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An update on active and passive surveillance for African swine fever in the Dominican Republic
A multiprotein regulatory module, MED16–MBR1&2, controls MED25 homeostasis during jasmonate signaling
Efficient IP address retrieval using a novel octet based encoding technique for high speed lookup to improve network performance
Cola beverage reduces risk of lead poisoning from accidental ingestion of contaminated soil particles in rat and swine models
Understanding rangeland desertification through pastoralist perspectives using a grounded theory approach
Nr4a1 and Nr4a3 redundantly control clonal deletion and contribute to an anergy-like transcriptome in auto-reactive thymocytes to impose tolerance in mice
Abstract The Nr4a nuclear hormone receptors are transcriptionally upregulated in response to antigen recognition by the T cell receptor (TCR) in the thymus and are implicated in clonal deletion, but the mechanisms by which they operate are not clear. Moreover, their role in central tolerance is obscured by redundancy among the Nr4a family members and by their reported functions in Treg generation and maintenance. Here we take advantage of competitive bone marrow chimeras and the OT-II/RIPmOVA model to show that Nr4a1 and Nr4a3 are essential for the upregulation of Bcl2l11/BIM and thymic clonal deletion by self-antigen. Importantly, thymocytes lacking Nr4a1/3 acquire an anergy-like signature after escaping clonal deletion and Treg lineage diversion. We further show that the Nr4a family helps mediate a broad transcriptional program in self-reactive thymocytes that resembles anergy and may operate at the margins of canonical thymic tolerance mechanisms to restrain self-reactive T cells after thymic egress.
Understanding the role of metabolic syndrome in prostate cancer risk: A UK Biobank prospective cohort study
High-performance solid-state proton gating membranes based on two-dimensional hydrogen-bonded organic framework composites
Weave structures of polyester fabric affect the tensile strength and microplastic fiber emission during the laundry process
Increased arterial stiffness is associated with poorer social cognition in older age
Abstract It is now well established that vascular aging is a significant predictor of cognitive decline in older age. But what remains less clear is the role that vascular health plays in social cognitive aging. Therefore, we aimed to provide the first test of the relationship between arterial stiffness and theory of mind (ToM) in late adulthood. In a sample of 50 healthy older adults (Age: M = 70.08, SD = 3.93), we measured arterial stiffness via carotid-femoral pulse wave velocity and social cognition using two well validated measures of ToM (RMET, TASIT). The results revealed that arterial stiffness was a significant predictor of ToM performance when indexed via the RMET and the TASIT, accounting for 11% and 9% of unique variance in scores, respectively. These findings add to the broader literature showing that arterial stiffness is a key predictor of cognitive aging and show that this relationship extends to the domain of social cognition.
Association between serum uric acid levels and left ventricular hypertrophy based on electrocardiographic findings: a sex-specific analysis across cardiometabolic diseases
Probabilistic assessment of the cumulative risk from dietary heavy metal exposure in Chongqing, China using a hazard-driven approach
The association between metabolomic profiles of lifestyle and the latent phase of incident chronic kidney disease in the UK Population
Zeta Potential Change and curing effects on Shield Muck solidified by Metal Ion Complex Catalysis
Comprehensive benefits evaluation of low impact development using scenario analysis and fuzzy decision approach
Molecular dynamics simulation of film water thickness and properties at different interfaces in partially saturated frozen soil systems
20-HETE mediates Ang II-induced cardiac hypertrophy via ROS and Ca2+ signaling in H9c2 cells
Abstract In the vascular system, angiotensin II (Ang II) mediated vasoconstriction by inducing the production of 20-hydroxyeicosatetraenoic acid (20-HETE). However, the role of 20-HETE in Ang II-induced cardiac dysfunction had yet to be fully elucidated. This study investigated the effects of Ang II on CYP4A expression and 20-HETE production in H9c2 cells using RT-qPCR, Western blot, and ELISA. The role of 20-HETE in Ang II-induced cardiac hypertrophy was examined using DHE, MitoSOX, and JC-1 staining to evaluate reactive oxygen species (ROS) generation and mitochondrial membrane potential changes. The ERK/Akt and CaN/NFAT3 signaling pathways were analyzed through Western blot. Ang II was found to promote CYP4A expression and 20-HETE production in H9c2 cells via an AT1 receptor-dependent mechanism. Additionally, the upregulation of AT1 receptor expression by 20-HETE further confirms its facilitatory effect on the Ang II signaling pathway. Inhibition of 20-HETE synthesis or blockade of its receptor, G-protein-coupled receptor 75 (GPR75), significantly reversed Ang II-induced cardiac hypertrophy. This reversal was closely associated with 20-HETE-induced ROS production, oxidative stress, and activation of the Ca2+/CaN/NFAT3 signaling pathway. This study demonstrated that 20-HETE mediated Ang II-induced cardiac hypertrophy and, for the first time, highlighted the significant role of the GPR75 receptor in this process. These findings suggested that targeting 20-HETE reduction or blocking its receptor action could offer a novel therapeutic approach for cardiovascular diseases associated with Ang II.
Role of transforming growth factor-β1 in regulating adipocyte progenitors
Inflammatory biomarkers profiles and cognition among older adults
Abstract Inflammation plays a major role in cognitive aging. Most studies on peripheral inflammation and cognitive aging focused on selected major inflammatory biomarkers. However, inflammatory markers are regulated and influenced by each other, and it is therefore important to consider a more comprehensive panel of markers to better capture diverse immune pathways and characterize the overall inflammatory profile of individuals. We explored 23 circulating inflammatory biomarkers using data from 1,743 participants without dementia (≥ 65 years-old) from the community-based, multiethnic Washington Heights Inwood Columbia Aging Project. Using principal component analysis (PCA), we developed six inflammatory profiles (PC-1 to PC-6) based on these 23 biomarkers and tested the association of resulting inflammatory profile with cognitive decline, over up to 12 years of follow-up. PC-1 described a pro-inflammatory profile characterized by high positive loadings for pro-inflammatory biomarkers. A higher PC-1 score was associated with lower baseline cognitive performances. No association of this profile with cognitive decline was observed in longitudinal analysis. However, PC-5 characterized by high PDGF-AA and RANTES was associated with a faster cognitive decline. Among older adults, a circulating pro-inflammatory immune profile is associated with lower baseline cognitive performance, and some specific pro-inflammatory cytokines might be associated with faster cognitive decline.