Hypertension is a major public health problem in the developing as well as in developed countries due to its high prevalence and its association with coronary heart disease, renal disease, stroke, peripheral vascular disease, and related disorders. Essential hypertension (EH) is the most common diagnosis in this disease, suggesting that a monocausal etiology has not been identified. However, a number of risk factors associated with EH have also been identified such as age, sex, demographic, environmental, genetic, and vascular factors. Recent advances in molecular biological research had achieved clarifying the molecular basis of Mendelian hypertensive disorders. Molecular genetic studies have now identified mutations in several genes that cause Mendelian forms of hypertension in humans. However, none of the single genetic variants has emerged from linkage or association analyses as consistently related to the blood pressure level in every sample and in all populations. Besides, a number of polymorphisms in candidate genes have been associated with differences in blood pressure. The most prominent candidate has been the polymorphisms in the renin-angiotensin-aldosterone system. In total, EH is likely to be a polygenic disorder that results from inheritance of a number of susceptibility genes and involves multiple environmental determinants. These determinants complicate the study of blood pressure variations in the general population. The complex nature of the hypertension phenotype makes large-scale studies indispensable, when screening of familial and genetic factors was intended. In this review, recent genetic studies exploring the molecular basis of EH, including different molecular pathways, are highlighted.

Selected isolates of Pseudomonas fluorescens (Pf1-94, Pf4-92, Pf12-94, Pf151-94 and Pf179-94) and chemical resistance inducers (salicylic acid, acetylsalicylic acid, DL-norvaline, indole-3-carbinol and lichenan) were examined for growth promotion and induced systemic resistance against Fusarium wilt of chickpea. A marked increase in shoot and root length was observed in P. fluorescens treated plants. The isolates of P. fluorescens systemically induced resistance against Fusarium wilt of chickpea caused by Fusarium. oxysporum f.sp. ciceri (FocRs1), and significantly (P = 0.05) reduced the wilt disease by 26-50% as compared to control. Varied degree of protection against Fusarium wilt was recorded with chemical inducers. The reduction in disease was more pronounced when chemical inducers were applied with P. fluorescens. Among chemical inducers, SA showed the highest protection of chickpea seedlings against wilting. Fifty two- to 64% reduction of wilting was observed in soil treated with isolate Pf4-92 along with chemical inducers. A significant (P = 0.05; r = -0.946) negative correlation was observed in concentration of salicylic acid and mycelial growth of FocRs1 and at a concentration of 2000 microg ml(-1) mycelial growth was completely arrested. Exogenously supplied SA also stimulated systemic resistance against wilt and reduced the disease severity by 23% and 43% in the plants treated with 40 and 80 microg ml(-1) of SA through root application. All the isolates of P. fluorescens produced SA in synthetic medium and in root tissues. HPLC analysis indicated that Pf4-92 produced comparatively more SA than the other isolates. 1700 to 2000 nanog SA g(-1) fresh root was detected from the application site of root after one day of bacterization whereas, the amount of SA at distant site ranged between 400-500 nanog. After three days of bacterization the SA level decreased and was found more or less equal at both the detection sites.

Fragile x syndrome (FXS) is the most common form of inherited mental retardation disease. This is caused due to expansion of CGG triplet in 5'-untranslated region of fragile x mental retardation 1 (FMR-1) gene. In most of the cases, abnormally large size of the CGG repeat (>200) undergoes hypermethylation, which in turn silences the FMR-1 gene causing thereby complete lack of its protein product called fragile x mental retardation protein (FMRP). Lack of FMRP due to gene silencing or production of faulty protein due to point mutation in KH2 domain of FMRP alters the translational process in neurons and leads to expression of mental retardation phenotype on the patients. The FMRP is expressed ubiquitously in all tissues; however, it is predominantly expressed in neurons and testis. It possesses heterogeneity and is found in many isoforms due to alternative splicing of the FMR-1 transcript. Based on our data from the Western-, slot-, Northern blotting and immunohistochemical studies, we report here the down regulation of Fmr-1 gene and FMRP in mice brain in age-dependent manner. The present finding is important in respect to FMRP-dependent various brain functions i.e., learning, memory, cognition etc. that decrease with advancing age.

Fragile X syndrome is caused by silencing of FMR-1 gene due to unusual expansion of CGG repeats (>200 repeats) and their hypermethylation in 5'-UTR. As a consequence, the expression of the RNA binding protein FMRP is stopped. Absence of this protein leads to several morphological and neurological symptoms. The symptoms of the syndrome in males are different than that in the females. We have previously reported that the Fmr1 gene is down regulated in males as a function of age. In the present communication, we have investigated expression of Fmr-1 mRNA, FMRP and analysis of interaction of trans-acting factors with E- and GC boxes in Fmr-1 promoter in female mouse brain as a function of age. Our Northern and Western blots data reveal that the level of Fmr-1 transcript decreases in adult as compared to young mouse but significantly increases in old age and that of FMRP decreases in brain of female old mouse as compared to young and adult age. The immunohistochemical analysis supported the results obtained from Western blot studies. Our EMSA data reveal that the intensity of USF1/USF2-E Box complex gradually increases during aging having significantly highest intensity in old age mouse whereas the intensity of alpha-Pal/Nrf1- GC-Box complex gradually decreases as a function of age. The increased intensity of the complex in old age mouse is correlated to higher level of Fmr-1 transcript in old age. The elevated level of Fmr-1 transcript in old mouse brain may be attributed to USF1/USF2 dependent increased transcription of Fmr-1 gene in old age and decrease in FMRP to altered translation of the transcript or high turn over of FMRP during aging. The present finding indicates age and sex as factors affecting the expression of Fmr-1 gene in mouse brain.

Glycine max-Rhizobium interaction is a well known symbiotic association occurring in nature and responsible for biological nitrogen fixation. Thiram a well-known fungicide has been in practice as seed dressing in order to prevent fungal colonization. In the present study the effect of various thiram concentrations is investigated. Thiram concentration beyond 500 g/ml was observed to be highly toxic with respect to plant growth factors and rhizobial infection to the G. max. The nodulation, nodule dry weight, nitrogenase activity were observed to be maximum at 100 g/ml of thiram. The study is useful in determining the threshold concentration of fungicide for soybean seed dressing for effective nitrogen fixation and crop yield.