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Built-in, multi-scale, spatial-temporal cell biology--A second step in the article genomic period.
OBJECTIVES Long-term care (LTC) facilities are particularly dangerous places for the spread of Covid-19 given that they house vulnerable, high-risk populations. Transmission-based precautions to protect residents, employees, and families alike must account for potential risks posed by LTC workers' second jobs and unpaid care work. This observational study describes the prevalence of their (1) second jobs and (2) unpaid care work for dependent children and/or adult relatives (double- and triple-duty caregiving) overall and by occupational group (registered nurses, licensed practical nurses, or certified nursing assistants). DESIGN A descriptive, secondary analysis of data collected as part of the final wave of the Work, Family and Health Study. SETTING Thirty nursing home facilities located throughout the northeastern United States. PARTICIPANTS A subset of 958 essential, facility-based LTC workers involved in direct patient care. MEASUREMENTS We present information on LTC workers' demographic characteristics,ate clinical, policy, and informal supports. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.BACKGROUND Trends in diet quality among US adults indicate a steady improvement, but data on longitudinal individual-level changes in diet quality are still limited. OBJECTIVE We examined changes in diet quality over 10 y and sought to determine whether baseline sociodemographic and lifestyle factors predicted the changes in a multiethnic population. METHODS Data were from 63,255 African American, Native Hawaiian, Japanese American, Latino, and white men and women (45-75 y old at baseline) in the Multiethnic Cohort, who completed a quantitative food frequency questionnaire at baseline (1993-1996) and 10-y follow-up (2003-2007) and had no prevalent cancer or heart disease at either survey. find more Overall diet quality was measured by use of the Healthy Eating Index-2015 (HEI-2015), the Alternative Healthy Eating Index-2010 (AHEI-2010), the alternate Mediterranean Diet score, and the Dietary Approaches to Stop Hypertension (DASH) score. We used a general linear model with adjustment for covariates to compare diet qualisubsequent changes in diet quality over time in this multiethnic population. Copyright © The Author(s) on behalf of the American Society for Nutrition 2020.The actin cytoskeleton is regulated by many proteins including capping proteins that stabilize actin filaments (F-actin) by inhibiting actin polymerization and depolymerization. Here we report two pediatric probands who carry damaging heterozygous de novo mutations in CAPZA2 (HGNC 1490) and exhibit neurological symptoms with shared phenotypes including global motor development delay, speech delay, intellectual disability, hypotonia and a history of seizures. CAPZA2 encodes a subunit of an F-actin-capping protein complex (CapZ). CapZ is an obligate heterodimer consisting of α and β heterodimer conserved from yeast to human. Vertebrate genomes contain three α subunits encoded by three different genes and CAPZA2 encodes the α2 subunit. The single orthologue of CAPZA genes in Drosophila is cpa. Loss of cpa leads to lethality in early development and expression of the human reference CAPZA2 rescues this lethality. However, the two CAPZA2 variants identified in the probands rescue this lethality at lower efficiency than the reference. Moreover, expression of the CAPZA2 variants affects bristle morphogenesis, a process that requires extensive actin polymerization and bundling during development. Taken together, our findings suggest that variants in CAPZA2 lead to a non-syndromic neurodevelopmental disorder in children. Published by Oxford University Press 2020.BREX (for BacteRiophage EXclusion) is a superfamily of common bacterial and archaeal defence systems active against diverse bacteriophages. While the mechanism of BREX defence is currently unknown, self versus non-self differentiation requires methylation of specific asymmetric sites in host DNA by BrxX (PglX) methyltransferase. Here, we report that T7 bacteriophage Ocr, a DNA mimic protein that protects the phage from the defensive action of type I restriction-modification systems, is also active against BREX. In contrast to the wild-type phage, which is resistant to BREX defence, T7 lacking Ocr is strongly inhibited by BREX, and its ability to overcome the defence could be complemented by Ocr provided in trans. We further show that Ocr physically associates with BrxX methyltransferase. Although BREX+ cells overproducing Ocr have partially methylated BREX sites, their viability is unaffected. The result suggests that, similar to its action against type I R-M systems, Ocr associates with as yet unidentified BREX system complexes containing BrxX and neutralizes their ability to both methylate and exclude incoming phage DNA. © The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.Dominant mutations in the mitochondrial paralogs CHCHD2 (C2) and CHCHD10 (C10) were recently identified as causing Parkinson's disease and ALS/FTD/myopathy, respectively. The mechanism by which they disrupt mitochondrial cristae, however, has been uncertain. Using the first C2/C10 double knockout (DKO) mice, we report that C10 pathogenesis and the normal function of C2/C10 are intimately linked. Similar to patients with C10 mutations, we found that C2/C10 DKO mice have disrupted mitochondrial cristae, due to cleavage of the mitochondrial shaping protein L-OPA1 by the stress-induced peptidase OMA1. OMA1 was found to be activated similarly in affected tissues of mutant C10 knock-in (KI) mice, demonstrating that L-OPA1 cleavage is a novel mechanism for cristae abnormalities due to both C10 mutation and C2/C10 loss. Using OMA1 activation as a functional assay, we found that C2 and C10 are partially functionally redundant, and some but not all disease-causing mutations have retained activity. Finally, C2/C10 DKO mice partially phenocopied mutant C10 KI mice with the development of cardiomyopathy and activation of the mt-ISR in affected tissues, tying mutant C10 pathogenesis to C2/C10 function. Published by Oxford University Press 2020.
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