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A new Complex Action involving Phytochrome T throughout Place Enviromentally friendly Variation.
Our findings add to our understanding of the genetic composition and local evolutionary process of Chinese goats. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.OBJECTIVE Prenatal opioid exposure has been linked with impaired cognitive development, with boys potentially at elevated risk. In the present study, we examined cognitive and language development of children prenatally exposed to opioids, with an additional focus on sex differences. METHODS A sample of 378 children (n = 194 girls and n = 184 boys) aged 1.2-42.8 months was drawn from the Danish Family Outpatient Clinic database. Developmental outcomes were assessed using the Bayley-III cognitive and language scales, and substance exposure was determined with urine screening and/or verbal report. Children exposed to opioids (n = 94) were compared to children with no prenatal substance exposure (n = 38), and children exposed to alcohol (n = 131) or tobacco (n = 115). Group and sex differences were investigated with separate linear mixed models for each Bayley scale, controlling for concurrent cannabis exposure. RESULTS There were significantly reduced scores in opioid-exposed boys compared to boys with no prenatal substance exposure, but no difference between opioid-exposed and nonexposed girls. Additionally, alcohol-exposed boys had lower cognitive scores than nonexposed boys, and alcohol-exposed girls had lower scores on both scales compared to opioid-exposed girls. There were otherwise no significant differences according to group, sex, or scale. CONCLUSIONS The present findings indicate poorer cognitive and language development in boys after prenatal opioid exposure. As academic performance is rooted in cognitive functioning, long-term follow-up might be necessary for exposed children. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society of Pediatric Psychology.BACKGROUND Body mass index (BMI) is a complex phenotype that may interact with genetic variants to influence colorectal cancer risk. METHODS We tested multiplicative statistical interactions between BMI (per 5 kg·m2) and approximately 2.7 million single nucleotide polymorphisms (SNPs) with colorectal cancer risk among 14,059 colorectal cancer case (53.2% women) and 14,416 control (53.8% women) participants. All analyses were stratified by sex a priori. Statistical methods included two-step (i.e., Cocktail method) and single-step (i.e., case-control logistic regression and a joint 2-degree of freedom test) procedures. All statistical tests were two-sided. RESULTS Each 5 kg·m2 increase in BMI was associated with higher risks of colorectal cancer, less so for women (odds ratio [OR] 1.14; 95% confidence intervals [CI] 1.11-1.18; p-value 9.75 x 10-17) than for men (OR 1.26; 95% CI 1.20-1.32; p-value 2.13 x 10-24). The two-step Cocktail method identified an interaction for women, but not men, between BMI and a SMAD7 intronic variant at 18q21.1 (rs4939827; p-observed 0.0009; p-threshold 0.005). A joint 2-degree of freedom test was consistent with this finding for women (joint p-value 2.43 x 10-10). Each 5 kg·m2 increase in BMI was more strongly associated with colorectal cancer risk for women with the rs4939827-CC genotype (OR 1.24; 95% CI 1.16-1.32; p-value 2.60 x 10-10) than for women with the CT (OR 1.14; 95% CI 1.09-1.19; p-value 1.04 x 10-8) or TT (OR 1.07; 95% CI 1.01-1.14; p-value 0.02) genotypes. read more CONCLUSION These results provide novel insights on a potential mechanism through which a SMAD7 variant, previously identified as a susceptibility locus for colorectal cancer, and BMI may influence colorectal cancer risk for women. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please email [email protected] methylation (DNAm) age acceleration, a parameter derived via the epigenetic clock, has recently been suggested as a biomarker of aging. We hypothesized that accelerated biological aging, measured by both this new and the established biomarker of aging, relative leukocyte telomere length (rLTL), are associated with vitamin D deficiency. Moreover, we tested for an association between rLTL/DNAm age acceleration and different clinical assessments for functional capacity, including the Fried frailty score. Cross-sectional data of 1,649 participants of the Berlin Aging Study II was available (∼50% female, age 22-37 and 60-84 years). A seven cytosine-phosphate-guanine clock was estimated to calculate the DNAm age acceleration. rLTL was measured by quantitative real-time PCR. 25-hydroxyvitamin D (25(OH)D) serum levels less then 25 nmol/L was defined as vitamin D deficiency and less then 50 nmol/L as vitamin Dinsufficiency. Vitamin D-sufficient individuals had a 1.4 years lower mean DNAm age acceleration (p less then 0.05, ANOVA) and a 0.11 longer rLTL (p less then 0.001, ANOVA) than vitamin D-deficient participants. Likewise, vitamin D sufficient participants had lower DNAm age acceleration (β=1.060, p=0.001) and longer rLTL (β=-0.070; p less then 0.001) than vitamin D non-sufficient subjects in covariate adjusted analysis. Neither DNAm age acceleration nor rLTL were significantly associated with the Fried frailty score or the functional assessments. Only the clock drawing test was associated with DNAm age acceleration (subgroup of older men β=1.898, p=0.002). Whether the analyzed biomarkers of aging can be used to predict an individual's functional capacity or will be associated with frailty in the advanced course of aging, will be clarified by future longitudinal analyses. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail [email protected] is an essential mechanism in the control of antiviral immunity upon virus infection. Here, we identify a series of ubiquitination-modulating enzymes that are modulated by vesicular stomatitis virus (VSV). Notably, TRIM24 is down-regulated through direct transcriptional suppression induced by VSV-activated IRF3. Reducing or ablating TRIM24 compromises type I IFN (IFN-I) induction upon RNA virus infection and thus renders mice more sensitive to VSV infection. Mechanistically, VSV infection induces abundant TRIM24 translocation to mitochondria, where TRIM24 binds with TRAF3 and directly mediates K63-linked TRAF3 ubiquitination at K429/K436. This modification of TRAF3 enables its association with MAVS and TBK1, which consequently activates downstream antiviral signaling. Together, these findings establish TRIM24 as a critical positive regulator in controlling the activation of antiviral signaling and describe a previously unknown mechanism of TRIM24 function. © 2020 Zhu et al.
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