This study was conducted as part of an epidemiological survey of 126 nonsmokers and 178 smokers, showing primary infertility residing around Kolkata region of Eastern India. Their lifestyle history including smoking habits along with semen and blood were collected. The study examined the association of cigarette smoking with the risk of infertility, by determining the semen quality, follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone levels, and androgen receptor (AR)-CAG repeat length in a group of smokers compared with a control group (non smokers). Based on conventional WHO criteria, lower sperm motility (P < 0.001) and increased sperm morphological defects (P < 0.0001) were associated with smoking habits. Binary logistic regression analysis for the effect of smoking status on sperm DNA integrity demonstrated significant positive correlation (p = 0.006). Serum FSH and LH levels were higher for smokers compared with non-smokers while the testosterone level decreased significantly with the increasing smoking habit. The mean length of CAG repeats in AR gene was significantly higher for smokers with low testosterone compared to non-smokers. The study suggested that smoking is associated with altered semen quality, endocrine hormonal status, and number of CAG repeats in the AR gene.

Context: With an increase in the abuse of various oral habitual products in India over the past few decades; the incidence of oral potentially malignant conditions as leukoplakia, oral submucous fibrosis and squamous cell carcinoma (SCC) rates have also increased. No recent study has been conducted reporting the scenario of oral cancer and potentially malignant conditions in Eastern India (specifically Kolkata). Aims: The present study was conducted at Dr. R. Ahmed Dental College, Kolkata during 2010-2011 to find a possible correlation between the effects of the different oral habits, age, sex and the different types of oral mucosal lesions among patients reported to the hospital. This study also enabled us to see the predilection of the various histopathological stages of the lesions for different sites of the oral cavity. Subjects and Methods: The study group consisted of 698 patients having either oral potentially malignant or malignant lesion. The control group consisted of 948 patients who had reported to the hospital for different oral/dental problems and had the habit of tobacco, areca nut and/or alcohol usage for at least 1 year. Statistical Analysis : The unadjusted odds ratio, the 95% confidence interval, and the P value were calculated to correlate patients with/without different kinds of habit and having/not having various kinds of oral lesions. Results: Our study shows that for males having the habit of taking smokeless tobacco or mixed habit poses the highest risk for developing SCC. For females, significant risk of developing SCC was found in patients habituated to processed areca nut chewing. Conclusion: This study presents probably for the first time in recent years the occurrence of oral potentially malignant and malignant conditions amongst patients having deleterious habits in a hospital based population of Kolkata.

Background: Aberrant methylation is a known cause of cancer initiation and/or progression. There are scant data on the genome‐wide methylation pattern of nonfunctioning pancreatic neuroendocrine tumors (NFPanNETs) and sporadic and hereditary NFPanNETs. Methods: Thirty‐three tissue samples were analyzed: they included samples from sporadic (n = 9), von Hippel‐Lindau (VHL)‐related (n = 10), and multiple endocrine neoplasia type 1 (MEN1)–related NFPanNETs (n = 10) as well as normal islet cells (n = 4) for comparison. Genome‐wide CpG methylation profiling was performed with the Infinium MethylationEPIC BeadChip assay and was analyzed with R‐based tools. Results: In unsupervised hierarchical clustering, sporadic and MEN1‐related NFPanNETs clustered together, and the VHL group was in a separate cluster. MEN1‐related NFPanNETs had a higher rate of hypermethylated CpG sites in comparison with sporadic and VHL‐related tumor groups. Differentially methylated region analysis confirmed the higher rate of hypermethylation in MEN1‐related tumors. Moreover, in an integrated analysis of gene expression data for the same tumor samples, downregulated gene expression was found in most genes that were hypermethylated. In a CpG island methylator phenotype analysis, 3 genes were identified and confirmed to have downregulated gene expression: secreted frizzle‐related protein 5 ( SFRP5 ) in sporadic NFPanNETs and cell division cycle–associated 7‐like ( CDCA7L ) and RNA binding motif 47 ( RBM47 ) in MEN1‐related NFPanNETs. Conclusions: MEN1 NFPanNETs have a higher rate of geno me‐wide hypermethylation than other NFPanNET subtypes. The similarity between the pathways enriched in a methylation analysis of known genes involved in NFPanNET tumorigenesis suggests a key role for aberrant methylation in the pathogenesis of NFPanNETs.

Early detection and quantification of DNA damage in oral premalignancy or malignancy may help in management of the disease and improve survival rates. The comet assay has been successfully utilised to detect DNA damage in oral premalignant or malignancy. However, due to the invasive nature of collecting blood, it may be painful for many unwilling patients. This study compares the micronucleus (MN) assay in oral buccal mucosa cells with the comet assay in peripheral blood cells in a subset of oral habit-induced precancer and cancer patients. For this, MN assay of exfoliated epithelial cells was compared with comet assay of peripheral blood leucocytes among 260 participants, including those with oral lichen planus (OLP; n = 52), leukoplakia (LPK; n = 51), oral submucous fibrosis (OSF; n = 51), oral squamous cell carcinoma (OSCC; n = 54) and normal volunteers (n = 52). Among the precancer groups, LPK patients showed significantly higher levels of DNA damage as reflected by both comet tail length (P < 0.0001) and micronuclei (MNi) frequency (P = 0.0009). The DNA damage pattern in precancer and cancer patients was OLP < OSF < LPK < OSCC, and with respective oral habits, it was multiple habits > cigarette + khaini > cigarette smokers > areca + khaini > areca. There was no significant difference in the comet length and MNi frequency between males and females who had oral chewing habits. An overall significant correlation was observed between MNi frequency and comet tail length with r = 0.844 and P < 0.0001. Thus, the extent of DNA damage evaluation by the comet assay in peripheral blood cells is perfectly reflected by the MN assay on oral exfoliated epithelial cells, and MNi frequency can be used with the same effectiveness and greater efficiency in early detection of oral premalignant conditions.

Context: The detrimental effects of arsenic on female reproductive functions may involve overt oxidative stress. Casein and pea [Pisum sativum Linn. (Fabaceae)] proteins have antioxidant properties. Objective: To investigate the role of casein- and pea-supplemented high-protein diet (HPD) in utero-ovarian protection from arsenic toxicity. Materials and methods: Adult female Wistar rats were orally gavaged with vehicle (Gr-I) or arsenic at 3 ppm/rat/d (Gr-II and Gr-III) for 30 consecutive days, when they were maintained on either regular diet containing 18% protein (Gr-I and Gr-II), or HPD containing 27% protein in the form of casein (20%) and pea (7%) (Gr-III). Reproductive functions were evaluated using a battery of biochemical and histological techniques. Results: As compared to Gr-I, the Gr-II rats suffered from loss of estrous cyclicity, reduction in weight (mg/100 g body weight) of ovary (Gr-I: 54.3 ± 4.2 versus Gr-II: 35.8 ± 1.6; p < 0.001) and uterus (Gr-I: 161.7 ± 24.6 versus Gr-II: 94.44 ± 13.2; p < 0.05), utero-ovarian degeneration, attenuated ovarian activities (unit/mg tissue/h) of Δ⁵, 3β-hydroxysteroid dehydrogenase (Gr-I: 3.41 ± 0.12 versus Gr-II: 2.31 ± 0.09; p < 0.01) and 17β-hydroxysteroid dehydrogenase (Gr-I: 3.82 ± 0.57 versus Gr-II: 1.24 ± 0.19; p < 0.001), and decreased serum estradiol level (pg/ml) (Gr-I: 61.5 ± 2.06 versus 34.1 ± 2.34; p < 0.001). Ovarian DNA damage was preponderant with blatant generation of malondialdehyde (nM/mg tissue; Gr-I: 15.10 ± 2.45 versus Gr-II: 29.51 ± 3.44; p < 0.01) and attenuated superoxide dismutase activity (unit/mg tissue) (Gr-I: 2.18 ± 0.19 versus Gr-II: 1.33 ± 0.18; p < 0.05). The Gr-III rats were significantly protected from these ill effects of arsenic. Discussion and conclusion: HPD, by way of antioxidant properties, may find prospective role in the protection of reproductive damage caused by arsenic.