Periodontitis is a chronic inflammatory disease which is caused by destruction of the tissues that surrounds and supports the tooth. Deregulation of microRNAs has been reported to cause several inflammatory diseases such as autoimmune disease, chronic periodontitis, and cancer. In the present study, we have investigated the expression pattern of microRNAs let-7a, miR-125b, miR-100, miR-21, and RNA-binding protein LIN-28A among healthy individuals and chronic periodontitis patients. Total RNA was isolated from gingival tissue samples collected from 100 healthy individuals and 100 chronic periodontitis patients. The expression of microRNAs and LIN-28 was performed by qPCR. Target prediction for the microRNAs was done using miRWalk and miRTarbase online databases and the experimentally validated targets were analyzed for their molecular function, biological processes, and related pathways using gProfiler software. The expression analysis revealed that let-7a and miR-21 were upregulated, whereas, miR-100, miR-125b, and LIN-28 were down regulated. The age dependent expression analysis revealed that the expression levels of all the microRNAs and LIN-28 were found to increase with age (more than 50 years), thereby suggesting an increased risk to chronic periodontitis. Among the various targets predicted using miRWalk and miRTarbase databases, NFKB was found to be a common target among all the four microRNAs. gProfiler revealed several functions such as NF-ĸB signaling pathway, cytokine-cytokine receptor interaction, osteoclast differentiation, etc., all of which specific to inflammation and periodontitis.

In conclusion, the present study reveals lack of association of MTHFR C677T and ACE I/D polymorphisms in RPL in South Indian women. However, we cannot exclude the possibility that other polymorphisms of ACE and MTHFR genes could be associated with the disease and might be clinically useful as a marker to assess risk for RPL.

Oral carcinogenesis, a multistep process with multifaceted etiology, arises due to accumulation of heterogeneous genetic changes in the genes involved in the basic cellular functions including cell division, differentiation, and cell death. These genetic changes in the affected cell progressively increase the cell proliferation, angiogenesis, and inhibition of apoptosis. The present study investigated the modulating effect of geraniol on the expression pattern of cell proliferative (PCNA, cyclin D1, c-fos), inflammatory (NF-κB, COX-2), apoptotic (p53, Bax, Bcl-2, caspase-3 and -9), and angiogenic (VEGF) markers in 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch carcinogenesis. Topical application of 0.5 % DMBA in liquid paraffin, three times a week, for 14 weeks, developed well-differentiated squamous cell carcinoma (SCC) in the buccal pouch of golden Syrian hamsters. All the hamsters treated with DMBA alone (100 %) developed oral tumors in the buccal pouch after 14 weeks. Over-expression of mutant p53, PCNA, Bcl-2, and VEGF accompanied by decreased expression of Bax were noticed in hamsters treated with DMBA alone. Increased expression of c-fos, COX-2, NF-κB, and cyclin D1 and decreased activities of caspase-3 and -9 were also noticed in hamsters treated with DMBA alone. Oral administration of geraniol at a dose of 250 mg/kg bw (body weight) not only completely prevented the formation of oral tumors but also prevented the deregulation in the expression of above mentioned molecular markers in hamsters treated with DMBA. The present results thus suggest that geraniol has potent anti-inflammatory, anti-angiogenic, anti-cell proliferative, and apoptosis-inducing properties in DMBA-induced hamster buccal pouch carcinogenesis.

IntroductionIn rapidly developing countries such as India, the ubiquity of air pollution sources in urban and rural communities often results in ambient and household exposures significantly in excess of health-based air quality guidelines. Few efforts, however, have been directed at establishing quantitative exposure–response relationships in such settings. We describe study protocols for The Tamil Nadu Air Pollution and Health Effects (TAPHE) study, which aims to examine the association between fine particulate matter (PM2.5) exposures and select maternal, child and adult health outcomes in integrated rural–urban cohorts.Methods and analysesThe TAPHE study is organised into five component studies with participants drawn from a pregnant mother–child cohort and an adult cohort (n=1200 participants in each cohort). Exposures are assessed through serial measurements of 24–48 h PM2.5 area concentrations in household microenvironments together with ambient measurements and time-activity recalls, allowing exposure reconstructions. Generalised additive models will be developed to examine the association between PM2.5 exposures, maternal (birth weight), child (acute respiratory infections) and adult (chronic respiratory symptoms and lung function) health outcomes while adjusting for multiple covariates. In addition, exposure models are being developed to predict PM2.5 exposures in relation to household and community level variables as well as to explore inter-relationships between household concentrations of PM2.5 and air toxics. Finally, a bio-repository of peripheral and cord blood samples is being created to explore the role of gene–environment interactions in follow-up studies.Ethics and disseminationThe study protocols have been approved by the Institutional Ethics Committee of Sri Ramachandra University, the host institution for the investigators in this study. Study results will be widely disseminated through peer-reviewed publications and scientific presentations. In addition, policy-relevant recommendations are also being planned to inform ongoing national air quality action plans concerning ambient and household air pollution.

The increase in incidence of prostate cancer in the Indian Population stresses the need to identify genetic markers for susceptibility and prognosis. Recent studies show that microRNAs play an important role in tumorigenesis by altering proliferation, differentiation and cell death. Gene polymorphisms not only in promoter region but also within miRNA gene have been shown to affect expression. The present study was aimed to analyze the role of miR-146a, miR-196a2 and miR-125a gene polymorphisms in prostate cancer. Genotyping of three SNPs rs73318382, rs57095329, rs2910164 in miRNA146a, rs11614913 in miR-196a2 and rs41275794, rs12976445, rs10404453 and rs1297533 in miR-125a was performed in 100 cases and 100 controls. Statistical analysis revealed the heterozygous AG genotype of the rs57095329 was significantly decreased in the cases when compared to the controls (OR-0.45, CI -0.24 to 0.85, p value-0.02) indicating an inverse association of this genotype with prostate cancer. Further the heterozygous CT of miR-196a2 (rs11614913) (OR-1.88, CI-1.06 to 3.35, p-0.02) and homozygous CC of miR-125a (rs12976445) (OR-2.55, CI -1.15 to 4.65, p-0.03) showed increased risk for prostate cancer. Combined analysis of all the genotypes revealed that the haplotype combination AGGCGTGG (OR = 0.09 at CI 95% (0.01-0.65) showed an inverse association with prostate cancer. Stratified analysis based on the age and tumor grade revealed no significant association.