Guldbrandsenfriedman3184

ter stroke by restoring blood flow to peri-infarct cortex.

The coronavirus disease 2019 (COVID-19) pandemic has fueled xenophobia against Chinese Americans. We examined the rates of 6 types of COVID-19 racism and racial discrimination experienced by Chinese American parents and youth and the associations with their mental health.

We recruited a population-based sample of Chinese American families to participate in this self-reported survey study conducted from March 14, 2020, to May 31, 2020. Eligible parent participants identified as ethnically/racially Chinese, lived in the United States, and had a 4- to 18-year-old child; their eligible children were 10 to 18 years old.

The sample included 543 Chinese American parents (mean [SD] age, 43.44 [6.47] years; 425 mothers [78.3%]), and their children (

= 230; mean [SD] age, 13.83 [2.53] years; 111 girls [48.3%]). Nearly half of parents and youth reported being directly targeted by COVID-19 racial discrimination online (parents 172 [31.7%]; youth 105 [45.7%]) and/or in person (parents 276 [50.9%]; youth 115 [50.2%]). A total of 417 (76.8%) parents and 176 (76.5%) youth reported at least 1 incident of COVID-19 vicarious racial discrimination online and/or in person (parents 481 [88.5%]; youth 211 [91.9%]). A total of 267 (49.1%) parents and 164 (71.1%) youth perceived health-related Sinophobia in America, and 274 (50.4%) parents and 129 (56.0%) youth perceived media-perpetuated Sinophobia. Higher levels of parent- and youth-perceived racism and racial discrimination were associated with their poorer mental health.

Health care professionals must attend to the racism-related experiences and mental health needs of Chinese Americans parents and their children throughout the COVID-19 pandemic via education and making appropriate mental health referrals.

Health care professionals must attend to the racism-related experiences and mental health needs of Chinese Americans parents and their children throughout the COVID-19 pandemic via education and making appropriate mental health referrals.Trypanosome U-insertion/deletion RNA editing in mitochondrial mRNAs involves guide RNAs (gRNAs) and the auxiliary RNA editing substrate binding complex (RESC) and RNA editing helicase 2 complex (REH2C). EHT 1864 supplier RESC and REH2C stably copurify with editing mRNAs but the functional interplay between these complexes remains unclear. Most steady-state mRNAs are partially edited and include misedited "junction" regions that match neither pre-mRNA nor fully edited transcripts. Editing specificity is central to mitochondrial RNA maturation and function, but its basic control mechanisms remain unclear. Here we applied a novel nucleotide-resolution RNA-seq approach to examine ribosomal protein subunit 12 (RPS12) and ATPase subunit 6 (A6) mRNA transcripts. We directly compared transcripts associated with RESC and REH2C to those found in total mitochondrial RNA. RESC-associated transcripts exhibited site-preferential enrichments in total and accurate edits. REH2C loss-of-function induced similar substrate-specific and site-specific editing effects in total and RESC-associated RNA. It decreased total editing primarily at RPS12 5' positions but increased total editing at examined A6 3' positions. REH2C loss-of-function caused site-preferential loss of accurate editing in both transcripts. However, changes in total or accurate edits did not necessarily involve common sites. A few 5' nucleotides of the initiating gRNA (gRNA-1) directed accurate editing in both transcripts. However, in RPS12, two conserved 3'-terminal adenines in gRNA-1 could direct a noncanonical 2U-insertion that causes major pausing in 3'-5' progression. In A6, a noncanonical sequence element that depends on REH2C in a region normally targeted by the 3' half of gRNA-1 may hinder early editing progression. Overall, we defined transcript-specific effects of REH2C loss.Stress granules (SGs) and processing bodies (PBs) are membraneless ribonucleoprotein-based cellular compartments that assemble in response to stress. SGs and PBs form through liquid-liquid phase separation that is driven by high local concentrations of key proteins and RNAs, both of which dynamically shuttle between the granules and the cytoplasm. SGs uniquely contain certain translation initiation factors and PBs are uniquely enriched with factors related to mRNA degradation and decay, although recent analyses reveal much broader protein commonality between these granules. Despite detailed knowledge of their composition and dynamics, the function of SGs and PBs remains poorly understood. Both, however, contain mRNAs, implicating their assembly in the regulation of RNA metabolism. SGs may also serve as hubs that rewire signaling events during stress. By contrast, PBs may constitute RNA storage centers, independent of mRNA decay. The aberrant assembly or disassembly of these granules has pathological implications in cancer, viral infection and neurodegeneration. Here, we review the current concepts regarding the formation, composition, dynamics, function and involvement in disease of SGs and PBs.Triacylglycerols are the main constituent of seed oil. The specific fatty acid composition of this oil is strongly impacted by the substrate specificities of acyltransferases involved in lipid synthesis, such as the integral membrane enzyme diacylglycerol acyltransferase (DGAT). Two forms of DGAT, DGAT1 and DGAT2, are thought to contribute to the formation of seed oil, and previous characterizations of various DGAT2 enzymes indicate that these often are associated with the incorporation of unusual fatty acids. However, the basis of DGAT2's acyl-donor specificity is not known because of the inherent challenges of predicting structural features of integral membrane enzymes. The recent characterization of DGAT2 enzymes from Brassica napus reveals that DGAT2 enzymes with similar amino acid sequences exhibit starkly contrasting acyl-donor specificities. Here we have designed and biochemically tested a range of chimeric enzymes, substituting parts of these B. napus DGAT2 enzymes with each other, allowing us to pinpoint a region that dramatically affects the specificity toward 221-CoA. It may thus be possible to redesign the acyl-donor specificity of DGAT2 enzymes, potentially altering the fatty acid composition of seed oil. Further, the characterization of a DGAT2 chimera between Arabidopsis and B. napus demonstrates that the specificity regulated by this region is transferrable across species. The identified region contains two predicted transmembrane helices that appear to reoccur in a wide range of plant DGAT2 orthologues, suggesting that it is a general feature of plant DGAT2 enzymes.Short tandemly repeated DNA sequences, termed microsatellites, are abundant in the human genome. These microsatellites exhibit length instability and susceptibility to DNA double-strand breaks (DSBs) due to their tendency to form stable non-B DNA structures. Replication-dependent microsatellite DSBs are linked to genome instability signatures in human developmental diseases and cancers. To probe the causes and consequences of microsatellite DSBs, we designed a dual-fluorescence reporter system to detect DSBs at expanded (CTG/CAG) n and polypurine/polypyrimidine (Pu/Py) mirror repeat structures alongside the c-myc replication origin integrated at a single ectopic chromosomal site. Restriction cleavage near the (CTG/CAG)100 microsatellite leads to homology-directed single-strand annealing between flanking AluY elements and reporter gene deletion that can be detected by flow cytometry. However, in the absence of restriction cleavage, endogenous and exogenous replication stressors induce DSBs at the (CTG/CAG)100 and Pu/Py microsatellites. DSBs map to a narrow region at the downstream edge of the (CTG)100 lagging-strand template. (CTG/CAG) n chromosome fragility is repeat length-dependent, whereas instability at the (Pu/Py) microsatellites depends on replication polarity. Strikingly, restriction-generated DSBs and replication-dependent DSBs are not repaired by the same mechanism. Knockdown of DNA damage response proteins increases (Rad18, polymerase (Pol) η, Pol κ) or decreases (Mus81) the sensitivity of the (CTG/CAG)100 microsatellites to replication stress. Replication stress and DSBs at the ectopic (CTG/CAG)100 microsatellite lead to break-induced replication and high-frequency mutagenesis at a flanking thymidine kinase gene. Our results show that non-B structure-prone microsatellites are susceptible to replication-dependent DSBs that cause genome instability.Recent proteomics studies of vertebrate striated muscle have identified lysine acetylation at several sites on actin. Acetylation is a reversible post-translational modification that neutralizes lysine's positive charge. Positively charged residues on actin, particularly Lys326 and Lys328, are predicted to form critical electrostatic interactions with tropomyosin (Tpm) that promote its binding to filamentous (F)-actin and bias Tpm to an azimuthal location where it impedes myosin attachment. The troponin (Tn) complex also influences Tpm's position along F-actin as a function of Ca2+ to regulate exposure of myosin-binding sites and, thus, myosin cross-bridge recruitment and force production. Interestingly, Lys326 and Lys328 are among the documented acetylated residues. Using an acetic anhydride-based labeling approach, we showed that excessive, nonspecific actin acetylation did not disrupt characteristic F-actin-Tpm binding. link2 However, it significantly reduced Tpm-mediated inhibition of myosin attachment, as reflected by increased F-actin-Tpm motility that persisted in the presence of Tn and submaximal Ca2+ Furthermore, decreasing the extent of chemical acetylation, to presumptively target highly reactive Lys326 and Lys328, also resulted in less inhibited F-actin-Tpm, implying that modifying only these residues influences Tpm's location and, potentially, thin filament regulation. To unequivocally determine the residue-specific consequences of acetylation on Tn-Tpm-based regulation of actomyosin activity, we assessed the effects of K326Q and K328Q acetyl (Ac)-mimetic actin on Ca2+-dependent, in vitro motility parameters of reconstituted thin filaments (RTFs). Incorporation of K328Q actin significantly enhanced Ca2+ sensitivity of RTF activation relative to control. Together, our findings suggest that actin acetylation, especially Lys328, modulates muscle contraction via disrupting inhibitory Tpm positioning.The deep relationship between plants and humans predates civilization, and our reliance on plants as sources of food, feed, fiber, fuels, and pharmaceuticals continues to increase. Understanding how plants grow and overcome challenges to their survival is critical for using these organisms to meet current and future demands for food and other plant-derived materials. link3 This thematic review series on "plants in the real world" presents a set of eight reviews that highlight advances in understanding plant health, including the role of thiamine (vitamin B1), iron, and the plant immune system; how plants use ethylene and ubiquitin systems to control growth and development; and how new gene-editing approaches, the redesign of plant cell walls, and deciphering herbicide resistance evolution can lead to the next generation of crops.