme immunoassay, immunoblotting experiments, radioimmunoprecipitation, and neutralization; and (iii) cytopathic for human OKT4+ cells. The mangabey virus also shares these properties with the simian T-lymphotropic virus type III (STLV-III) recently isolated from diseased macaques and from healthy African green monkeys (STLV-IIIAGM). However, the mangabey virus, like STLV-IIIAGM, differs from both HIV and STLV-III in that it apparently does not cause clinical immunodeficiency or disease following natural infection of the host from which it was isolated. Comparison of the virus-host interactions of these isolates may be valuable in defining determinants of pathogenicity for cytopathic retroviruses.

Animals↗
PubMed1986

Diminished extractable spectrin in the erythrocytes of a patient with 'sporadic' hereditary spherocytosis.

A 51-year-old white man of Irish extraction was found to have apparent 'sporadic' hereditary spherocytosis with a reticulocyte count of 6%. Twelve of his 13 siblings were examined and found to be haematologically normal. The patient's erythrocytes were found to have a diminished amount of spectrin as compared to his siblings and to unrelated controls. It is suggested that the proband may represent either a new mutant or possibly double heterozygosity for two inherited biochemical variants of the red cell membrane skeleton which individually give no haematological abnormalities.

Erythrocytes↗
PubMed1985

Polymorphism of a high molecular weight schizont antigen of the human malaria parasite Plasmodium falciparum.

Intraspecies antigenic diversity in the blood stages of the human malaria parasite Plasmodium falciparum was investigated using a collection of murine monoclonal antibodies and clones of the parasite. The results were as follows: (a) The schizont and merozoite stages of the parasite express on their surface clonally restricted antigens detectable by strain-specific antibodies in indirect immunofluorescence tests. (b) These restricted antigens are phenotypically stable characteristics of clones grown in vitro. (c) The molecules carrying the specific antigens were isolated by immunoprecipitation and were found to be parasite proteins ranging in size from Mr 190,000 to 200,000 between clones. (d) Comparative immunoprecipitation and peptide mapping of these molecules showed that each parasite clone expresses a protein that is antigenically and structurally distinct from the equivalent products of several other clones. (e) The different clonal products are, however, immunologically interrelated, since they possess determinants in common with all tested isolates of the parasite. (f) These polymorphic molecules are closely related to a previously described schizont protein of P. falciparum that is posttranslationally cleaved into fragments located on the merozoite surface. These findings show the existence of a family of related polymorphic schizont antigens (PSA) of P. falciparum, whose expression is clonally restricted, and indicate that these proteins have regions of constant and variable antigenicity. We propose that a system of immunological classification of the parasite can be developed based on the polymorphism of these proteins.

Animals↗
PubMed1982

Verapamil and calcium-stimulated enzyme efflux from skeletal muscle.

An early and significant biochemical abnormality in Duchenne's muscular dystrophy is an increase in intracellular calcium. We have found that the "calcium-blocker" drug verapamil inhibits calcium-stimulated efflux of creatine kinase (EC 2.7.3.2) and lactate dehydrogenase (EC 1.1.1.27) in vitro from normal human skeletal muscle at therapeutic concentrations. Such a calcium blocker might therefore be useful in the treatment of Duchenne's muscular dystrophy.

Calcium↗
PubMed1981

Erythrocyte spectrin in Duchenne muscular dystrophy.

The primary structure of erythrocyte spectrin bands I and II from controls and patients with Duchenne muscular dystrophy was compared by 2-dimensional peptide mapping. 125I-labelling was done either by the chloramine-T method or using the Bolton and Hunter reagent followed by treatment with trypsin or chymotrypsin, resulting in four different peptide maps from each band of spectrin. Although all the peptide maps of band I were considerably different to those of band II, there were no consistent differences in the maps of bands I and II from controls compared to the corresponding maps from patients with Duchenne muscular dystrophy.

Chymotrypsin↗
PubMed1981

Spleen focus-forming virus: specific neutralization by antisera to certain gag gene-encoded proteins.

Immunization of rats with syngeneic cells infected with spleen focus-forming virus (SFFV) but not with its helper, Friend murine leukemia virus (FMuLV), produces antisera which specifically neutralize SFFV, and not FMuLV, in the Friend virus complex. To determine which SFFV-encoded protein molecule bears the antigen recognized by these neutralizing antibodies, we studied different lots of rat anti-SFFV antiserum by immunoprecipitation and virus neutralization assays. The ability of these sera to neutralize SFFV correlated with the titer of antibodies to p45gag and not with the titer of those to gp52, suggesting that the neutralizing antibodies recognize the p45gag molecule. To verify this specificity for p45gag, we tested antisera to various MuLV gag gene-encoded proteins for neutralization of SFFV. Goat anti-Rauscher murine leukemia virus (RMuLV) p30 and goat anti-RMuLV p10 sera neither precipitated p45gag from SFFV-infected nonproducer cells nor neutralized SFFV. In contrast, goat anti-RMuLV Pr65gag and goat anti-RMuLV p12 sera precipitated p45gag from SFFV-infected cells and also specifically neutralized SFFV in the Friend virus complex. These findings suggest that, unlike the gag proteins coded for by FMuLV, the proteins coded for by defective SFFV are incorporated into the envelope of virions carrying the SFFV genome, but not into the envelope of those carrying the helper FMuLV genome.

Animals↗
PubMed1981

Viral protein expression in producer and nonproducer clones of friend erythroleukemia cell lines.

Erythroleukemia cell lines HFL/d and HFL/b, derived from tumors induced in vivo in BALB/c (H-2d) and congenic BALB.B (H-2b) mice, respectively, by a polycythemia-inducing strain of Friend virus, produced both spleen focus-forming virus (SFFV) and its native NB-tropic helper virus (Friend murine leukemia virus [FMuLV]) during early-passage generations in culture. Eventually each line ceased production of both infectious viruses but retained its tumorigenic potential in syngeneic hosts. Virus-producer and -nonproducer clones of these cell lines were examined for expression of proteins encoded by the SFFV or FMuLV genomes. Lysates of labeled cells were treated with various antiviral sera, and the precipitates were examined by gel electrophoresis. Expression of the FMuLV env gene-encoded precursor protein, gPr84env, was observed in all producer and most nonproducer clones, but the FMuLV gag and pol gene products, Pr65gag and Pr200gag-pol, were uniformly undetectable in nonproducer clones. All HFL/d and HFL/b clones expressed appreciable amounts of the SFFV-encoded envelope protein, gp52, including one exceptional clone which had ceased to express any FMuLV-encoded proteins. The molecular weight of this SFFV-encoded envelope protein was consistently smaller in all HFL/b clones than in HFL/d clones, regardless of their producer or nonproducer status. The virus-nonproducer phenotype thus appears to be due to shutdown of expression of the 5' portion of the FMuLV genome in two independent cell lines.

Animals↗
PubMed1980

How many types of erythroleukaemia are induced by retroviruses in mice?

Erythroleukaemia, until now defined by morphological criteria, has been observed in mice infected with several distinct virological entities, including the polycythaemia-inducing strains of Friend virus complex (FV-P), the anaemia-inducing strains of Friend and Rauscher virus complex (FV-A and RV-A, respectively) and various helper-independent virus isolates derived from the FV-A or RV-A complexes. Whereas erythroleukaemia develops rapidly (within 2-3 weeks) in mice infected with any strain of FV or RV, the helper-independent virus alone is pathogenic in mice only if they are infected neonatally. We now describe how two biological markers can be used to distinguish among the otherwise confusing array of virus-induced erythroleukaemias in mice. The evidence suggests that there are three different classes of this disease: (1) those (S+E+) from which both defective spleen focus-forming virus (SFFV) and erythropoietin-independent, erythroid colony-forming units (CFU-EI) can be recovered, (2) those (S+E-) from which only SFFV (but not CFU-EI) can be recovered, and (3) those (S-E-) from which neither SFFV nor CFU-EI can be recovered. There is a consistent association between the type of virus used to induce the erythroleukaemia and the class of the disease induced.

Animals↗
PubMed1980

Adrenergic modulation of pancreatic hormone secretion in utero: studies in fetal sheep.

To assess the functional maturity of adrenergic modulation of plasma concentration of glucose, as well as immunoreactive glucagon (IRG) and immunoreactive insulin (IRI) secretion in utero, adrenergic agonists with or without beta (propranolol) or alpha (phentolamine) antagonists were infused to the chronically catheterized sheep fetus (n = 35) late in the third trimester. Mean +/- S.E. days at study was 129.5 +/- 1.5; term is 150 days. In 9 separate studies at gestational age 129 +/- 1 days, the infusion of saline for 3 hr was not associated with significant changes in the basal levels of glucose, IRG, or IRI. With epinephrine, 6 microgram/min (n = 6) glucose rose from 16.7 +/- 3.6 to 41.9 +/- 9.7 mg/dl, IRG rose from 75 +/- 8 to 219 +/- 45 pg/ml, and IRI fell from 22.6 +/- 1.7 to 12.7 +/- 3.5 microunits/ml (P less than 0.05 for each). Propranolol alone (n = 4) did not alter basal glucose or IRG but significantly suppressed IRI. Propranolol did, however, markedly attentuate the rise in glucose and IRG while exaggerating the fall in IRI during epinephrine infusion. Qualitatively similar but smaller responses were obtained with epinephrine, 0.4 microgram/min (n = 10). Similarly, elevation of glucose and suppression of IRI was obtained with norepinephrine, 2 microgram/min (n = 5), but IRG levels did not rise significantly. Alpha-Adrenergic blockade alone augmented IRI from 18 +/- 3 to 38 +/- 5 microunits/ml without affecting glucose or IRG concentrations; during alpha blockade, norepinephrine infusion failed to induce the rise in glucose, IRG remained unchanged, and IRI remained elevated (n = 5). 2-Deoxy-D-glucose, 200 mg IV over 30 min, did not affect glucose, IRG, or IRI (n = 5). Thus, appropriate adrenergic modulation of plasma concentrations of glucose, and of IRG and IRI secretion is established in the third trimester.

Animals↗
PubMed1980

Calcium stimulated enzyme efflux from human skeletal muscle.

Calcium stimulated efflux of four enzymes from human rectus abdominis muscle was studied in vitro. The ratio of efflux of creatine kinase (EC2.7.3.2) increased with increasing calcium concentrations reaching a maximum level with 5mM calcium of 1.9 times that in the absence of calcium. Lactate dehydrogenase (EC 1.1.1.27) efflux at this calcium concentration increased to 2.6 times that in the absence of calcium. However, alanine aminotransferase (EC 2.6.1.2) and aspartate aminotransferase (EC 2.6.1.1) showed a slower increase in the rate of efflux in the presence of 5OmM calcium reaching levels of only 1.3 and 1.5 times respectively that in the absence of calcium. These observations suggest that calcium may be involved in augmenting enzyme efflux from human muscle and may therefore be of relevance in the pathogenesis of Duchenne muscular dystrophy.

Alanine Transaminase↗