Emerging drug resistance varieties and hyper-virulent strains of microorganisms have compelled the scientific fraternity to develop more potent and less harmful therapeutics. Antimicrobial peptides could be one of such therapeutics. This review is an attempt to explore antifungal peptides naturally produced by prokaryotes as well as eukaryotes. They are components of innate immune system providing first line of defence against microbial attacks, especially in eukaryotes. The present article concentrates on types, structures, sources and mode of action of gene-encoded antifungal peptides such as mammalian defensins, protegrins, tritrpticins, histatins, lactoferricins, antifungal peptides derived from birds, amphibians, insects, fungi, bacteria and their synthetic analogues such as pexiganan, omiganan, echinocandins and Novexatin. In silico drug designing, a major revolution in the area of therapeutics, facilitates drug development by exploiting different bioinformatics tools. With this view, bioinformatics tools were used to visualize the structural details of antifungal peptides and to predict their level of similarity. Current practices and recent developments in this area have also been discussed briefly.

Mustard is widely used in a variety of foods/food products to enhance the flavor and nutritional value that subsequently raise the risk of hypersensitivity reactions. Mustard allergy has been reported for many years and is increasing gradually especially in the areas where its consumption is comparatively higher, and it may be considered among the most important food allergies. A number of relevant clinical studies focused on mustard-induced allergic manifestations are summarized in the current review. In addition, the knowledge regarding the immunological as well as biochemical characteristics of mustard allergens that have been known till date and their cross-reactivity with other food allergens have also been discussed here. Notably, mustard may also be present as a hidden allergen in foods; therefore, it is important to recognize food products that may contain mustard as it may pose potential risk for the allergic individuals. Additionally, the better understanding of the underlying mechanism in mustard allergy is a prerequisite for the development of specific therapeutic procedures. Conclusively, mustard sensitivity should be routinely tested in patients with idiopathic anaphylaxis for the safety of the allergic patients.

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Purpose We investigated if substitutions in the ERCC1, ERCC2, and XRCC1 genes of the DNA repair pathway correlate with non-obstructive azoospermia and male infertility. Methods A total of 548 azoospermic infertile males and 410 fertile controls were genotyped for XRCC1 399A > G, 280G > A, and ERCC1 C > A 3′ UTR and 541 azoospermic infertile males and 416 fertile controls were genotyped for ERCC2 751A > C using iPLEX Gold Assay. Meta-analyses were performed on XRCC1 399A > G (1022 cases and 1004 controls), ERCC1 C > A 3′ UTR (879 cases and 1059 controls), and ERCC2 751A > C (914 cases and 850 controls) polymorphisms to quantitatively estimate the significance of the association between these polymorphisms and the risk of infertility. Results Statistically significant association between ERCC2 751A > C SNP and male infertility was found using the codominant model (p = 0.03). Results of meta-analysis suggested a lack of correlation with male infertility risk, which could be due to pooling of studies from different ethnic populations. Due to limited the number of studies, a stratified analysis for different ethnic groups could not be performed. Conclusion (s) In conclusion, AA genotype of 751A > C SNP in ERCC2 correlated with a higher risk of male infertility and may contribute to an increased risk of azoospermia and male infertility in Indian men.

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We describe Mus musculus castaneus as a new mammalian host for Cryptococcus neoformans var. grubii (VNI). Eighteen apparently healthy adults and pups of the rodent were collected from human dwellings in Varanasi, a city of India. Both clinical and behavioral examinations of the rodents did not reveal any sign of the disease. Among visceral organs, histological examination of only liver exhibited the presence of single celled, encapsulated, Southgate's mucicarmine positive fungal structures consistent with C. neoformans. Nevertheless, culture of tissue homogenates of brain, lungs, liver, and kidneys yielded white colonies on Sabouraud's dextrose agar and brown mucoid colonies of C. neoformans on Staib's and Tobacco agar media. The pathogen was isolated from habitat soil as well as fresh faeces of the animals. All isolates were urease positive, nitrate and canavanine-glycine bromothymol blue negative, exhibited phenoloxidase activity and grew at 37°C. The isolates were identified as C. neoformans var. grubii with ITS primers and unique marker (GACA)4. The pathogen when inoculated in immunosuppressed mice showed low pathogenicity. To our knowledge, we for the first time report case cluster of Mus musculus castaneus as new passenger host for C. neoformans var. grubii (VNI).

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