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Shared genetic architecture of posttraumatic stress disorder with cardiovascular imaging, risk, and diagnoses
Understanding deinstitutionalization policies for older adults through sarcopenia and the place of aging in Spain
Adaptive neuro-fuzzy inference system optimization of natural rubber latex modified concrete’s mechanical Properties
Subglottic imaging puncture scope (SIPS) for minimally invasive endoscopy
Impact of prenatal Di(2-ethylhexyl) phthalate exposure on pubertal development in female offspring rats: A focus on ERα-Mediated IGF-1/NKB crosstalk in the hypothalamus
Measurement of the Poisson expansion effect on crack openings in self-sensing concrete
Abstract Concrete infrastructure tends to degrade with extended service life, but detecting deterioration with conventional inspection methods can be challenging. Existing approaches such as developing self-sensing concrete by adding electrically conductive fillers to the cement matrix often suffer from high costs and complex manufacturing processes for casting the concrete from fresh. This study looks beyond the commonly discussed resistance-based and capacitance-based self-sensing mechanisms in the elastic deformation regime of the concrete and investigates the changes in electrical conductivity due to micro-crack opening through Poisson expansion by utilising the measurement technique of drilling the concrete to insert conductive epoxy for electrode embedment to achieve intrinsic self-sensing on as-built regular concrete (i.e. without conductive fillers). Experimental results on existing plain concrete samples showed a good correlation between the compressive load and the fractional change in resistivity (FCR). Finite element analysis (FEA) was then used to further investigate the effect of changes in conductivity in the direction of loading and orthogonal directions on the measured electrical behaviour of the concrete. Results showed that the correlation between the FCR and the compressive load depends on the relationship between the load-parallel and -orthogonal gauge factors. Beyond a threshold level, the electrical signal picked up by the electrodes reflects the material’s behaviour in the direction orthogonal to the loading direction due to Poisson expansion. Further numerical simulation has suggested that to achieve a stable measurement, the electrodes’ penetration should equal the spacing.
Polarization filtering with isomaterial multifocal metalenses at ultraviolet frequencies
Deep learning model for hair artifact removal and Mpox skin lesion analysis and detection
Solitary waves, bifurcation, chaos, sensitivity, and multistability of electrical transmission line model
The effects of social media criticism against public health institutions on trust, emotions, and social media engagement
In recent years, trust in US public health and science institutions has faced unprecedented declines, particularly among Republicans/conservatives. To what extent might institutional criticism on social media be responsible for such politically polarized declines in institutional trust? Two online survey experiments (total N = 6,800), using samples roughly reflective of the US adult population, examined the effects of key types of criticism against the Agency for Healthcare Research and Quality (AHRQ) and the Centers for Disease Control and Prevention (CDC). The results suggest that just a single exposure to any of the key types of criticism was sufficient to undermine institutional trust. While an institutional rebuttal was partially able to reverse these effects, residual declines in trust were substantial enough to cause decreased intentions to adhere to the AHRQ/CDC health recommendation featured in the experiments. While institutions should, therefore, be concerned about all types of social media criticism, those featuring morally charged trust-undermining narratives attacking the integrity of the AHRQ/CDC generated dramatically more anger (i.e., moral outrage), which in turn attracted social media engagement preferences likely to promote viral spread and exacerbate preexisting institutional politicization and issue polarization. These results suggest that efforts to bolster institutional trust should pay special attention to criticisms featuring integrity-based trust-undermining narratives.
Flow-induced 2D nanomaterials intercalated aligned bacterial cellulose
Brain region-specific gain modulation of place cells by VIP neurons
A ferritin-targeted biohybrid triggering ferroptosis immunotherapy via activating endogenous iron and replenishing exogenous iron simultaneously
Organic Cage Encapsulated Within Metal Cluster‐Based Open Frameworks: A Single‐Crystal Host‐in‐Host Material with Inter‐Host Charge Cooperation
Abstract Integrating dissimilar building units of discrete organic cages and inorganic clusters into single‐crystal supramolecular frameworks with tailored architectures and synergistic functions presents a significant challenge. Here, we presented our discovery of achieving such hybrids through electrostatically driven self‐assembly of cationic ammonium organic cages with anionic lead iodide clusters. Notably, by carefully modulating the size, shape, and composition of cationic organic cages, we have constructed an integrated porous host‐in‐host architecture. In this system, the internal cationic cage snugly resided, encapsulated within the external network constructed from anionic lead iodide clusters. This unique nested hierarchy showcased enhanced interhost interactions facilitated by electrostatic forces, which intricately tailored the electronic structure of the outer lead iodide moiety. As a result, the hybrid demonstrated distinguished photophysical properties, including efficient oxygen activation and enhanced photothermal conversion capability, as confirmed by comprehensive experimental and theoretical analyses. The critical role of interhost electrostatic interactions was further demonstrated through a systematic comparison with a structurally similar host‐in‐host architecture comprising lead iodide clusters and neutral amine cages. Furthermore, the integrated and compartmentalized dual‐host served as spatially isolated dual active sites for cascade reactions, exhibiting 33–47‐folds enhancement in activity compared to structural counterparts lacking charge cooperation.
The impact of total joint arthroplasty on arterial stiffness in osteoarthritis patients: a 7-year prospective cohort study (CAMERA study)
Enhancing education quality with hybrid clustering and evolutionary neural networks in a multi phase framework
Feasibility of long-read sequencing to identify molecular alterations in an Indonesian cohort of locally advanced to advanced nasopharyngeal cancer
LncRNA CTD-2555A7.2 promotes bone formation with LncRNA-specific cascade amplification strategy
Abstract Osteoporosis poses a significant threat to human health. Long non-coding RNAs (LncRNAs) have been deemed as crucial regulators in the pathogenesis of osteoporosis. However, the accuracy and efficiency of LncRNA-mediated regulation of bone formation require further improvement. Our previous study identified a repeat sequence in the human-derived LncRNA CTD-2555A7.2, suggesting its potential role in osteoporosis regulation. To investigate this hypothesis, we conducted systematic functional analyses of CTD-2555A7.2 in osteogenesis and explored its mechanisms and potential therapeutic applications. Through over-expression, siRNA silencing and repeat sequence over-expression in vitro and in vivo, our research demonstrate that CTD-2555A7.2 enhances bone formation by sequestering multiple miR-381-3p molecules through its repeat sequence. Through Western blot, siRNA silencing and luciferase reporter assay, we illuminated miR-381-3p suppresses osteogenic differentiation by concurrently targeting four essential genes of the Wnt signaling pathway: Apc , Lef1 , wnt5a , and Lrp6 . Notably, the mRNA of CTD-2555A7.2 repeat sequence exhibited pronounced therapeutic efficacy in ovariectomy osteoporosis models. Taken together, we identified a dual-amplification osteogenic axis (CTD-2555A7.2-miR-381-Wnt) that demonstrates significant regulatory effects on osteoporosis. This study has established an important theoretical framework for understanding osteogenic LncRNA mechanisms and provides novel insights for developing targeted therapeutics against osteoporosis.
Genetic association analysis between LDL-c lowering drugs and portal hypertension using Mendelian randomization analysis
Abstract Clinical guidelines recommend the use of statins to reduce portal pressure and alleviate portal hypertension (PH). However, there is a lack of population-level studies on the use of non-statin Low-Density Lipoprotein Cholesterol (LDL-c) reduction agents for the treatment of PH. This study utilized a novel method, Mendelian Randomization (MR) analysis, to investigate the impact of commonly used LDL-c-lowering medications on PH. Instrumental variables (IVs) for eight lipid-lowering drug-related genes were extracted from three large-scale LDL-c databases of Genome-Wide Association Studies (GWAS), followed by MR analysis. The MR results indicated that, compared to normal individuals, lower expression of CETP and NPC1L1 in whole blood (result of meta-analysis: CETP [OR: 0.322, 95%CI:0.130–0.795, P = 1.396e-02], NPC1L1 [OR: 0.057, 95%CI: 0.022–0.146, P = 2.670e-09]) is associated with reduced portal pressure. The IVs of target genes were subjected to MR analysis with coronary atherosclerosis (CAD) as a positive control, confirming that the IVs can effectively substitute for the biological function of the target gene, thereby further enhancing the reliability of the results. Subsequently, Summary-based Mendelian Randomization (SMR) analysis was conducted by using expression quantitative trait loci (eQTL) data to validate the results of the MR analysis. The SMR results suggested that only NPC1L1 is associated with PH (OR: 0.648, 95%CI: 0.472–0.891, P SMR = 7.502e-3, P HEIDI = 0.747) from genetic correlation. Additionally, mediation analysis indicates that the therapeutic effect of NPC1L1 inhibitors on PH is partially mediated by tissue factor (mediating effect accounted for 18.52%, and the P value was 0.01). Phenome-Wide MR indicated that NPC1L1 inhibitors may be associated with 23 diseases or symptoms. In addition, NPC1L1 had genetic correlation between and alkaline phosphatase as well as total bilirubin, but no genetic correlation with alanine aminotransferase, aspartate aminotransferase, direct bilirubin, or gamma glutamyltransferase. In conclusion, this study systematically analyzed the genetic correlation between lipid-lowering drug targets and PH. From a genetic correlation perspective, we revealed that the potential therapeutic effect of NPC1L1 on PH may not be mediated through the reduction of LDL-c but rather through the modulation of tissue factors. Additionally, the potential side effects associated with NPC1L1 inhibition also were explored.