Fusarium wilt (FW) and Ascochyta blight (AB) are two major constraints to chickpea (Cicer arietinum L.) production. Therefore, two parallel marker-assisted backcrossing (MABC) programs by targeting foc1 locus and two quantitative trait loci (QTL) regions, ABQTL-I and ABQTL-II, were undertaken to introgress resistance to FW and AB, respectively, in C 214, an elite cultivar of chickpea. In the case of FW, foreground selection (FGS) was conducted with six markers (TR19, TA194, TAA60, GA16, TA110, and TS82) linked to foc1 in the cross C 214 × WR 315 (FWresistant). On the other hand, eight markers (TA194, TR58, TS82, GA16, SCY17, TA130, TA2, and GAA47) linked with ABQTL-I and ABQTL-II were used in the case of AB by deploying C 214 × ILC 3279 (AB-resistant) cross. Background selection (BGS) in both crosses was employed with evenly distributed 40 (C 214 × WR 315) to 43 (C 214 × ILC 3279) SSR markers in the chickpea genome to select plant(s) with higher recurrent parent genome (RPG) recovery. By using three backcrosses and three rounds of selfing, 22 BC 3 F 4 lines were generated for C 214 × WR 315 cross and 14 MABC lines for C 214 × ILC 3279 cross. Phenotyping of these lines has identified three resistant lines (with 92.7-95.2% RPG) to race 1 of FW, and seven resistant lines to AB that may be tested for yield and other agronomic traits under multilocation trials for possible release and cultivation.

Our findings suggest that the polymorphic variants of AGT gene-M235T and T174M-show association with hypertension.

Systemic PFOA was at least as or more efficacious than ASA or dexamethasone in reducing carrageenan-induced edema. RU-486 did not change the anti-edema effect of PFOA, ruling out a contribution of endogenous release of glucorticoids. I. c. v. PFOA, but not perfluorooctanes, dramatically reduced multiple signs of inflammation at doses well below the systemically-effective dose. We conclude that the anti-edema effect of high systemic doses of PFOA (> or =100 mg/kg, i. p.) is mediated in part by actions in the brain.

The present study revealed a strong synergistic effect of CYP11B2 C-344T and IC polymorphisms causing susceptibility to EHT and haplotype H1 (-344T-Conv-Lys173) as the risk-conferring factor for hypertension predisposition.

Background: Renin is a rate-limiting enzyme of the renin-angiotensin-aldosterone system (RAAS) that plays a crucial role in the regulation of blood pressure. The renin gene has been suggested as a marker for genetic predisposition to essential hypertension (EHT) in humans. The purpose of the study is to explore the association of a genetic marker of renin gene Mbo I polymorphism with EHT in the South Indian population. Methods: A total of 279 hypertensive and 200 normotensive subjects were genotyped for REN Mbo I polymorphism (RFLP) using the PCR-restriction fragment length polymorphism method.Results: There were no significant differences in the distribution of genotypes and alleles for REN gene Mbo I polymorphism between hypertensive cases and controls (p>0.05). The genotypic and allele frequencies were in Hardy-Weinberg equilibrium both in cases and controls. Females with Mbo I AA+GA genotypes had 1.87-fold higher risk to develop hypertension as compared with those with GG genotype (odds ratio 1.87; 95% confidence interval = 0.98-3.56, p = 0.057). Conclusions: Our results indicate that renin gene Mbo I site polymorphism is not associated with blood pressure levels and risk of hypertension. However, the present study demonstrates risk for females who are carriers of REN Mbo I A allele for developing essential hypertension.