Breast carcinogenesis is a multistep process, involving both genetic and epigenetic modification process of genes, involved in diverse pathways ranging from DNA repair to metabolic processes. This study was undertaken to assess the role of promoter methylation of GSTP1 gene, a member of glutathione-S-transferase family of enzymes, in relation to its expression, polymorphism, and clinicopathological parameters. Tissue samples were taken from breast cancer patients and paired with their normal adjacent tissues. A total of 51 subjects were studied, in which the frequency of promoter methylation in cancerous tissue was 37.25% as against 11% in the normal tissues (p ≤ 0.001). The hypermethylated status of the gene was significantly associated with the loss of the protein expression (r = −0.449, p = 0.001, odds ratio = 7.42, 95% confidence interval = 2.05-26.92). Furthermore, when compared with the clinical parameters, the significant association was found between the promoter hypermethylation and lymph node metastasis (p ≤ 0.001), tumor stage (p = 0.039), tumor grade (p = 0.028), estrogen receptor status (p = 0.018), and progesterone receptor status (p = 0.046). Our study is the first of its kind in Kashmiri population, which indicates that GSTP1 shows aberrant methylation pattern in the breast cancer with the consequent loss in the protein expression. Furthermore, it also shows that the gene polymorphism (Ile105Val) at codon 105 is not related to the promoter methylation and two are the independent events in breast cancer development.

Coronary artery disease (CAD) is a clinical manifestation of atherosclerosis in the arteries supplying myocardium. Inflammation is the cornerstone in the development and progression of atherosclerosis. Amongst the various biomolecules tumour necrosis factor-a (TNF-a), interleukin-18 (IL-18) and interleukin-1b (IL-1b) build an inflammatory bionetwork in developing the disease. In this study we investigated the association of TNF-a SNPs [-308G/A (rs1800629), À1031T/C (rs1799964), À863C/A (rs1800630)]; IL-18 [-137G/C (rs187238)] and IL-1b SNPs [+3954C/T (rs1143634), À31C/T (rs1143627), and À511C/T (rs16944)] with coronary artery disease risk in Kashmiri population. A total of 200 cases and 260 controls were recruited in the study. Logistic regression analysis was done to investigate the association between SNPs and CAD risk. In case of TNF-a, the À308G/A-A/A and À863A/A showed an association with disease while À1031T/C was found to have an inverse relation. The IL-18-137G/C showed no statistically significant difference between controls and cases. For IL-1b the +3954C/T and À31C/T SNP variants showed no disease association while À511T/T showed significant association. Haplotypic analysis revealed the haplotype ATCGCC and GTACCTC to be associated with CAD risk and GTCGTTT, in particular, showing a profound association. Overall, our study suggests that TNF-a and IL-1b promoter polymorphisms may act as genetic risk factors in developing the coronary artery disease.

In the present world a significant threat to human health is posed by zoonotic diseases. Helminth parasites of ruminants are one of the most common zoonotic organisms on the planet. Among them, trichostrongylid nematodes of ruminants, found worldwide, parasitize humans in different parts of the world with varying rates of incidence, particularly among rural and tribal communities with poor hygiene, pastoral livelihood and poor access to health services. In the Trichostrongyloidea superfamily, Haemonchus contortus, Teladorsagia circumcincta, Marshallagia marshalli, Nematodirus abnormalis and Trichostrongylus spp. are zoonotic in nature. Species of the genus Trichostrongylus are the most prevalent gastrointestinal nematode parasites of ruminants that transmit to humans. This parasite is prevalent in pastoral communities around the world and causes gastrointestinal complications with hypereosinophilia which is typically treated with anthelmintic therapy. The scientific literature from 1938 to 2022 revealed the occasional incidence of trichostrongylosis throughout the world with abdominal complications and hypereosinophilia as the predominant manifestation in humans. The primary means of transmission of Trichostrongylus to humans was found to be close contact with small ruminants and food contaminated by their faeces. Studies revealed that conventional stool examination methods such as formalin-ethyl acetate concentration or Willi's technique combined with polymerase chain reaction-based approaches are important for the accurate diagnosis of human trichostrongylosis. This review further found that interleukin 33, immunoglobulin E, immunoglobulin G1, immunoglobulin G2, immunoglobulin M, histamine, leukotriene C4, 6-keto prostaglandin F1α, and thromboxane B2 are vital in the fight against Trichostrongylus infection with mast cells playing a key role. This review focuses on the prevalence, pathogenicity and immunological aspects of Trichostrongylus spp. in humans.

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