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Under the influence of development strategies with regard to national fitness and health in China, the interactive development between national fitness and national health is becoming increasingly strong. To explore the coupling and coordination relationship between national fitness and national health, this paper conducts an empirical analysis of the coupling and coordination relationship between national fitness and national health in 11 provinces and cities in Eastern China using the entropy weight method, a coupling coordination model, spatial visualization of the coupling coordination degree and spatial autocorrelation analysis. The research confirms that the comprehensive development level of national fitness and national health in Eastern China shows a steady upward trend, with a lag in national fitness as a whole, and that the growth rate of national fitness development is faster than that of national health development. The coupling coordination degree of the two systems of national fitness and national health in Eastern China shows a slow upward trend, and the coupling coordination degree rises from barely coordinated to primary coordination. There are significant differences in the spatial pattern of coupling coordination: the spatial pattern from north to south generally shows ‘low-high-high-low-high-low’ characteristics, and the spatial spillover effect of coupling coordination in various regions has not yet appeared. The revised GM(1.1) prediction results indicate that the level and improvement rate of coupling coordination will accelerate significantly in the next 10 years, but the spatial differences will still exist. Finally, suggestions are proposed to optimize the coupling and coordinated development of national fitness and national health based on policy guarantees as well as strengthening and cross-regional cooperation.

Purpose. Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common urological disorder. Although ferroptosis is closely associated with inflammation, oxidative stress, and neuropathic pain, its role in CP/CPPS has not yet been elucidated. Therefore, we sought to explore the role and mechanism of ferroptosis in the prostatitis development. Methods. The experimental autoimmune prostatitis (EAP) was established through intradermal immunization of prostate extract. Iron chelator deferoxamine (DFO) and free radical scavenger edaravone (EDA) were applied to evaluate the effects of ferroptosis inhibition on oxidative stress, ferroptosis, inflammation, fibrosis, and mast cell activation in the context of CP/CPPS. Results. Increased generation of lipid peroxidation products (ROS and MDA) and decreased activities of antioxidant enzymes (SOD and CAT) suggested an aberrant oxidative stress status in EAP model. Elevated iron concentration was observed in the EAP model. Meanwhile, we discovered significant biological performances associated with ferroptosis in CP/CPPS, including the downregulation of the system Xc-/GPX4 axis and the upregulation of the ACSL4/LPCAT3 axis. EAP rats performed serious leukocyte infiltration, advanced inflammatory grade, and abnormal expression of inflammatory mediators. Abundant collagen deposition, enhanced RhoA, ROCK1, and α-SMA protein levels indicated that EAP rats were prone to suffer from stromal fibrosis compared with control group. An elevated number of degranulated mast cells and corresponding marker TPSB2 represented that mast cell-sensitized pain was amplified in the EAP model. Furthermore, reduction of NRF2/HO-1 indicated a vulnerability of EAP towards ferroptosis response. However, application of DFO and EDA had partially reversed the adverse influences mentioned above. Conclusion. We first demonstrated that ferroptosis might be a crucial factor of chronic prostatitis progression. Inhibition of ferroptosis using DFO and EDA represented a promising approach for treating prostatitis by ameliorating inflammation, fibrosis, and mast cell activation.

Stability and scalability are essential and urgent requirements for the commercialization of perovskite solar cells (PSCs), which are retarded by the non‐ideal interface leading to non‐radiative recombination and degradation. Extensive efforts are devoted to reducing the defects at the perovskite surface. However, the effects of the buried interface on the degradation and non‐radiative recombination need to be further investigated. Herein, an omnibearing strategy to modify buried and top surfaces of perovskite film to reduce interfacial defects, by incorporating aluminum oxide (Al2O3) as a dielectric layer and growth scaffolds (buried surface) and phenethylammonium bromide as a passivation layer (buried and top surfaces), is demonstrated. Consequently, the open‐circuit voltage is extensively boosted from 1.02 to 1.14 V with the incorporation of Al2O3 filling the voids between grains, resulting in dense morphology of buried interface and reduced recombination centers. Finally, the impressive efficiencies of 23.1% (0.1 cm2) and 22.4% (1 cm2) are achieved with superior stability, which remain 96% (0.1 cm2) and 89% (1 cm2) of its initial performance after 1200 (0.1 cm2) and 2500 h (1 cm2) illumination, respectively. The dual modification provides a universal method to reduce interfacial defects, revealing a promising prospect in developing high‐performance PSCs and modules. The aluminum oxide (Al2O3) nanoparticles are imbedded into the buried interface, which fills the voids and grain boundaries of perovskite, leading to compact morphology and reduced dangling bonds and defects. The suppressed trap‐assisted recombination, better energy alignment, and decreased J–V hysteresis in the modified device with Al2O3 nanoparticles and phenethylammonium bromide contribute to a significant increase in voltage and stability.

As men age, a growing number develop benign prostatic hyperplasia (BPH). According to previous research, diabetes may be a risk factor. Pyruvate dehydrogenase kinase 4 (PDK4) is closely related to glucose metabolism and plays a role in the onset and progression of numerous illnesses. This study aimed to determine the direct effects of high glucose environment on prostate epithelial cells, in particular by altering PDK4 expression levels. In this investigation, normal prostatic epithelial cells (RWPE-1) and human benign prostatic hyperplasia epithelial cells (BPH-1) were treated with 50 mM glucose to show the alteration of high glucose in prostate cells. PDK4-target siRNA, PDK4-expression plasmid were used to investigate the effects of PDK4. Rosiglitazone (RG), a PPARγ agonist, with the potential to up-regulate PDK4 expression was also used for treating prostate cells. The expression of PDK4 in human prostate samples was also analyzed. The effects of high glucose therapy on BPH-1 and RWPE-1 cells were demonstrated to enhance proliferation, epithelial-mesenchymal transition (EMT), suppress apoptosis, and down-regulate PDK4 expression. Additionally, diabetes-related BPH patients had reduced PDK4 expression. Following the application of PDK4-target siRNA, a comparable outcome was seen. The PDK4-expression plasmid therapy, however, produced the opposite results. RG with the ability to elevate PDK4 expression might be used to treat BPH. Changes in the metabolism of lipids and glucose may be the cause of these consequences. These findings showed that high glucose treatment might facilitate BPH development, and may be related to the down-regulation of PDK4. PDK4 might be a potential therapeutic target of BPH.

Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin's anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-α [TNF-α, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt and translocation of NF-κB. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators release in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.

In-sensor computing is proposed to reduce energy expenditure and processing latency by unifying sensing and computation within the hardware layer, yet the application under extreme illuminating scenario remains constrained by simultaneously obtaining broadband responsivity, large linear dynamic range and fast response. Here, we report a fully vapor-deposited graded Pb-Sn alloyed perovskite heterojunction photodiode with improved crystal quality. It enables the detection of light from visible to infrared light with a 230 dB linear dynamic range and 33 ns response time. We also develop a wafer-scale imaging processor by integrating the photodiode to a reconfigurable array. With this approach, we demonstrate biomedical detection and spatiotemporal trajectory encoding. The in-sensor processor realizes low-power high-resolution visible to infrared wavelength edge detection, adaptive background suppression under dim light and noise-immune high-speed dynamic imaging. Our results extend the options for in-sensor computing hardware, and thus pave a way toward practical artificial intelligent machine vision. Zhan et al. report a fully vapor-deposited graded perovskite photodiode for visible-to-IR imaging with 230 dB linear dynamic range and 33 ns response time. Wafer-scale reconfigurable imaging processor is developed for edge detection, adaptive background suppression under dim light, and noise-immune high-speed dynamic imaging.

Background Bladder outlet obstruction (BOO), initiated by abnormal mechanical stress, leads to progressive bladder fibrosis and functional decompensation. Abnormal mechanical stress plays a key role in the pathogenesis of various diseases, including fibrosis. However, the mechanisms through which BOO-induced abnormal mechanical stress drives bladder fibrosis remain poorly understood. Recent studies have highlighted that Yes-associated protein 1 (YAP1) serves as a critical integrator of mechanical signals and metabolic alterations. Abnormal mechanical stress can promote disease progression by regulating metabolic enzymes such as glutaminase 1 (GLS1) through YAP1. Alterations in cellular behavior and disease progression induced by abnormal mechanical stress are closely linked to metabolic reprogramming. Targeting this metabolic reprogramming may effectively counteract the resulting cellular alterations and disease progression. Methods KEGG pathway enrichment was performed using RNA-seq data from a rat BOO model, and YAP1 expression was examined in human and rat bladder tissues. Fibroblasts were cultured under high hydrostatic pressure (HHP) to mimic BOO-induced stress, and YAP1 nuclear translocation and GLS1 expression were assessed by immunofluorescence and western blotting. Fibroblast proliferation, migration, and activation were measured via functional assays and fibrotic protein expression. To clarify the roles of Piezo1 and YAP1, we performed siRNA, inhibitor, and rescue experiments and evaluated their effects on GLS1, glutamine metabolism, and fibroblast activation. In vivo, bladder function and histology were assessed following GLS1 inhibition in BOO rats. Results YAP1 expression was significantly increased in human and rat bladders with BOO. HHP enhanced nuclear translocation of YAP1 and upregulated GLS1. HHP stimulation also promoted fibroblast proliferation, migration, and activation. Under HHP, Piezo1 acted as the upstream mechanotransducer that activated YAP1, which in turn induced GLS1 expression. Inhibition of Piezo1 or YAP1 reduced GLS1 expression, and blockade of this axis suppressed fibroblast activation in vitro. HHP-induced fibroblast activation relied on GLS1-driven glutamine metabolic reprogramming, and pharmacological blockade of GLS1 effectively attenuated fibrosis and improved bladder function in BOO rats. Conclusions This study identifies a Piezo1/YAP1/GLS1 axis linking mechanical stress to metabolic reprogramming and fibroblast activation in BOO, which may serve as a therapeutic target to prevent fibrosis and preserve bladder function.

Chronic prostatic inflammation promotes cell survival and fibrosis, leading to benign prostatic hyperplasia (BPH) with aggravated urinary symptoms. It is investigated whether yes‐associated protein 1 (YAP1), an organ size controller and mechanical transductor, is implicated in inflammation‐induced BPH. The correlation between YAP1 expression and fibrosis in human and rat BPH specimens is analyzed. Furthermore, the effects of YAP1 activation on prostatic cell survival and fibrosis, as well as the underlying mechanism, are also studied. As a result, total and nuclear YAP1 expression, along with downstream genes are significantly upregulated in inflammation‐associated human and rat specimens. There is a significant positive correlation between YAP1 expression and the severity of fibrosis or clinical performance. YAP1 silencing suppresses cell survival by decreasing cell proliferation and increasing apoptosis, and alleviates fibrosis by reversing epithelial‐mesenchymal transition (EMT) and extracellular matrix (ECM) deposition in prostatic BPH‐1 and WPMY‐1 cells. Mechanistically, inflammatory stimulus and rigid matrix stiffness synergistically activate the RhoA/ROCK1 pathway to provoke cytoskeleton remodeling, thereby promoting YAP1 activation to exacerbate BPH development. Overall, inflammation‐triggered mechanical stiffness reinforcement activates the RhoA/ROCK1/F‐actin/YAP1 axis, thereby promoting prostatic cell survival and fibrosis to accelerate BPH progression. Chronic inflammation promotes activation of the RhoA/ROCK1 pathway and facilitates YAP1 nuclear translocation to interact with TEAD1, thereby promoting cell survival and fibrosis. The fibrotic microenvironment reinforces mechanical stiffness and, in combination with inflammatory stimulus, synergistically promotes cytoskeleton‐dependent YAP1 reactivation. Targeting YAP1 may represent a promising approach to break the vicious cycle and alleviate inflammation‐associated benign prostatic hyperplasia (BPH) progression.

Background Long noncoding RNAs (lncRNAs) and N6-methyladenosine (m6A) modification of RNA play pivotal roles in tumorigenesis and cancer progression. However, knowledge regarding the expression patterns of m6A-related lncRNAs and their corresponding m6A regulators in prostate cancer (PCa) is limited. This study aimed to delineate the landscape of m6A-related lncRNAs, develop a predictive model, and identify the critical m6A regulators of prognostic lncRNAs in PCa. Methods Clinical and transcriptome data of PCa patients were downloaded from The Cancer Genome Atlas (TCGA) database. Prognostic m6A-related lncRNAs were subsequently identified through Pearson correlation and univariate Cox regression analyses. The prognostic lncRNAs were clustered into two groups by consensus clustering analysis, and a risk signature model was constructed using least absolute shrinkage and selection operator (LASSO) regression analysis of the lncRNAs. This model was evaluated using survival, clinicopathological, and immunological analyses. Furthermore, based on the constructed lncRNA-m6A regulatory network and RT-qPCR results, RBM15 was identified as a critical regulator of m6A-related lncRNAs. The biological roles of RBM15 in PCa were explored through bioinformatics analysis and biological experiments. Results Thirty-four prognostic m6A-related lncRNAs were identified and categorized into two clusters with different expression patterns and survival outcomes in PCa patients. Seven m6A lncRNAs (AC105345.1, AL354989.1, AC138028.4, AC022211.1, AC020558.2, AC004076.2, and LINC02666) were selected to construct a risk signature with robust predictive ability for overall survival and were correlated with clinicopathological characteristics and the immune microenvironment of PCa patients. Among them, LINC02666 and AC022211.1 were regulated by RBM15. In addition, RBM15 expression correlated with PCa progression, survival, and the immune response. Patients with elevated RBM15 expression were more susceptible to the drug AMG-232. Moreover, silencing RBM15 decreased the viability of PCa cells and promoted apoptosis. Conclusion RBM15 is involved in the regulation of prognostic lncRNAs in the risk signature and has a robust predictive ability for PCa, making it a promising biomarker in PCa.

Mechanisms of DNA repair and mutagenesis are defined on the basis of relatively few proteins acting on DNA, yet the identities and functions of all proteins required are unknown. Here, we identify the network that underlies mutagenic repair of DNA breaks in stressed Escherichia coli and define functions for much of it. Using a comprehensive screen, we identified a network of ≥93 genes that function in mutation. Most operate upstream of activation of three required stress responses (RpoS, RpoE, and SOS, key network hubs), apparently sensing stress. The results reveal how a network integrates mutagenic repair into the biology of the cell, show specific pathways of environmental sensing, demonstrate the centrality of stress responses, and imply that these responses are attractive as potential drug targets for blocking the evolution of pathogens.