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Accumulating evidence demonstrates that the host genome's epigenetic modifications are essential for living organisms to adapt to extreme conditions. DNA methylation, covalent modifications of histone and interassociation of noncoding RNAs facilitate the cellular manifestation of epigenetic changes in the genome. Out of various factors involved in the epigenetic programming of the host, noncoding RNAs (ncRNAs) such as microRNA (miRNA), long noncoding RNA (lncRNA), circular RNA, snoRNA and piRNA are new generation noncoding molecules that influence a variety of cellular processes like immunity, cellular differentiation and tumor development. During tumor development, temporal changes in miRNA/lncRNA rheostat influence sterile inflammatory responses accompanied by the changes in the carcinogenic signaling in the host. At the cellular level, this is manifested by the upregulation of inflammasome and inflammatory pathways, which promotes cancer-related inflammation. Given this, we discuss the potential of lncRNAs, miRNAs, circular RNA, snoRNA and piRNA in regulating inflammation and tumor development in the host.

The biological applications of germylenes remain an unconceivable domain owing to their unstable nature. We report the isolation of air, water, and culture-medium stable germylene DPMGeOH (3) and its potential biological application (DPM = dipyrromethene ligand). Compound 3 exhibits antiproliferative effects comparable to that of cisplatin in human cancer cells. The cytotoxicity of compound 3 on normal epithelial cells is minimal and is similar to that of the currently used anti-cancer drugs. These findings provide a framework for a plethora of biological studies using germylenes and have important implications for low-valent main group chemistry.

Silver coating of different thicknesses ranging from 5 to 20 nm was deposited on the Ti6Al4V substrate using DC sputtering followed by thermal annealing at 750 °C for 15 min in an ambient environment. The surface topography and elemental composition of annealed samples were analyzed using different characterization techniques. The silver ions (Ag+) concentration released from the modified titanium surface was calculated through inductive coupled plasma mass spectroscopy (ICP-MS). The plate counting method was used to quantify the bacteria-killing potential of modified titanium surface against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), Fluoroquinolones-resistant Salmonella typhi (FRST) and Methicillin-resistant Staphylococcus aureus (MRSA) bacteria. The cell membrane integrity study of E. coli and S. aureus bacterium was done qualitatively using scanning electron microscopy and further confirmed with fluorescence microscopy. Due to thermal annealing, polygonal shaped oxide nanoparticles were formed on the titanium substrate. Moreover, the surface topography of modified titanium surface changes with the thickness of the silver film. In order to check the cytotoxic effect of modified titanium surface, mouse fibroblast cells (NIH3T3) were used for 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay. The limited (

The method for fast fabrication of superhydrophobic surfaces was proposed to resist the formation of biofilm of Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) for orthopedic and dental implants. Laser beam machining with nanosecond pulsed laser (Nd:YAG) was used to fabricate pit structure on Grade-5 Ti–6Al–4V alloy followed by annealing (at 300 °C with different time scales) in order to reduce the transition time from hydrophilic to superhydrophobic surface generation. Field emission scanning electron microscopy (FE-SEM) and X-ray diffraction (XRD) techniques were used to characterize the textured samples. The surface wettability of plain and textured samples was measured by the sessile drop method using goniometer. The biofilm formation was qualitatively and quantitatively evaluated by FE-SEM and crystal violet binding assay, respectively. The biofilm formation was observed on plain (hydrophilic) surface for both the types of bacteria, whereas significantly less biofilm formation was observed on the laser textured (superhydrophobic) surfaces. The proposed method helps in reducing the risk of infection associated with implants without using cytotoxic bactericidal agents.

The clinical course of HIV-1 varies greatly among infected individuals. Despite extensive research, virus factors associated with slow-progression remain poorly understood. Identification of unique HIV-1 genomic signatures linked to slow-progression remains elusive. We investigated CpG dinucleotide content in HIV-1 envelope gene as a potential virus factor in disease progression. We analysed 1808 HIV-1 envelope gene sequences from three independent longitudinal studies; this included 1280 sequences from twelve typical-progressors and 528 sequences from six slow-progressors. Relative abundance of CpG dinucleotides and relative synonymous codon usage (RSCU) for CpG-containing codons among HIV-1 envelope gene sequences from typical-progressors and slow-progressors were analysed. HIV-1 envelope gene sequences from slow-progressors have high-CpG dinucleotide content and increased number of CpG-containing codons as compared to typical-progressors. Our findings suggest that observed differences in CpG-content between typical-progressors and slow-progressors is not explained by differences in the mononucleotide content. Our results also highlight that the high-CpG content in HIV-1 envelope gene from slow-progressors is observed immediately after seroconversion. Thus CpG dinucleotide content of HIV-1 envelope gene is a potential virus-related factor that is linked to disease progression. The CpG dinucleotide content of HIV-1 envelope gene may help predict HIV-1 disease progression at early stages after seroconversion.

The major challenge faced in biomedical field is the formation of biofilm on polymer devices like catheters. It is important to functionalize the biomedical devices with a bactericidal agent through an easy and safe process in order to protect them from bacterial attack. In this article, the new method of impregnation of silver nanoparticles (AgNPs) into polymer film was proposed and tested against bacterial cells. The different sizes of silver nanoparticles were embedded in polystyrene film using thermal annealing and soft molding technique. Silver films having different thickness were deposited on the highly polished machinable glass ceramic (MACOR) substrate using direct current (DC) sputtering and subjected to at 750 °C for 15 min. After the heat treatment, AgNPs were formed on MACOR sample. It was then characterized using field emission scanning electron microscope (FE-SEM). Image-J software was used to analysed shape, size and distribution of AgNPs. The spin coating method was adopted to coat polystyrene film on to MACOR substrate supported AgNPs and allow it to cure for 24 h. After curing, the polystyrene film was peeled off and finally, AgNPs got transferred to polystyrene film. The AgNPs embedded polystyrene film was analyzed using FE-SEM and atomic force microscopy (AFM). Spread plate (plate counting) method was used to evaluate the bacterial killing potential of modified polystyrene film against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) bacteria. The modified polystyrene film shows effective antibacterial ability against both the types of bacteria compared to the plain polystyrene surface.

Polymorphisms in DNA repair and cell cycle genes contribute to increased breast cancer (BC) risk. Their association and interaction in relation to betel quid and tobacco chewing habits need exhaustive multi-analytical investigation to explain BC predisposition due to DNA damage. Polymorphism in TP53-72Arg>Pro, RAD51-135G>C, BRCA2, and CCND1-G870A were examined in 204 BC cases and 217 controls from Northeast Indian population. Multifaceted analytic approaches were used to explore relationships between polymorphisms, tobacco history, and BC susceptibility. Betel quid chewing was identified as the predominant risk factor. CCND-AA and dominant model showed protection towards BC in betel quid chewer (BQC) [(0.28 (0.10–0.77), 0.01 and 0.32 (0.12–0.81), 0.01)] and non-betel quid chewers (NBQC) [(0.26 (0.09–0.78), 0.01 and 0.37 (0.16–0.87), 0.02)]. TP53-Pro/Pro genotype showed protection towards BC in NBQC (0.29 (0.10–0.81), p = 0.01) and (0.51 (0.32–0.80), p = 0.003, respectively). RAD51-C allele was associated with BC risk (2.03 (1.26–3.30) 0.002) in BQC. Two BQC cases had BRCA2 8415G>T:K2729N mutation in Exon18. MDR analysis showed best four locus model with TBA 0.6765 (0.005) and CVC of 10/10 in NBQC. Interaction diagram concurred the interactions between TP53 and RAD51 (1.32 %) with independent effect (1.89 %) of CCND1in NBQC. In CART analysis, BQC with CCND1 GG genotype were at risk (OR = 33.0; 95 % CI = 6.08–179.07), p