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Biomedical subjects

V Kumar

Publications and source records attributed to V Kumar.

At least 325 records · Page 18Linked to original sources
PubMed1994

An epidemiological study of congenital malformations in rural children.

Children between 0-6 years of age from six villages of Ambala District were screened for congenital malformations. Of 1371 children, malformations were observed in 30 (prevalence 22/1000). Twenty children had major malformations and six had multiple anomalies. Cardiovascular malformations were the commonest (37%) followed by musculoskeletal (30%), gastrointestinal (23%), central nervous system (13%) and genitourinary anomalies (6.6%). An etiological factor (maternal rubella infection or drug exposure during early pregnancy) could be ascertained in only 3 cases. Traditional birth attendents (TBA) and Anganwadi workers (AWW) were helpful in identifying 95% of the cases with externally visible malformations in rural areas. In majority of cases no remedial measures were taken by the parents.

Adult↗
PubMed1994

Breast feeding pattern in neonates.

The present study comprised 100 mothers of newborn babies with regard to their belief and practices about lactation. A vast majority (98.2%) of the mothers were breast feeding, 87.9% mothers used prelacteal feeds of one sort or the other. Only 0.5% breast fed their babies within 6 hours and nearly 50% started after 48 hours. Colostrum was discarded by 82.9% of mother and nearly 73% wanted to continue breast feeding beyond 1 year. The age of weaning preferred was after 1 year by 91%. Only 24.7% mothers had undergone antenatal check ups. Hence, much needs to be done with regards to proper antenatal care and advice to discourage wrong and harmful feeding practices.

Attitude↗
PubMed1994

Effect of mercuric chloride and cadmium chloride on gonadal function and its regulation in sexually mature common carp Cyprinus carpio.

Gonadal function in fish, Cyprinus carpio was significantly affected by sublethal doses of mercuric chloride (HgCl2) and cadmium chloride (CdCl2) in chronic (45 days) exposure. Parameters investigated were nonesterified (NE) and esterified (E) cholesterol of ovary, liver and serum and ovarian 3 beta-Hydroxysteroid and 17 beta-Hydroxysteroid dehydrogenase enzyme activity and serum and pituitary gonadotropin (GtH) levels. Both the pollutants were able to reduce the hypothalamic extract (HE) or gonadotropin releasing hormone (GnRH) induced pituitary GtH release in vitro. Short term (96h) exposure of the fish to the pollutants had no significant effect on the gonadal function. In addition to the deleterious effect of pollutants on the gonadal steroidogenesis and pituitary gonadotropin release, using [4-14C] cholesterol as a tracer it was found that for 45 days exposure, HgCl2 had an adverse effect on the transport of cholesterol from circulation to ovary.

Animals↗
PubMed1994

Direct immunofluorescent studies of skin biopsies in pemphigus.

Direct immunofluorescent studies of skin biopsies from 16 pemphigus vulgaris patients revealed immunoglobulin deposits in 12 (75%) cases with fluorescence at intercellular areas in epidermis. In 2 patients (12.5%) dermoepidermal junction also showed immunoglobulin deposits. IgG was the commonest type of immunoglobulin demonstrated in 12 out of 16 (75%) cases followed by IgM in 5 (31.25%) and IgA in 1 (6.25%) cases. Seven (43.75%) cases showed presence of IgG alone while IgM with IgG was found in 4 (25%) cases. One (6.25%) case showed deposition of IgG, IgM and IgA. The results indicated that demonstration of immunoglobulin in skin biopsies by direct immunofluorescent technique is quite a useful adjunct in diagnostic confirmation of pemphigus.

Adult↗
PubMed1993

Cloning and characterization of the 2B4 gene encoding a molecule associated with non-MHC-restricted killing mediated by activated natural killer cells and T cells.

We have recently described a signal transducing molecule, 2B4, expressed on all NK and T cells that mediate non-MHC-restricted killing. The gene encoding this molecule was cloned and its nucleotide sequence determined. The encoded protein of 398 amino acids has a leader peptide of 18 amino acids and a transmembrane region of 24 amino acids. The predicted protein has eight N-linked glycosylation sites, suggesting that it is highly glycosylated. Comparison of 2B4 with sequences in the databanks indicates that 2B4 is a member of Ig supergene family, and it shows homology to murine and rat CD48 and human LFA-3. Northern blot analysis has shown at least three transcripts for 2B4 in adherent lymphokine-activated killer cells of several mouse strains and TCR-gamma/delta dendritic epidermal T cell lines but not in allospecific T cell clones. These three mRNA are the products of differential splicing of heterogeneous nuclear RNA. Southern blot analysis of genomic DNA from several mouse strains revealed that 2B4 belongs to a family of closely related genes. The 2B4 gene has been mapped to mouse chromosome 1 by analysis of 2B4 expression in recombinant inbred mouse strains.

Amino Acid Sequence↗
PubMed1993

Degenerate recognition of a dissimilar antigenic peptide by myelin basic protein-reactive T cells. Implications for thymic education and autoimmunity.

The key event in the induction of an immune response is the recognition by a T lymphocyte of an antigenic peptide bound to a MHC molecule. In the absence of structural coordinates of the TCR and class II MHC molecules, various models of T cell recognition have been proposed, with the emerging dogma that T cell recognition is exquisitely specific. We show here that T cell clones specific for the N-terminal fragment of myelin basic protein, acetylated Ac1-11, recognize a set of unrelated peptides in the context of the same I-Au molecule. Moreover, immunization with the peptide mimic is sufficiently cross-reactive with Ac1-9 to either induce the Ac1-9-reactive clones or to induce tolerance as well as protection against Ac1-9-induced EAE. This observed degeneracy in T cell recognition has important implications for thymic selection and induction of autoimmune disease states by "molecular mimicry."

Amino Acid Sequence↗
PubMed1993

Non-steroidal glucocorticoid-like substances: receptor binding and in vivo activity.

Compounds of general structure I, prepared by a Diels-Alder reaction with diene 3, are relatives of the known potent glucocorticoid II but possess a markedly modified C- and D-ring environment. Despite these structural changes, 4, 5, 9, 10, 12a, 13, and 14 bound to the glucocorticoid receptor with an affinity which approximated that of the reference standard, 6-alpha-methylprednisolone. Four of these compounds not only exhibited antiinflammatory activity in the alpha-tocopherol pouch test but also exhibited marked adrenal suppression and other typical glucocorticoid properties at doses in the same range as the effective antiinflammatory doses.

Animals↗
PubMed1993

Characterization of the promoter region of the membrane cofactor protein (CD46) gene of the human complement system and comparison to a membrane cofactor protein-like genetic element.

Membrane cofactor protein (MCP; CD46) is a widely expressed C regulatory protein that inhibits C activation on self-tissue. MCP binds C3b and C4b deposited on autologous cells and then serves as a cofactor for their inactivation by limited proteolytic cleavage. To characterize the DNA sequence elements responsible for controlling MCP expression, the 5' flanking region of the human MCP gene was cloned. Sequencing of 1350 nucleotides upstream from the ATG codon revealed a GC-rich region in the initial 500 nucleotides that is especially rich in the CpG dinucleotide. A CAAT box in reverse orientation, surrounded by four putative SP1 binding sites but lacking a typical TATA element, was within the first 200 nucleotides of this GC-rich region. The major transcriptional initiation site for HeLa cells, determined by primer extension and S1 nuclease protection analyses, was located 105 nucleotides from the translational start site. This overall orientation of the promoter region is characteristic of "housekeeping" genes. The MCP promoter region was further examined in HEp-2 cells by the chloramphenicol acetyltransferase (CAT) reporter gene assay, using various constructs derived from the 5' region of the MCP gene. The MCP promoter activity was confined to the GC-rich region from -624 to +96 (start site of transcription being +1). Inclusion of an AT-rich sequence from -624 to -1204 resulted in a 42% reduction in CAT activity suggesting that an inhibitor is present among the AT-rich sequences. The 5' flanking region of a highly homologous partial duplication of the MCP gene was also cloned and sequenced, and various constructs were assessed in the CAT reporter system. Many of the functionally relevant sequences seen in MCP are also found in the MCP-like 5' UT region, which is 85% homologous to MCP. The most striking difference was a 224 nucleotide deletion that was upstream from the corresponding MCP region harboring most of the promoter activity. Although expression of an MCP-like protein has not been reported, the MCP-like promoter region produced promoter activity comparable with that of MCP. These results serve as a basis for subsequent analyses of the expression of MCP in various cells and tissues and for understanding the mechanism of its modulation in inflammatory conditions. Also, through a comparison of the 5' region of MCP with other genes in the regulators of C activation gene cluster (at 1 q32), we propose a model for the evolution of the promoters in this tight linkage group.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigens, CD↗
PubMed1993

The involvement of T cell receptor peptide-specific regulatory CD4+ T cells in recovery from antigen-induced autoimmune disease.

Experimental allergic encephalomyelitis (EAE) is a prototype for CD4+ T cell-mediated autoimmune diseases. Immunization with myelin basic protein (MBP) in B10.PL mice results in EAE, and a majority of animals recover permanently from the disease. Most MBP-reactive encephalitogenic T cells recognize an immunodominant NH2-terminal peptide, Ac1-9, and predominantly use the T cell receptor (TCR) V beta 8.2 gene segment. Here we report that in mice recovering from MBP-induced EAE, peripheral T cells proliferate in response to a single immunodominant TCR peptide from the V beta 8.2 chain (amino acids 76-101), indicating natural priming during the course of the disease. Cloned T cells, specific for this TCR peptide, specifically downregulate proliferative responses to Ac1-9 in vivo and also protect mice from MBP-induced EAE. These regulatory T cells express CD4 molecules and recognize a dominant peptide from the TCR variable framework region of V beta 8.2, in the context of the major histocompatibility complex class II molecule, I-Au, and predominantly use the TCR V beta 14 gene segment. This is the first demonstration of the physiological induction of TCR peptide-specific CD4+ T cells that result from MBP immunization and that are revealed only during the recovery from disease. The downregulation of disease-causing T cells by TCR peptide-specific T cells offers a mechanism for antigen-specific, network-induced recovery from autoimmune disease.

Amino Acid Sequence↗
PubMed1993

Use of newborn liver cells as a murine model for cord blood cell transplantation.

There is current interest in using umbilical cord blood cells as a substitute for bone marrow cells (BMC) in human transplantation. However, T cell-depleted BMC are more susceptible to rejection. Because CBC lack mature T cells, mouse newborn liver cells (NLC) were used as a model to investigate the role of T cells in engraftment. BALB/c BMC, C.B-17 scid/scid (SCID) BMC, and BALB/c NLC were transplanted into lethally irradiated BALB/c and (B6 x DBA/2) F1 (B6D2F1) hosts. Splenic 125IUdR incorporation 5 days later assessed engraftment. BALB/c BMC, NLC, and SCID BMC grew well in BALB/c hosts, but only BALB/c BMC grew in B6D2F1 hosts. This suggests that T cells are necessary for engraftment of H-2d stem cells in the B6D2F1 host. Addition of BALB/c thymocytes to SCID BMC or NLC allowed engraftment in the F1 hosts. It appears that NK cells mediated the resistance because their depletion by mAb increased engraftment of SCID BMC or NLC. Anti-NK1.1 mAb and -asialo GM1 serum eliminate all NK cells, although anti-5E6 mAb eliminate a subpopulation of NK cells that responds to Hh-1d (determinant 2+) stem cells. Treatment of F1 hosts with any of these mAb prevented rejection of SCID BMC or BALB/c NLC. Also, activation of NK cells by poly I:C caused rejection of donor cells in the F1 that could not be overcome by the presence of thymocytes. This effect of the poly I:C could also be reversed by mAb depletion of host NK cells. Thus, engraftment of stem cells is influenced by the presence of donor T cells and the activation level of host NK cells.

Animals↗
PubMed1993

A detailed genetic map for the X chromosome of the malaria vector, Anopheles gambiae.

Anopheles gambiae, the primary vector of human malaria in Africa, is responsible for approximately a million deaths per year, mostly of children. Despite its significance in disease transmission, this mosquito has not been studied extensively by genetic or molecular techniques. To facilitate studies on this vector, a genetic map has been developed that covers the X chromosome at an average resolution of 2 centimorgans. This map has been integrated with the chromosome banding pattern and used to localize a recessive, sex-linked mutation (white eye) to within 1 centimorgan of flanking markers.

Alleles↗
PubMed1993

A novel function-associated molecule related to non-MHC-restricted cytotoxicity mediated by activated natural killer cells and T cells.

NK cells and IL-2-propagated splenic T cells mediate non-MHC-restricted cytotoxicity. The molecules involved in this process are not well defined. We describe a novel 66-kDa cell surface molecule called 2B4 that is expressed on cells that mediate non-MHC-restricted cytotoxicity. All resting and rIL-2 cultured NK cells and a significant number of T cells cultured in high doses of rIL-2 are 2B4+. In fresh as well as cultured spleen cells, all non-MHC-restricted cytotoxicity is contained within the 2B4+ population. In addition to defining cells capable of non-MHC-restricted killing, the 2B4 molecule is also involved in modulation of their function. In the presence of anti-2B4, the lytic activity of cultured NK cells and non-MHC-restricted T cells against a wide variety of FcR- and FcR+ targets is greatly augmented. Anti-2B4 is also able to transduce other signals in IL-2-activated NK cells such as IFN-gamma secretion and granule exocytosis. In addition, 2B4+ T cells can specifically lyse the 2B4 hybridoma cells. Unlike many other activation and adhesion molecules (such as murine CD2, LFA-1, and CD16), 2B4 expression is restricted to cells that mediate NK-like killing. Conversely, highly activated T cells that do not express 2B4 do not mediate non-MHC-restricted killing. Together these data suggest that the 2B4 molecule is likely to be a part of a receptor complex or a component of signal-transducing complex on cells that mediate non-MHC-restricted killing.

Animals↗
PubMed1993

Mapping of neutralizing epitopes and the receptor binding site of human interleukin 1 beta.

Antibodies to synthetic peptides of human interleukin 1 beta (IL-1 beta) and to recombinant human IL-1 beta were used to identify epitopes of IL-1 beta associated with the neutralization of its biological activity. Analysis of antisera raised to 17 synthetic peptides derived from the mature IL-1 beta sequence showed that five regions (residues 6-15, 49-80, 58-80, 92-101, and 120-133) were both immunoprecipitating and neutralizing. Using a hexamer epitope mapping method, comparison of the regions recognized by four neutralizing rabbit antisera with those recognized by a rabbit antiserum raised to denatured IL-1 beta suggested two further neutralizing epitopes, residues 39-48 and 83-95. Finally, a neutralizing monoclonal antibody was shown to bind to the peptides 6-11 and 87-95 by peptide binding and mutagenesis. All of these regions appear predominantly on one face of IL-1 beta. The effect of mutations in residues 4-11 and 88-97, which lie within this face, on receptor binding and biological activity was determined. Most of the mutations tested affected both receptor binding and activity, whereas mutations in another face of IL-1 beta (residues 74-80) had no effect. Purification of two of the mutants with reduced bioactivity and receptor binding and analysis by two-dimensional NMR indicated no gross changes in tertiary structure. A third mutant had reduced bioactivity in two different bioassays but no change in receptor binding. Although two-dimensional NMR revealed no gross changes in conformation, small changes did occur at a site distal from that mutated. The data are consistent with other epitope mapping and receptor binding mutagenesis data and suggest that the neutralizing antibodies and receptor recognize different but overlapping regions of IL-1 beta.

Amino Acid Sequence↗