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Background. Globally, more than 350 million people of all ages suffer from depression. Elderly persons are more vulnerable to depression. We conducted this study to estimate the prevalence of depression, and to study the association of depression with sociodemographic and clinical variables among elderly persons in a rural community. Methods. We conducted a community-based cross-sectional study among 395 randomly selected elderly persons aged 60 years and above in a rural area of Ballabgarh, Haryana, India. The participants were screened by using the Geriatric Depression Scale, and diagnosis was confirmed by the Mini International Neuropsychiatric Interview. Multivariate analysis was done for independent predictors of depression. Results. The prevalence of depression was 11.4% (95% CI 8.6%–14.9%). Living in a nuclear family (adjusted odds ratio [AOR] 8.98, 95% CI 3.40–23.71), lack of physical activity (AOR 4.95, 95% CI 2.00–12.27), whole-time involvement in household work (AOR 4.47, 95% CI 1.18–16.93), presence of two or more chronic diseases (AOR 4.45, 95% CI 1.60–12.35), having no role in family decision-making (AOR 2.77, 95% CI 1.19–6.42), sleep problems in past one year (AOR 2.97, 95% CI 1.32–6.69) and bilateral hearing impairment (AOR 4.00, 95% CI 1.80–8.88) were factors associated with depression in elderly persons. Conclusions. Depression is common among elderly persons in rural areas. Individuals providing healthcare to elderly persons need to be trained to identify depression and take appropriate action; elderly persons with chronic diseases and hearing impairment deserve special attention. Natl Med J India 2016;29:129–35
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Background & objectives: Genetic polymorphisms in glutathione-S-transferase genes (GSTM1 and GSTT1) have been studied intensively for their potential role in lung cancer susceptibility. However, most of the studies on association between the polymorphisms and lung cancer do not distinguish between genotypes with one or two copies of the genes. The present study investigates the gene dosage effects of GSTT1 and GSTM1 copy number and their environmental interactions to examine the association of lung cancer risk with trimodular genotypes of the GSTs in a high-risk population from north-east India. Methods: A total of 154 lung cancer cases and 154 age and sex matched controls from the high risk region of north-east India were analyzed by multiplex real-time PCR to determine the trimodal genotypes (+/+, +/- and -/-) in both the genes (GSTM1 and GSTT1). Results: No significant association and gene dosage effect of GSTM1 gene copy number with lung cancer risk (Ptrend=0.13) were found. However, absence of GSTT1 conferred 68 per cent (OR=0.32;95%CI=0.15-0.71;P=0.005) reduced risk compared to the two copy number of the gene. tThere was evidence of gene dosage effect of GSTT1 gene (Ptrend=0.006). Tobacco smoking was a major environmental risk factor to lung cancer (OR=3.03;95%CI=1.73-5.31;P<0.001). However, its interaction with null genotype of GSTT1 conferred significant reduced risk to lung cancer (OR=0.30;95%CI=0.10-0.91;P=0.03). Further in only tobacco smokers, null genotype was associated with increased reduced risk [0.03(0.001-0.78)0.03; Ptrend=0.006]. No effect modification of GSTM1 was observed with lung cancer risk by environmental risk factors. Interpretation & conclusions: The results suggest that absence of GSTT1 null genotype may be associated with a reduced risk of lung cancer and the effect remains unchanged after interaction with smoking.
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Background & objectives: Prostate cancer (CaP) is the fifth most common cancer among Indian men. Tumour protein p53 (TP53) gene increases the fidelity of DNA replication and homologous recombination by transcriptional transactivation of mismatch repair (MMR) genes. DNA repair thus has a potential role in molecular carcinogenesis of CaP. The aim of the present study was to identify mutations, and polymorphisms in TP53 gene and MMR protein expression in CaP in Indian male population. Methods: TP53 codon 72 polymorphism was analysed in 105 CaP, 120 benign prostatic hyperplasia (BPH) cases and 106 normal controls. Mutational analysis of TP53 was done in DNA extracted from formalin fixed paraffin embedded tissue of 80 CaP and 24 BPH cases. Expression of MMR proteins viz. hMLH1, hMSH2, hPMS1 and hPMS2 was studied in 80 CaP, 15 prostatic intraepithelial neoplasia (PIN) and 15 BPH cases. Results: A somatic C/A variation at the intronic boundary of exon 7 in TP53 gene was observed in one each biopsy samples from CaP and BPH. A significant association of codon 72 TP53 Pro/Pro genotype was observed with the risk of CaP (OR, 2.59, P=0.02) and BPH (OR, 6.27, P<0.001). Immunohistochemical analysis of MMR proteins showed maximum loss of hPMS1 expression in cases of CaP and PIN while no loss in expression of MMR proteins was observed in BPH cases. The study also identified a significant loss of hPMS2 protein in poorly differentiated tumours (Gleason score >7) than in well differentiated tumours (Gleason score 3-6) (P<0.05). Interpretation & conclusions: The results of the present study demonstrate that TP53 codon 72 polymorphism plays significant role in the pathogenesis and susceptibility to CaP and BPH. Also, an aberrant MMR protein expression could be involved in progression of prostate cancer through PIN, early CaP to aggressive CaP. The loss of hPMS2 protein expression may serve as a marker for progression of CaP.