The paper presents major lipid classes and their fatty acids investigated from Ascaridia galli, a nematode parasite of country fowl. Thin layer chromatography (TLC) reveals that the percent of total lipid, neutral lipid, phospholipids, and glycolipids are 1.94, 54.39, 26.95 and 18.66, respectively. Gas-liquid chromatography (GLC) analysis shows that the saturated fatty acids are the major components in all the lipid fractions followed by monoenes and dienes. Polyunsaturated fatty acids (PUFA) were present in low amount. Stearic acids (C 18 ) were the chief components among all the fatty acids in all the lipid fractions.

A new strain of the beta coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is solely responsible for the ongoing coronavirus disease 2019 (COVID-19) pandemic. Although several studies suggest that the spike protein of this virus interacts with the cell surface receptor, angiotensin-converting enzyme 2 (ACE2), and is subsequently cleaved by TMPRSS2 and FURIN to enter into the host cell, conclusive insight about the interaction pattern of the variants of these proteins is still lacking. Thus, in this study, we analyzed the functional conjugation among the spike protein, ACE2, TMPRSS2, and FURIN in viral pathogenesis as well as the effects of the mutations of the proteins through the implementation of several bioinformatics approaches. Analysis of the intermolecular interactions revealed that T27A (ACE2), G476S (receptor-binding domain [RBD] of the spike protein), C297T (TMPRSS2), and P812S (cleavage site for TMPRSS2) coding variants may render resistance in viral infection, whereas Q493L (RBD), S477I (RBD), P681R (cleavage site for FURIN), and P683W (cleavage site for FURIN) may lead to increase viral infection. Genotype-specific expression analysis predicted several genetic variants of ACE2 (rs2158082, rs2106806, rs4830971, and rs4830972), TMPRSS2 (rs458213, rs468444, rs4290734, and rs6517666), and FURIN (rs78164913 and rs79742014) that significantly alter their normal expression which might affect the viral spread. Furthermore, we also found that ACE2, TMPRSS2, and FURIN proteins are functionally co-related with each other, and several genes are highly co-expressed with them, which might be involved in viral pathogenesis. This study will thus help in future genomics and proteomics studies of SARS-CoV-2 and will provide an opportunity to understand the underlying molecular mechanism during SARS-CoV-2 pathogenesis.

No abstract

Aberrant expression of long non-coding RNAs (lncRNAs), caused by alterations in DNA methylation, is a driving factor in several cancers. Interplay between lncRNAs’ aberrant methylation and expression in prostate cancer (PC) progression still remains largely elusive. Therefore, this study characterized the genome-wide epigenetic landscape and expression profiles of lncRNAs and their clinical impact by integrating multi-omics data implementing bioinformatics approaches. We identified 62 differentially methylated CpG-sites (DMCs) and 199 differentially expressed lncRNAs (DElncRNAs), where 32 DElncRNAs contain 32 corresponding DMCs within promoter regions. Significant negative correlation was observed between 8 DElncRNAs-DMCs pairs. 3 (cg23614229, cg23957912, and cg11052780) DMCs and 4 (CACNA1G-AS1, F11-AS1, NNT-AS1, and MSC-AS1) DElncRNAs were identified as high-risk factors for poor prognosis of PC patients. Overexpression of hypo-methylated CACNA1G-AS1, F11-AS1, and NNT-AS1 and down-regulation of hyper-methylated MSC-AS1 significantly lower the survival of PC patients and could be a potential prognostic and therapeutic biomarker. These DElncRNAs were found to be associated with several molecular functions whose deregulation can lead to cancer. Involvement of these epigenetically deregulated DElncRNAs in cancer-related biological processes was also noticed. These findings provide new insights into the understanding of lncRNA regulation by aberrant DNA methylation which will help to clarify the epigenetic mechanisms underlying PC.

No abstract