Search PubMed⌕ Search

Biomedical subjects

H Singh

Publications and source records attributed to H Singh.

At least 199 records · Page 11Linked to original sources
PubMed1995

A controlled study of the effect of balanced general anaesthesia on cognitive functions in hypertensives on propranolol.

The aim of this study was to observe the effect of general anaesthesia (GA) on multiple dimensions of cognitive functioning in hypertensives on propranolol therapy (group A) in comparison to a control group (group B). Ten subjects in each group were administered a battery of six psychological cognitive tests pre- and post-intervention under GA. Both groups showed a significant decrement in memory scores on the 4th postoperative day which showed signs of recovery on seventh day (P < 0.05 for both groups). The group A patients were further compromised in one of the intelligence test scores (Standard progressive matrices) from the beginning (P < 0.05). Although this intergroup deficit persisted even on the 7th postoperative day (P < 0.05), no added effects of GA on this parameter was observed in group A (P > 0.05). In conclusion, GA induced transient memory deficit in both groups. This should be kept in mind while considering 'street fitness' following general anaesthesia.

Adult↗
PubMed1995

Polymorphic protein expression (profile) in numigall.

Ten protein and enzyme polymorphic systems, viz. haemoglobin, albumin, transferrin, adenosine deaminase, adenylate kinase phosphoglucomutase, esterase-D, glyoxalase, alkaline phosphatase and amylase were studied in numigall (guinea fowl x chicken hybrids) to assess structural gene expression and regulatory gene divergence between the parental species. The investigation revealed presence of both the maternal and paternal electrophoretic components in case of adenosine deaminase, alkaline phosphatase, amylase, albumin and transferrin although no clear differences could be identified for haemoglobin and glyoxalase. Esterase-D and adenylate kinase phenotypes showed a dominance of the chicken type.

Animals↗
PubMed1994

Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages.

The transcription factor PU.1 is a hematopoietic-specific member of the ets family. Mice carrying a mutation in the PU.1 locus were generated by gene targeting. Homozygous mutant embryos died at a late gestational stage. Mutant embryos produced normal numbers of megakaryocytes and erythroid progenitors, but some showed an impairment of erythroblast maturation. An invariant consequence of the mutation was a multilineage defect in the generation of progenitors for B and T lymphocytes, monocytes, and granulocytes. Thus, the developmental programs of lymphoid and myeloid lineages require a common genetic function likely acting at the level of a multipotential progenitor.

Animals↗
PubMed1994

RNA trans-splicing in Fasciola hepatica. Identification of a spliced leader (SL) RNA and SL sequences on mRNAs.

We have identified a new spliced leader (SL) in Fasciola hepatica by characterizing the 5'-terminal sequences of its enolase mRNA, an mRNA also trans-spliced in the flatworm Schistosoma mansoni (Rajkovic, A., Davis, R.E., Simonsen, J.N., and Rottman, F.M. (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 8879-8883). This 37-nucleotide spliced leader is at the 5' ends of multiple Fasciola mRNAs and is likely to be derived from the 5' terminus of a nonpolyadenylated, 108-nucleotide RNA with a trimethylguanosine cap. The SL RNA gene is present in approximately 100 copies within a 1.1-kilobase genomic tandem repeat. Secondary structure predictions indicate that the Fasciola SL RNA contains three stem loops in contrast to two previously observed in S. mansoni. Fasciola and S. mansoni SLs are likely to be evolutionarily related although their sequence identity is only 65%. In contrast with nematodes, absolute conservation of SL sequences and secondary structure does not occur in trematodes. A spliced leader in Fasciola indicates that trans-splicing is likely to be a common feature in other trematodes and perhaps other flatworms.

Amino Acid Sequence↗
PubMed1994

In vitro and in vivo genotoxicity evaluation of hormonal drugs. II. Dexamethasone.

Genotoxicity evaluation of a widely used glucocorticoid medicine, dexamethasone, was undertaken using in vitro and in vivo assays. Analyses of chromosomal aberrations, sister-chromatid exchanges (SCEs) in human lymphocytes and micronuclei and SCEs in mouse bone marrow showed the drug to be capable of attacking the genetic material. However, the Ames/Salmonella assay, both with and without S9 mix, did not show any increase in His+ revertants.

Animals↗
PubMed1994

Peroxisomal beta-oxidation of branched chain fatty acids in rat liver. Evidence that carnitine palmitoyltransferase I prevents transport of branched chain fatty acids into mitochondria.

Fatty acid beta-oxidation was investigated in highly purified mitochondrial and peroxisomal preparations from rat liver. Under isotonic conditions, pristanic and homophytanic acid beta-oxidation in purified peroxisomes was severalfold greater compared to the oxidation in purified mitochondria. Branched chain fatty acid beta-oxidation in purified mitochondria was very low, and the oxidation was not stimulated by exogenous L-carnitine or L-malate. In contrast, stearic acid beta-oxidation by purified mitochondria depended upon exogenous L-carnitine, and the oxidation was stimulated by L-malate. Both mitochondrial and peroxisomal beta-oxidation of branched chain fatty acids was strongly inhibited by fatty acid-free bovine serum albumin, whereas stearic acid oxidation was either unaffected or slightly inhibited by bovine serum albumin. The results presented clearly indicate that branched chain fatty acids are mainly degraded in peroxisomes in rat liver. Branched chain fatty acids were efficiently converted to coenzyme A thioesters by purified mitochondria, peroxisomes, and microsomes. Although pristanic and phytanic acids were rapidly converted to pristanoyl-CoA and phytanoyl-CoA, respectively, they were not converted to carnitine esters by mitochondrial outer membranes. The results indicate that acyl-CoA synthetase and carnitine acyltransferase located at the mitochondrial outer membranes regulate entry of branched chain fatty acids into mitochondria. Mitochondrial carnitine acyltransferase I appears to be highly specific for straight chain fatty acids and restricts entry of branched chain fatty acids into mitochondria. Thus, branched chain fatty acids which cannot be transported across the mitochondrial membranes via the carnitine acyltransferase system are directed to peroxisomes for beta-oxidation. The results reported indicate that phytanic acid, the fatty acid which can be initially degraded by alpha-oxidation due to the presence of a beta-methyl group in the molecule, cannot be transported across the mitochondrial membranes. The data presented strongly suggest that phytanic acid alpha-oxidation occurs in organelles other than mitochondria and possibly in peroxisomes.

Acyl Coenzyme A↗
PubMed1994

The v-abl tyrosine kinase negatively regulates NF-kappa B/Rel factors and blocks kappa gene transcription in pre-B lymphocytes.

Transformation of B-lineage precursors by the Abelson murine leukemia virus appears to arrest development at the pre-B stage. Abelson-transformed pre-B cell lines generally retain transcriptionally inactive, unrearranged immunoglobulin kappa alleles. We demonstrate that nontransformed pre-B cells expanded from the mouse bone marrow efficiently transcribe unrearranged kappa alleles. In addition, they contain activated complexes of the NF-kappa B/Rel transcription factor family, in contrast with their Abelson-transformed counterparts. Using conditionally transformed pre-B cell lines, we show that the v-abl viral transforming protein, a tyrosine kinase, blocks germ-line kappa gene transcription and negatively regulates NF-kappa B/Rel activity. An active v-abl kinase specifically inhibits the NF-kappa B/Rel-dependent kappa intron enhancer, which is implicated in promoting both transcription and rearrangement of the kappa locus. v-abl inhibits the activated state of NF-kappa B/Rel complexes in a pre-B cell via a post-translational mechanism that results in increased stability of the inhibitory subunit I kappa B alpha. This analysis suggests a molecular pathway by which v-abl inhibits kappa locus transcription and rearrangement.

Animals↗
PubMed1994

Effect of Calphostin C (PKC inhibitor) on daunorubicin resistance in P388/ADR and HL60/AR cells: reversal of drug resistance possibly via P-glycoprotein.

Calphostin C is a potent and specific inhibitor of protein kinase C (PKC). In this investigation we examined the effect of Calphostin C (without prior exposure to light) on daunorubicin (DNR) accumulation and sensitivity to DNR in multidrug-resistant (MDR) murine leukemia P388/ADR and human myeloid leukemia HL60/AR cells. P388/ADR cells overexpress P-glycoprotein, whereas HL60/AR cells lack any expression of P-glycoprotein (both at mRNA and protein levels). Calphostin C, in a concentration-dependent manner, increased the accumulation of DNR in P388/ADR cells and partially reversed (threefold) the DNR resistance in P388/ADR cells but had no effect on either of the parameters in HL60/AR cells. Calphostin C-induced increased accumulation of DNR in P388/ADR cells was due to increased uptake and decreased efflux of DNR. Furthermore, Calphostin C increased the uptake and decreased the efflux of rhodamine 123 (a substrate for P-gp) in P388/ADR cells but had no such effect in P388 cells. In addition, Calphostin C without exposure to light did not inhibit PKC activity in any of the cell lines studied. Taken together, these data suggest that Calphostin C may reverse drug resistance via P-glycoprotein independently of its effect on PKC activity. Therefore, any data regarding the effect of Calphostin C on the reversal of MDR should be interpreted in the light of these findings.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Histochemical/histoenzymic studies in broiler chicks fed aflatoxin, ochratoxin and inoculated with inclusion body hepatitis virus singly and in concurrence.

The effect of feeding mycotoxins, i.e. aflatoxin B1 (1.25 ppm from 3 to 38 days of age) and ochratoxin A (0.5 ppm from 3 to 38 days of age) along with inclusion body hepatitis virus (IBHV) inoculation (at 10 days of age) singly and in combination was studied in broiler chicks. Birds in combined treatment groups, i.e. aflatoxin fed and virus inoculated and ochratoxin fed and virus inoculated, showed more changes in activities of phosphatases (AKPase, ATPase, G-6-Pase and ACPase) in liver and kidney tissues than their respective individual treatment groups with a few exceptions. Reduction in the activities of oxido-reductases in liver and kidney tissues were almost comparable in different treatment groups. The increase in muco-polysaccharides reaction was more marked in both the combined treatment groups than the single treatment groups. Intensity of lipid reaction was more in ochratoxin virus combination group than either alone.

Acid Phosphatase↗
PubMed1994

Genetic analysis of transcription factors implicated in B lymphocyte development.

The transcription factors Oct-2, NF-kappa B and PU.1 have been implicated in regulating the development of B lymphocytes. Genetic approaches have been used to analyze the developmental functions of these regulatory proteins. Using gene targeting in murine embryonic stem cells, PU.1 is shown to be required for the development of progenitor B cells. Strikingly, PU.1 is also essential for the development of T lymphoid, granulocytic and monocytic progenitors. Transcription factors of the NF-kappa B/Rel family, which appear to regulate immunoglobulin kappa gene expression, are shown to be a target of the viral transforming protein (v-abl) which arrests B lineage development at the precursor B stage. This suggests a mechanism by which v-abl blocks precursor B cell differentiation. The Oct-2 transcription factor was considered to represent a development regulator of immunoglobulin gene expression. Using gene targeting in a murine B cell, Oct-2 is shown to be dispensable for immunoglobulin gene expression. This suggests the existence of an alternate pathway, involving the ubiquitous related protein, Oct-1, in immunoglobulin gene regulation.

Animals↗
PubMed1994

In vitro and in vivo genotoxicity evaluation of hormonal drugs v. mestranol.

Genotoxicity of a widely used estrogen, Mestranol, was undertaken using in vitro, in vivo and host-mediated assay with bacteria as indicator organism. Analyses of chromosome aberrations and sister chromatid exchanges (SCEs) in human lymphocytes and chromosome aberrations, micronuclei and sister chromatid exchanges (SCEs) in bone-marrow cells of mice showed the drug to be capable of attacking the genetic material. However, both Ames Salmonella/S9 assay with and without S9 mix and host-mediated assay using same tester strains of Salmonella, did not show any significant increase/decrease in the His+ revertants.

Animals↗
PubMed1994

Bacteriophage typing in Salmonella bareilly.

A total of 675 strains of Salmonella bareilly received from different parts of India and France during 1959-92 were phage typed using six bacteriophages. Overall typability achieved was 90.8% with 23 distinct phage types excluding a group of untypable strains. Phage types have been defined in octal code. Simpson's coefficient was applied for diversity index having a value of 0.839. This system was found to be reproducible, stable and epidemiologically useful.

Animals↗
PubMed1994

Angiotensin II-dependent proximal tubule sodium transport is mediated by cAMP modulation of phospholipase C.

Angiotensin II (ANG II) stimulates proximal tubule sodium transport by decreasing adenylyl cyclase activity. The role of ANG II-dependent phospholipase C is less certain. To determine the contribution of phospholipase C and adenylyl cyclase to apical (AP) ANG II-dependent sodium transport, unidirectional (AP to basolateral) 22Na flux was measured in rat proximal tubule cells cultured on permeable supports. AP ANG II (100 nM)-dependent sodium flux was prevented by preincubation with concentrations of the phospholipase C inhibitor U-73122 (1 microM) that blocked ANG II-dependent inositol phosphate formation. AP ANG II-dependent sodium flux was also abolished by preincubation with the intracellular calcium mobilization inhibitor 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), further suggesting that ANG II-dependent sodium transport was mediated by inositol phosphates. Neither U-73122 nor TMB-8 prevented ANG II-dependent adenosine 3',5'-cyclic monophosphate (cAMP) decreases. Incubation with dibutyryl cAMP (10 microM) or forskolin (10 microM) prevented ANG II-dependent sodium flux as well as ANG II-dependent inositol phosphate formation. In conclusion, ANG II-dependent proximal tubule sodium transport in cultured cells was transduced by phospholipase C and adenylyl cyclase. The adenylyl cyclase effect on ANG II-dependent sodium transport was mediated by phospholipase C.

Adenylyl Cyclases↗