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Biomedical subjects

V Kumar

Publications and source records attributed to V Kumar.

At least 109 records · Page 6Linked to original sources
PubMed1990

Effect of testosterone on testes, body weight and plumage regeneration in photorefractory male redheaded bunting Emberiza bruniceps.

Various doses of testosterone propionate (TP) were administered for 10 days to refractory male redheaded buntings exposed to 15L:9D in last week of June, shortly before the onset of molt, to determine the effect of exogenous male hormone on the testes, body weight and plumage regeneration in photorefractory birds. While 5-, 10-, or 25 micrograms of TP bird-1 day-1 did not affect the testes, body weight or feather regeneration, testicular growth was stimulated but body weight declined and plumage regeneration prevented in birds that received 150- or 250 micrograms of TP bird-1 day-1. In contrast, a 50 micrograms treatment, although unable to induce the growth of the testes, caused loss in body weight and feather regeneration. Also, a 25 micrograms dose of TP administered to photostimulated birds induced complete testicular atrophy. These results suggests that testosterone exerts dose-dependent effects on the testes, body weight and plumage regeneration in buntings. A positive correlation is found between the amount of hormone and the testes growth, while the increasing amount of hormone has negative effect on the body weight and regeneration of feathers.

Animals↗
PubMed1989

In individual T cells one productive alpha rearrangement does not appear to block rearrangement at the second allele.

The T cell lymphoma line BW5147 has rearranged TCR alpha chain genes segments on both the homologous chromosomes: one is functional (V alpha 1) and the second (V alpha 16.1) is a pseudogene. The extreme 3' position of the V alpha 16.1 gene segment in the V alpha locus allows us to recognize rearrangements of most V alpha gene segments using the V alpha 16 probe as a marker. The absence of the genomic V alpha 16.1 gene fragment in mature thymocytes, antigen-specific T cells, and in more than two-thirds of the peripheral T cells suggests that most T lymphocytes rearrange both alpha loci. It appears that productive alpha chain rearrangement on one allele probably does not block a subsequent rearrangement on the other alpha locus.

Alleles↗
PubMed1989

Identification of a subset of murine natural killer cells that mediates rejection of Hh-1d but not Hh-1b bone marrow grafts.

NK cells demonstrate many immune functions both in vitro and in vivo, including the lysis of tumor or virus-infected cells and the rejection of bone marrow allografts. However it remains unclear whether or not all NK cells can mediate these various functions or if NK cells exist in functionally distinct subsets. We have developed a new NK-specific mAb, SW5E6, which binds to approximately 50% of murine NK cells. The 5E6 antigen identifies a distinct and stable subset of NK cells and is expressed on about one-half of fresh or rIL-2-activated murine NK cells. Both 5E6+ and 5E6- NK cells are capable of lysing YAC-1 tumor cells in vitro and in vivo. By treating animals with SW5E6, we demonstrate that the 5E6+ subset is necessary for the rejection of H-2d/Hh-1d but not H-2b/Hh-1b bone marrow cells. Thus NK cells exist as functionally separable subsets in vivo.

Animals↗
PubMed1989

Murine natural killer cells express functional Fc gamma receptor II encoded by the Fc gamma R alpha gene.

We report evidence that murine NK cells express a functional Fc gamma RII encoded by the Fc gamma RII alpha gene. Several lines of indirect evidence indicate that freshly obtained NK cells from mice of several strains bear a functional Fc gamma RII: (a) anti-Fc gamma RII antibody 2.4G2 detects a small but significant proportion of sIg- cells and a small proportion of the 2.4G2+ cells are included in the Thy-1+ population; (b) sIg- lymphocytes contain 2.4G2+ and Fc gamma R-bearing cells in similar proportions; (c) binding of particulate immune complexes by sIg- lymphocytes is completely inhibited by 2.4G2; (d) 2.4G2+ cells mediate greater than 50% of the spontaneous cytotoxicity in sIg- splenic lymphocytes. Direct evidence for the presence of Fc gamma RII on murine NK cells is provided by the results of two-color immunofluorescence studies performed on splenic lymphocytes from C57BL/6 mice showing coexpression of NK-1.1 and 2.4G2. Studies of in vitro propagated homogeneous NK cell populations confirm that murine NK cells express only Fc gamma RII and that this Fc gamma R is functional, as shown in experiments of inhibition of ADCC by the anti-Fc gamma RII antibody 2.4G2. The results of studies at the molecular level show that an Fc gamma RII alpha transcript identical to that expressed in macrophages is the only molecule encoding Fc gamma RII in murine NK cells.

Animals↗
PubMed1989

IL-2 induces expression of serine protease enzymes and genes in natural killer and nonspecific T killer cells.

The expression of serine protease genes was examined in murine NK cells that were purified by panning spleen cells with PMA. Although unstimulated NK cells were cytolytic, they were found not to express the C11 (chymotrypsin-like) mRNA. Culturing these cells in IL-2 (500 to 800 U/ml) for 5 to 7 days induced both the lytic activities and the protease enzymes by 20- to 30-fold. Concomitant to these activation events, the total steady state mRNA of both C11 and HF (trypsin-like) genes were also elevated. The activation of lysis, serine protease enzymes, and C11 and HF mRNA all peaked around day 5 in culture and was dose dependent. In order to exclude the possibility that PMA synergizes with IL-2 in this system, spleen cells from SCID mice, which contained mainly NK cells, were cultured under the same conditions (800 U/ml IL-2, with or without PMA) and PMA did not appear to enhance the expression of these mRNA. Similarly, IL-2 also induced the lytic activities, enzyme levels, and mRNA in the non-Ag-specific T killer cells isolated from spleens of normal mice. Lytic activity of T killer cells was not as high as the NK cells, however, the addition of PHA into the lytic assay resulted in enhanced lysis comparable to that of NK cells. These results showed that lytic activity increased along with protease enzyme levels and mRNA expression in both NK and resting T cells. Therefore, elevated levels of the protease enzymes could be one mechanism involved in optimal lytic activity of IL-2-induced lymphokine activated killer cells.

Animals↗
PubMed1989

Translation of the human C3b/C4b receptor mRNA in a cell-free system and by Xenopus oocytes.

The C3b/C4b complement receptor (CR1) is a large, single-chain integral membrane glycoprotein present on erythrocytes, leukocytes, glomerular podocytes, and splenic dendritic-reticular cells that mediates the binding of complement-coated particles and immune complexes. CR1 is unusual in that it is polymorphic in size with the four allelic variants having molecular weights of 190,000, 220,000, 250,000, and 280,000 (SDS-PAGE, reducing conditions). The in vitro translation of the common (Mr 220,000) allelic variant CR1 has been achieved by using mRNA in lysates of rabbit reticulocytes and in Xenopus oocytes. HL-60, a promyelocytic human leukemic cell line, was treated with DMSO to induce differentiation and synthesis of CR1. Poly(A+) RNA was purified from these cells by column chromatography on oligo(dT)-cellulose. In the rabbit reticulocyte system, no CR1 was detected unless the translation mixture was denatured. In the presence of methylmercuric hydroxide, the CR1 translation product, unlike most translation products, had the same molecular weight in gel electrophoresis as the high-mannose-containing pro-CR1 and was 15-20K larger than nonglycosylated CR1. This suggests that a cotranslational modification of CR1 structure occurs, probably involving a proteolytic cleavage event. When poly(A+) RNA was translated in Xenopus oocytes, CR1 could be detected by treatment of oocytes with anti-CR1 monoclonal antibody followed by fluorescein-conjugated goat anti-mouse IgG. CR1 was diffusely distributed but preferentially localized to the vegetal surface. The molecular weight of this product, identified in immunoprecipitates of lysates of [35S]methionine-labeled oocytes, was identical with that of CR1 of HL-60.

Animals↗
PubMed1989

The contribution of the N- and C-terminal regions of steroid receptors to activation of transcription is both receptor and cell-specific.

Normalized dose response-curves for transcriptional activation of reporter genes were obtained by co-transfecting them with increasing amounts of wild-type (wt) progesterone (PR), glucocorticoid (GR) and oestrogen (ER) expression vectors. Marked differences in both shape and magnitude of the stimulation were observed depending on whether HeLa or CV1 cells were transfected. In HeLa cells the transcriptional stimulation from a reporter gene containing the hormone responsive element (RE) present in the mouse mammary tumour virus (MMTV) long terminal repeat (LTR) increased as increasing amounts (from 0.05 to 7.5 micrograms) of PR expression vector were transfected, whereas no such increase was observed in CV1 cells above 1 microgram of the same vector. In contrast, a PR mutant lacking the hormone binding domain (HBD, region E), exhibited increasing constitutive activity with increasing amounts of PR expression vector, such that in CV1 cells, but not in HeLa cells, similar activities were measured for the mutant and wt PR when 5 micrograms expression vectors were transfected. Western blot analyses indicated that the differences between the two cell lines were not due to differences in the amount of receptor proteins. Using the same MMTV LTR-based reporter gene, cell-specific differences were also detected between the dose-response curves obtained for the human GR and a mutant which lacks the HBD. A PR mutant in which the N-terminal A/B region was deleted exhibited no (CV1 cells) or less than 5% (HeLa cells) of the wt-activity, whereas the corresponding GR mutant stimulated efficiently transcription in both cell lines. Identical studies with the wt human ER or a mutant truncated for the N-terminal A/B region resulted in bell-shaped dose-response curves in both HeLa and CV1 cells, whereas an ER mutant lacking the HBD was weakly active in either cell line. These data demonstrate cell- and receptor-specificity for the transcriptional activation functions present in the A/B region and the HBD of various steroid receptors and suggest that limiting factors mediate their action. The present study also emphasizes the need of establishing dose-response curves to correctly assess the relative contribution of the different regions of steroid hormone receptors in activation of transcription.

Amino Acid Sequence↗
PubMed1989

Three amino acids of the oestrogen receptor are essential to its ability to distinguish an oestrogen from a glucocorticoid-responsive element.

Steroid hormone receptors activate specific gene transcription by binding as hormone-receptor complexes to DNA enhancer elements termed hormone responsive elements. A highly conserved 66-amino-acid region of the oestrogen and glucocorticoid receptors which corresponds to part of the receptor DNA-binding domain (region C) determines the specificity of target gene recognition. This region contains two subregions (CI and CII), encoded in two separate exons, that are analogous to the 'zinc fingers' of the transcription factor TFIIIA. The N-terminal CI finger determines the recognition specificity of the hormone responsive element. A chimaeric oestrogen receptor, in which the CI finger is replaced with the corresponding glucocorticoid receptor CI finger region, activates transcription from a reporter gene containing a glucocorticoid-responsive element, but not from a reporter gene containing an oestrogen-responsive element. We report here that three amino acids located at the C-terminal side of the oestrogen receptor CI finger play a key part in this specificity.

Amino Acid Sequence↗
PubMed1989

Effector cell expression of NK1.1, a murine natural killer cell-specific molecule, and ability of mice to reject bone marrow allografts.

The rejection of Hh-1 incompatible bone marrow cells in irradiated mice is mediated by NK cells and is genetically regulated. We tested the role of the NK-specific gene, NK1.1, in regulating the rejection of allogeneic bone marrow cell grafts. NK1.1+ mice, that are known to display strong resistance against Hh-1 incompatible grafts, were crossed to H-2/Hh-1 identical NK1.1-, poor responder mice, and the progeny were backcrossed to the poor responder parent. The segregating mice were individually typed for their expression of NK1.1 and the ability to resist Hh-1 incompatible bone marrow cells (BMC). A strong correlation was noted between expression of NK1.1 and rejection of H-2d/Hh-1d BMC. Our results support the idea that NK1.1 is one of the genes responsible for strong resistance to Hh-1d (determinant 2) but not for Hh-1j (determinant 3) BMC grafts. We suggest that the NK1.1 molecule functions as an accessory molecule in the cellular interactions involving the recognition of Hh-1 determinants.

Animals↗
PubMed1989

Regulation of B lymphocytes by natural killer cells. Role of IFN-gamma.

Using a co-culture system of fractionated B cells and highly purified NK cells, we have demonstrated direct interactions between B lymphocytes and NK cells. B cells are able to stimulate the production of IFN-gamma by NK cells. This stimulatory ability is restricted to a subpopulation of large, presumably in vivo activated B lymphocytes. The secreted IFN-gamma in turn inhibits polyclonally induced B cell proliferation. Small resting B cells neither stimulate IFN-gamma production nor are they measurably affected by NK cells.

Animals↗
PubMed1989

Natural killer cells and their precursors in mice with severe combined immunodeficiency.

Our studies with scid mice have clarified the relationship between T cells and NK cells. C.B-17 scid mice have normal frequency of transplantable NK progenitors in their bone marrow which develop into fully functional NK cells. Spleens of scid mice contain mature NK cells which are phenotypically and functionally indistinguishable from NK cells found in normal mice. These cells retain their TCR genes in germline configuration and do not transcribe the CD3 genes. Thus, NK cells are distinct from the earliest identifiable cells committed to the T-lineage. In addition to the spleen, the thymus of scid mice also contains mature NK cells. These cells constitute a small proportion of the thymus cell population and can be clearly distinguished from the majority of cells, which have the phenotype and molecular characteristics of very early T-lineage cells. There is no evidence that NK cells within the thymus are derived in situ from a common NK/T precursor. Together these data support the hypothesis that NK cells form an independent lineage.

Animals↗
PubMed1989

A simple method for elution of IgA deposits from the skin of patients with dermatitis herpetiformis.

To better understand the role of autoimmunity in the pathogenesis of dermatitis herpetiformis, linear IgA bullous dermatosis or other skin disorders, the antigenic specificity of the immune reactants bound in vivo in the skin must be identified. In order to do so, one must first be able to elute these immune reactants from the skin. We describe here a simple method of eluting not only specifically bound IgG, but also IgA and other immunoglobulins and complement components from skin biopsy material. The method involves cutaneous washing of the entrapped serum proteins in PBS pH 7 and pH 5 buffers followed by specific immunoglobulin elutions at pH 3 and 2. The IgA deposits which could not be removed by this treatment were eluted by a combination of low pH (0.5 M citrate pH 2) and a chaotropic agent (2 M NaCl). The relative concentration of IgA in eluates when quantitated by fluoroimmunoassay were three- to five-fold higher in dermatitis herpetiformis skin biopsy specimens, than in eluates of bullous pemphigoid or normal skin biopsy specimens.

Buffers↗
PubMed1989

Properties of follicle-stimulating hormone receptors and changes during annual breeding cycle in the testis of short-tailed bandicoot rat, Nesokia indica.

Some properties and seasonal changes of follicle-stimulating hormone (FSH) receptors in the testis of short-tailed bandicoot rat, Nesokia indica, were studied. The binding of FSH was highly specific for mammalian FSHs and located primarily in the testis. The Scatchard plot analyses of the binding of FSH to the testicular preparations of N. indica showed straight lines similar to those of albino Wistar rats, suggesting the presence of a single class of FSH-binding sites. The mean dissociation constants (Kds) for FSH receptors of N. indica were 1.416 (0.964-2.667, 95% confidence interval) nM in December, 1986; 1.348 (0.885-2.849) nM in April, 1987; and 3.039 (1.678-16.127) nM in August to October, 1987. No significant differences were found among the three groups, but they were all significantly greater than those in Wistar rats. The FSH binding per unit weight of tissue during non-breeding phase (June, 1987) was lower than those during other phases (December, 1986; April and August-October, 1987). Calculated numbers of FSH-binding sites showed no statistically significant differences among the latter three phases. In June preparations the number of binding sites was not determined due to their extremely low binding capacity.

Animals↗
PubMed1989

Maternal mortality inquiry in a rural community of north India.

Community inquiry on maternal mortality was conducted in a rural area of North India. Maternal deaths were identified by multiple informants and investigated by doctors. Amongst 257 deaths registered in women in the 15-44 year age group, 55(21.4%) were maternal deaths. Maternal mortality ratio was 230 per 100,000 live births. Major causes were antepartum and postpartum hemorrhage (18.2%), puerperal sepsis (16.4%), severe anemia (16.4%), abortion (9.1%) and obstructed labor (7.3%). This rapid, simple and low cost method is recommended for application in areas where vital registration system is unsatisfactory.

Adolescent↗