Spermatogenesis is collaboratively controlled by testosterone and follicle stimulating hormone. Testosterone and its immediate metabolite dihydrotestosterone affect their roles through the androgen receptor (AR). Mutations in the AR gene have been shown to cause partial to complete androgen insensitivity or infertility in otherwise normal males. The dependence of germ cells upon Sertoli and Leydig cells for their differentiation into sperms and deletion studies of the AR gene in animal models indicate a direct or indirect role of the AR gene in spermatogenesis. Although a few studies worldwide have reported AR mutations in male infertility, no similar study has been conducted on Indian populations. Therefore, we undertook this study to look at the contribution of AR mutations in male infertility among Indian men. We have sequenced the complete coding region of the AR gene in a total of 399 infertile samples, comprising 277 azoospermic, 100 oligozoospermic, and 22 oligoteratozoospermic samples. A total of 100 healthy males with proven fertility and the same ethnicity as the experimental group served as controls. Sequence analysis revealed no mutation in any of these samples. Our study suggests that mutations in the AR gene are less likely to cause azoospermia and oligozoospermia; however, it was difficult to rule out its effect in oligoteratozoospermia, as the sample size was small.

ObjectiveThe main aim of the study was to explore the factors causing delay in seeking treatment among adult patients diagnosed with CAAs acute myocardial infarction (AMI) and compare the factors between timely and late treatment seeking groups.MethodA total of 93 subjects were included in the study diagnosed with AMI interviewed within 48 h of hospitalization. Data were collected from onset of symptoms to arrival at hospital on demography, clinical profile, clinical factors, cognitive factors and social support factors. Subjects were categorized in two study groups i.e. timely treatment seeking group (<120 min from onset of symptoms) and delayed treatment seeking group (>120 min from onset of symptoms).ResultsThe minimum and maximum time took by subjects to seek treatment was 10 and 5450 min, respectively. The mean pain score of subjects who sought delayed treatment (2.2619) is less than those who sought timely treatment (3.3725). The mean knowledge score (12.2754), mean symptom perception (3.6667), mean perceived seriousness (4.7647) is more in subjects who sought timely treatment than those who sought delayed treatment (5.7381), (1.3095), (1.8333) respectively. The mean family support score (57.4492), mean non-family support score (24.902), mean social support score (48.3002) is more in timely treatment group than in delayed treatment seeking group (42.6829), (4.7619), (29.2138) respectively.ConclusionDecreased pain, knowledge about AMI, symptom perception, perceived seriousness respectively and inadequate family & non-family support i.e. social support were the factors related to treatment seeking delay among adults diagnosed with AMI.

Testosterone is converted to 5 a-dihydrotestosterone (DHT) by 5 a-reductase enzyme, which is encoded by the SRD5A2 gene. DHT is the main androgen responsible for prostate growth. We have analyzed the complete coding region of the SRD5A2 gene in 87 histologically confirmed prostate cancer (PC) patients, 40 benign prostatic hyperplasia (BPH) cases, and 96 control samples from southern parts of India. The study revealed the A49T site to be monomorphic, the V89L site to be highly polymorphic, and the (TA) n repeat site to be polymorphic with only 2 alleles in our populations. The distribution of V89L alleles between PC cases and controls was not significantly different; however, (TA) 9 alleles distributed differently between the 2 groups. BPH cases exhibited alleles similar to controls at all polymorphic sites. The sequencing of the whole coding region did not reveal any other known or novel polymorphism in this gene. Our study emphasizes that the (TA) 9 allele might confer certain PC risk but that A49T and V89L polymorphisms do not confer PC risk in South Indian men.