Mitochondrial Stress Induces Grow Resistance Through Chromatin Adjustments

There has been a need for research on the association between metabolic syndrome (MetS) and obstructive sleep apnea syndrome (OSAS) using large data such as nationwide population-based data that adjusts important confounding factors. Therefore, we investigated the relationship between MetS and OSAS. The data source we used was the National Health Insurance Service claims database managed by the Republic of Korea government, in which 10,113,560 individuals were enrolled in 2009 and followed up until 2018. The independent association of MetS with the risk of OSAS was determined using a Cox proportional hazards model with adjustment for age, sex, smoking status, alcohol consumption, regular physical exercise, and body mass index. Our results showed that MetS were strongly associated to OSAS which was adjusted for several confounding factors. Also, we found men, increased waist circumference and increased triglyceride are important risk factors for OSAS.The ventral tegmental area (VTA) is the origin of dopaminergic neurons and the dopamine (DA) reward pathway. This pathway has been widely studied in addiction and drug reinforcement studies and is believed to be the central processing component of the reward circuit. In this study, we used a well-established rat model to expose mother dams to alcohol, nicotine-alcohol, and saline perinatally. DA and non-DA neurons collected from the VTA of the rat pups were used to study expression profiles of miRNAs and mRNAs. miRNA pathway interactions, putative miRNA-mRNA target pairs, and downstream modulated biological pathways were analyzed. In the DA neurons, 4607 genes were differentially upregulated and 4682 were differentially downregulated following nicotine-alcohol exposure. However, in the non-DA neurons, only 543 genes were differentially upregulated and 506 were differentially downregulated. Cell proliferation, differentiation, and survival pathways were enriched after the treatments. Specifically, in the PI3K/AKT signaling pathway, there were 41 miRNAs and 136 mRNAs differentially expressed in the DA neurons while only 16 miRNAs and 20 mRNAs were differentially expressed in the non-DA neurons after the nicotine-alcohol exposure. These results depicted that chronic nicotine and alcohol exposures during pregnancy differentially affect both miRNA and gene expression profiles more in DA than the non-DA neurons in the VTA. Understanding how the expression signatures representing specific neuronal subpopulations become enriched in the VTA after addictive substance administration helps us to identify how neuronal functions may be altered in the brain.To explore the pathogenesis of high myopia (HM) using quantitative proteomics. The aqueous humor of patients with simple nuclear cataract and nuclear cataract complicated with HM (hereinafter referred to as "C" and "HM" groups, respectively) were collected. GDC-0084 The isobaric tags for relative and absolute quantitation (iTRAQ)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteomics approach was employed to explore differentially expressed proteins (DEPs). Bioinformatics was used to interpret the proteomic results. Furthermore, the plasminogen (PLG) protein was confirmed by enzyme-linked immunosorbent assay (ELISA) as the candidate biomarker for HM through a receiver operating characteristic curve analysis. The study showed 32 upregulated and 26 downregulated proteins. The gene ontology analysis demonstrated that 58 DEPs corresponded to 325 biological processes, 33 cell components, and 45 molecular functional annotations. The Kyoto Encyclopedia of Genes and Genomes analysis showed that the upregulated DEPs were highly enriched in the coagulation and complement cascades, consistent with the gene set enrichment analysis. Our data suggested that some DEPs might be hallmarks of the development of HM. ELISA confirmed that the PLG expression levels were significantly upregulated in HM. This was a new study investigating alterations in protein levels and affected pathways in HM using iTRAQ-based quantitative proteomics. Our study provided a comprehensive dataset on overall protein changes and shed light on its potential molecular mechanism in human HM.Increasing sea temperature is a driver of change for many fish traits, particularly for fast-growing epipelagic species with short life spans. With warming, altered spawning phenology and faster growth may produce substantially larger body sizes of the new cohort, affecting fishery productivity. We present an individual-based model (IBM) that predicts the distribution of fish length at catch under observed and projected thermal scenarios, accounting for mortality, temperature-dependent spawning phenology, temperature- and photoperiod- dependent growth. This IBM was demonstrated with Coryphaena hippurus (common dolphinfish), a circumglobally-distributed and highly thermophilic species sustaining commercial and recreational fisheries where it is present. The model projected a 13.2% increase in the average length at catch under marine heatwave conditions compared to the current thermal regime (1995-2005 average). Projections under RCP scenarios 4.5 and 8.5 by the end of the century led to 5.1% and 12.8% increase in average length, respectively. Furthermore, these thermal scenarios affected spawning phenology differently, producing higher variance in body size under RCP 8.5 scenario with respect to marine heatwave conditions. This study highlights how the environmental effects of climate change can alter the distribution of species length at catch.Tyrosine kinase inhibitor is an effective chemo-therapeutic drug against tumors with deregulated EGFR pathway. Recently, a genetic variant rs10251977 (G>A) in exon 20 of EGFR reported to act as a prognostic marker for HNSCC. Genotyping of this polymorphism in oral cancer patients showed a similar frequency in cases and controls. EGFR-AS1 expressed significantly high level in tumors and EGFR-A isoform expression showed significant positive correlation (r = 0.6464, p  less then  0.0001) with reference to EGFR-AS1 expression levels, consistent with larger TCGA HNSCC tumor dataset. Our bioinformatic analysis showed enrichment of alternative splicing marks H3K36me3 and presence of intronic polyA sites spanning around exon 15a and 15b of EGFR facilitates skipping of exon 15b, thereby promoting the splicing of EGFR-A isoform. In addition, high level expression of PTBP1 and its binding site in EGFR and EGFR-AS1 enhances the expression of EGFR-A isoform (r = 0.7404, p  less then  0.0001) suggesting that EGFR-AS1 expression modulates the EGFR-A and D isoforms through alternative splicing.