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Biomedical subjects

R S Chauhan

Publications and source records attributed to R S Chauhan.

At least 19 recordsLinked to original sources
PubMed2002

Genetic and physical mapping of a rice blast resistance locus, Pi-CO39(t), that corresponds to the avirulence gene AVR1-CO39 of Magnaporthe grisea.

We have identified, genetically mapped and physically delineated the chromosomal location of a new rice blast resistance locus, designated Pi-CO39(t). This locus confers resistance to Magnaporthe grisea isolates carrying the AVR1-CO39 avirulence locus. The AVR1-CO39 locus is conserved in non-rice (cereals and grasses)-infecting isolates of M. grisea, making Pi-CO39(t) useful for engineering M. grisea resistance in rice and other cereals. The resistance in the rice line CO39 was inherited as a single dominant locus in segregating populations derived from F(2) and F(3) crosses between disease-resistant (CO39) and susceptible (51583) rice genotypes. Microsatellite, RFLP and resistance gene analog (RGA) markers were used to map the Pi-CO39(t) locus to a 1.2-cM interval between the probenazole-responsive ( RPR1) gene (0.2 cM) and RFLP marker S2712 (1.0 cM) on the short arm of rice chromosome 11. RFLP markers G320 and F5003, and resistance gene analogs RGA8, RGA38 and RGACO39 were tightly linked to the Pi-CO39(t) locus (no recombination detected in a sample of ~2400 gametes). A large-insert genomic library of CO39 was constructed in the binary plant transformation vector pCLD04541. A library screen using RGA8, RGA38 and probes derived from the ends of CO39 clones, as well as BAC end probes from the corresponding locus in the rice cv. Nipponbare, resulted in the assembly of three CO39 contigs of 180 kb, 110 kb and 145 kb linked to the Pi-CO39(t) locus. A 650-kb contig was also constructed representing the susceptible locus, pi-CO39(t), in the Nipponbare genome. The two genomes are highly divergent with respect to additions, deletions and translocations at the Pi-CO39(t) locus, as revealed by the presence or absence of mapping markers.

Blotting, Southern↗
PubMed2002

Meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA effect on gallium arsenide induced pathological liver injury in rats.

The effect of meso 2,3-dimercaptosuccinic acid (DMSA) and monoisoamyl DMSA (MiADMSA) on gallium arsenide (GaAs) induced liver damage was studied. The oral feeding rat model was used in this study. The animals were exposed to 10 mg/kg GaAs, orally, once daily, 5 days a week for 24 weeks and treated thereafter with single oral daily dose of either 0.3 mmol/kg DMSA or MiADMSA for two course of 5 days treatment. The animals were sacrificed thereafter. Lipid peroxidation was assessed by measuring liver thiobarbituric acid reactive substance (TBARS). Liver damage was assessed by number of biochemical variables and by light microscopy. The activity of superoxide dismutase (SOD) and delta-aminolevulinic acid dehydratase (ALAD) beside reduced glutathione (GSH) concentration was measured in blood. Exposure to GaAs produced a significant reduction in GSH while, increased the oxidized glutathione (GSSG) concentration. Hepatic glutathione peroxidase (GPx) and catalase activity increased significantly while level of serum transaminase increased moderately. Gallium arsenide exposure also produced marked hepatic histopathological lesions. Overall, treatment with MiADMSA proved to be better than DMSA in the mobilization of arsenic and in the turnover of some of the above mentioned GaAs sensitive biochemical alterations. Histopathological lesions also, responded more favorably to chelation treatment with MiADMSA than DMSA.

Alanine Transaminase↗
PubMed1992

Cell-mediated immune response in rotavirus-infected calves: leucocyte migration inhibition assay.

The cell-mediated immune (CMI) response was determined in rotavirus-infected calves by leucocyte migration inhibition assay with blood, spleen, mesenteric lymph node and intestinal lymphocytes. The inhibition of migration was more prominent in intestinal and mesenteric lymph node lymphocytes than in spleen and blood. In rotavirus-infected calves, the assay indicated the presence of CMI response which was more prominent at the local site of infection.

Animals↗
PubMed1991

Isolation of enterotoxigenic Escherichia coli from camels with diarrhoea.

E. coli serogroups 02, 08, 083, 0103 and 0120 were isolated from seven camels with diarrhoea of which 02, 08, and 083 were found to be enterotoxigenic on rabbit ligated ileal loop test. Out of 125 apparently healthy camels, 75 strains of E. coli were isolated. The majority of isolates were susceptible to gentamycin, nitrofurantoin, trimethoprim plus sulphonamide, neomycin, kanamycin and chloramphenicol.

Animals↗
PubMed1989

Separation of some antihistamines on impregnated TLC silica plates.

Different metal salts have been tried as impregnating reagents for developing TLC separation schemes for some antihistamines on silica gel 'G' plates, using a new solvent system benzene + dimethyl formamide + acetic acid (30:10:7). Spots were visualized by spraying with a solution of Dragendroff's reagent.

Chromatography, Thin Layer↗
PubMed1989

Comparison of the dot-immunobinding assay with the complement fixation test for the detection of Brucella antibodies in sheep.

A dot-immunobinding assay (DIA), using as antigen a sonic extract of Brucella abortus dotted on nitrocellulose bound to a plastic strip, was employed for the detection of Brucella antibodies in 666 sheep sera. The results were compared with the complement fixation test (CFT). All the 242 sera belonging to two flocks were found to be negative by DIA. CFT was negative in 239 cases, whereas three samples showed anti-complementary activity. Of the 424 sera from the remaining three flocks, 98 were positive by both tests and six were positive in DIA, but negative in CFT. In addition, 14 of the 19 anti-complementary sera were also positive by DIA.

Animals↗
PubMedDate not supplied

Structural changes induced by sulphur mustard in rabbit skin.

Sulphur mustard (SM) is a bifunctional alkylating agent which can react with a wide variety of molecules of biological interest. The interaction of SM with animal skin elicits a varied histopathological response in cellular components on a temporal scale. The extracellular matrix (ECM) undergoes tremendous structural changes as a result of SM exposure. Sulphur mustard induces oedema, infiltration of polymorphonuclear cells and destruction of cells. Injury appeared to be most severe on the third day after exposure, when the thickness of the skin registered the maximum change from the control. The initiation of recovery could be noticed on the 6th day, when the intercellular gap in the ECM began to reduce significantly, indicating reformation of damaged skin. Simultaneous reformation was also noticed in the epidermis and other cellular components. However, recovery was far from complete and continued beyond the 6th day.

Animals↗
PubMedDate not supplied

Effect of topically applied sulphur mustard on guinea pig liver.

The study revealed that topically applied sulphur mustard, which is a potent blistering agent with mutagenic and carcinogenic properties, is also hepatotoxic. It produces severe steatosis and other pathological alterations, accompanied by biochemical changes. There is a significant rise in the levels of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvate transaminase (GPT) after exposure. The liver injury appeared to peak on the third day. Recovery at the ultrastructural level could be noticed on the sixth day but was far from complete because the gross pathological changes were still severe.

Administration, Topical↗