Notes

Post-operative outcomes of inflammatory thoracic aortitis: a study involving 41 people from a cohort of 1119 operative instances.
Cyclic GMP-AMP-synthase is a sensor of endogenous nucleic acids, which subsequently elicits a stimulator of interferon genes (STING)-dependent type I interferon (IFN) response defending us against viruses and other intracellular pathogens. This pathway can drive pathological inflammation, as documented for type I interferonopathies. In contrast, specific STING activation and subsequent IFN-β release have shown beneficial effects on experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Although less severe cases of relapse-remitting MS (RRMS) are treated with IFN-β, there is little information correlating aberrant type I IFN signaling and the pathologic conditions of MS. We hypothesized that there is a link between STING activation and the endogenous production of IFN-β during neuroinflammation. Gene expression analysis in EAE mice showed that Sting level decreased in the peripheral lymphoid tissue, while its level increased within the central nervous system over the course of the disease. Similar patterns could be verified in peripheral immune cells during the acute phases of RRMS in comparison to remitting phases and appropriately matched healthy controls. Our study is the first to provide evidence that the STING/IFN-β-axis is downregulated in RRMS patients, meriting further intensified research to understand its role in the pathophysiology of MS and potential translational applications.Background This field experiment investigated the acute effects of brief mindfulness-based intervention (MBI) coupled with carbohydrate (CHO) intake on players' recovery from half-time break in a simulated soccer competition. Methods In a single-blinded randomized crossover experiment, 14 male players received 3 treatments (Control non-carbohydrate solution + travelling introduction audio; CHO CHO-electrolyte solution + travelling introduction audio; and CHO_M CHO-electrolyte solution + MBI) during simulated half-time breaks. Vertical jump, sprint performance, mindfulness level, rate of perceived exertion, muscle pain, mental fatigue, blood glucose, and lactate were measured immediately before, during, and after the exercise. Results (1) MBI significantly increased participants' mindfulness level (Control vs. CHO_M, p less then 0.01; CHO vs. learn more CHO_M, p less then 0.01) and decreased mental fatigue for CHO_M condition (pre vs. post, p less then 0.01); (2) participants in the CHO_M condition performed better in the repeated sprint tests than in the Control and CHO condition (Control vs. CHO_M, p = 0.02; CHO vs. CHO_M, p = 0.02). Conclusion Findings of this study provide preliminary evidence of the positive effect of MBI coupled with CHO ingestion on athletes' recovery from fatigue in the early stage of the second half of a game.Background In utero smoke (IUS) exposure is associated with asthma susceptibility. Objective We sought to test the hypothesis that changes in miRNA expression by IUS exposure during human lung development is associated with asthma susceptibility. Methods Gene expression was profiled from 53 IUS unexposed and 51 IUS exposed human fetal lung tissues. We tested for the differential expression of miRNAs across post-conception age and by IUS using linear models with covariate adjustment. We tested the IUS-associated miRNAs for association with their gene expression targets using pair-wise inverse correlation. Using our mouse model, we investigated the persistence of the IUS-associated miRNA signature using RT-PCR from the lungs of mouse pups with and without IUS at postnatal day 14. MiRNAs were then tested for association with asthma and exacerbations using whole blood gene expression profiles from Asthma BRIDGE. Results Five miRNAs were differentially expressed across post-conception age (adjusted p less then 0.0002) including two that were differentially expressed by IUS exposure in human fetal lung (p less then 0.05). MiR-15a was differentially expressed by post-conception age (p = 0.00002), IUS exposure in human fetal lung (p = 0.005), and in the post-natal mouse lung (p = 0.01). MiR-15a was also associated with the in utero expression of GSDMB (adjusted p = 0.0002), a known childhood asthma gene and with asthma exacerbations (p = 0.0009) in Asthma BRIDGE. Thus, miR-15a is expressed during human lung development, is impacted by IUS exposure, regulates the intrauterine expression of asthma genes, and is associated with asthma severity. Conclusions These results provide evidence for the role of miR-15a in the fetal origin of asthma.Due to the increasing anthropogenic CO2 emissions, Ocean Acidification (OA) is progressing rapidly around the world. Despite the major role that microorganisms play on the marine biogeochemical cycling and ecosystem functioning, the response of bacterial communities upon OA scenarios is still not well understood. Here, we have conducted a detailed characterization of the composition and relative abundance of bacterial communities in the water column of an open-ocean station in the Eastern Tropical South Pacific (ETSP) off northern Chile and their interactions with environmental factors. In addition, through a short-term microcosm experiment, we have assessed the effect of low pH/high pCO2 conditions over the abundance and genetic diversity of bacterial communities. Our results evidence a clear partitioning of community composition that could be attributed mostly to dissolved oxygen. However, our experimental approach demonstrated that low pH/high pCO2 conditions might modify the structure of the bacterial community, evidencing that small changes in pH may impact significantly the abundance and diversity of key microorganisms. This study constitutes a first step aiming to provide insight about the influence of changing carbonate chemistry conditions on natural bacterial communities and to shed light on the potential impact of OA in biogeochemical cycles on the ETSP region.Cisplatin is a chemotherapeutic drug used for the treatment of a number of cancers. The efficacy of cisplatin relies on its binding to DNA and the induction of cytotoxic DNA damage to kill cancer cells. Cisplatin-based therapy is best known for curing testicular cancer; however, treatment of other solid tumors with cisplatin has not been as successful. Pre-clinical and clinical studies have revealed nucleotide excision repair (NER) as a major resistance mechanism against cisplatin in tumor cells. NER is a versatile DNA repair system targeting a wide range of helix-distorting DNA damage. The NER pathway consists of multiple steps, including damage recognition, pre-incision complex assembly, dual incision, and repair synthesis. NER proteins can recognize cisplatin-induced DNA damage and remove the damage from the genome, thereby neutralizing the cytotoxicity of cisplatin and causing drug resistance. Here, we review the molecular mechanism by which NER repairs cisplatin damage, focusing on the recent development of genome-wide cisplatin damage mapping methods.
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