Short-term association of particulate matter and cardiovascular disease mortality in Shanghai, China between 2003 and 2020.

Objective: Evidence regarding the effects of particulate matter (PM) pollutants on cardiovascular disease (CVD) mortality remains limited in Shanghai, China. Our objective was to thoroughly evaluate associations between PM pollutants and CVD mortality. Methods: Daily data on CVD mortality, PM (PM10 and PM2.5) pollutants, and meteorological variables in Shanghai, China were gathered from 2003 to 2020. We utilized a time-series design with the generalized additive model to assess associations between PM pollutants and CVD mortality. Additionally, we conducted stratified analyses based on sex, age, education, and seasons using the same model. Results: We found that PM pollutants had a significant association with CVD mortality during the study period. Specifically, there was a 0.29% (95%CI: 0.14, 0.44) increase in CVD mortality for every 10 µg/m3 rise in a 2-day average (lag01) concentration of PM10. A 0.28% (95% CI: 0.07, 0.49) increase in CVD mortality was associated with every 10 µg/m3 rise in PM2.5 concentration at lag01. Overall, the estimated effects of PM10 and PM2.5 were larger in the warm period compared with the cold period. Furthermore, males and the older adult exhibited greater susceptibility to PM10 and PM2.5 exposure, and individuals with lower education levels experienced more significant effects from PM10 and PM2.5 than those with higher education levels. Conclusion: Our findings suggested that PM pollutants have a substantial impact on increasing CVD mortality in Shanghai, China. Moreover, the impacts of air pollution on health may be altered by factors such as season, sex, age, and educational levels.

Immune responses induced by Mycobacterium tuberculosis heat-resistant antigen (Mtb-HAg) upon co-administration with Bacillus Calmette-Guérin in mice.

OBJECTIVES: To preliminarily assess the immunogenicity of Mtb-HAg in mice and the synergistic effect provided by HAg when co-immunised with BCG. METHODS: Mice were randomly grouped for different immunisations and then spleens were aseptically removed and lymphocytes were extracted for immediate detection of cytokines transcript levels and stimulation index(SI), cytokine secretion and multifunctional antigen-specific T cells were detected after incubation for different times. RESULTS: HAg extracted from active Mtb is a group of mixed polypeptides with molecular weights of (10-14) kDa. It can significantly stimulate lymphocytes proliferation and increase SI. Injection of HAg alone and in combination with BCG induced significantly higher numbers of multifunctional antigen-specific T cells including CD4+ IFN-γ+, CD4+ IL-2+, CD8+ IFN-γ+, and CD8+ IL-2+ cells than that in BCG-treated mice. Co-immunisation induced the secretion of higher levels of IFN-γ, TNF-α, IL-2 and IL-4 and increased their mRNA expression levels. Significant increases in the transcription levels of IL-10, IL-12 and IL-17 were observed in the co-immunised group with the assistance of HAg. CONCLUSION: We demonstrated that HAg has favourable immunogenicity, triggers a stronger Th1-type immune response and proposed the hypothesis that HAg can be used as a BCG booster to further enhance the benefits of BCG.

Loss-of-function mutation in PRMT9 causes abnormal synapse development by dysregulation of RNA alternative splicing.

Protein arginine methyltransferase 9 (PRMT9) is a recently identified member of the PRMT family, yet its biological function remains largely unknown. Here, by characterizing an intellectual disability associated PRMT9 mutation (G189R) and establishing a Prmt9 conditional knockout (cKO) mouse model, we uncover an important function of PRMT9 in neuronal development. The G189R mutation abolishes PRMT9 methyltransferase activity and reduces its protein stability. Knockout of Prmt9 in hippocampal neurons causes alternative splicing of ~1900 genes, which likely accounts for the aberrant synapse development and impaired learning and memory in the Prmt9 cKO mice. Mechanistically, we discover a methylation-sensitive protein-RNA interaction between the arginine 508 (R508) of the splicing factor 3B subunit 2 (SF3B2), the site that is exclusively methylated by PRMT9, and the pre-mRNA anchoring site, a cis-regulatory element that is critical for RNA splicing. Additionally, using human and mouse cell lines, as well as an SF3B2 arginine methylation-deficient mouse model, we provide strong evidence that SF3B2 is the primary methylation substrate of PRMT9, thus highlighting the conserved function of the PRMT9/SF3B2 axis in regulating pre-mRNA splicing.

SIRT1 coordinates transcriptional regulation of neural activity and modulates depression-like behaviors in the nucleus accumbens.

BACKGROUND: Major depression and anxiety disorder are significant causes of disability and socio-economic burden. Despite the prevalence and considerable impact of these affective disorders, their pathophysiology remains elusive. Thus, there is an urgent need to develop novel therapeutics for these conditions. We evaluated the role of SIRT1 in regulating dysfunctional processes of reward by using chronic social defeat stress (CSDS) to induce depression- and anxiety-like behaviors. CSDS induces physiological and behavioral changes that recapitulate depression-like symptomatology and alters gene expression programs in the nucleus accumbens, yet cell type-specific changes in this critical structure remain largely unknown. METHODS: We examined transcriptional profiles of D1-MSNs lacking deacetylase activity of SIRT1 by RNA sequencing (RNA-Seq) in a cell-type specific manner using the RiboTag line of mice. We analyzed differentially expressed genes using gene ontology tools including SynGO and EnrichR, and further demonstrated functional changes in D1-MSN specific SIRT1-KO mice using electrophysiological and behavioral measurements. RESULTS: RNAseq revealed altered transcriptional profiles of D1-MSNs lacking functional SIRT1 and showed specific changes in synaptic genes including glutamatergic and GABAergic receptors in D1-MSNs. These molecular changes may be associated with decreased excitatory and increased inhibitory neural activity in Sirt1-KO D1-MSNs, accompanied by morphological changes. Moreover, the D1-MSN-specific Sirt1-KO mice exhibited pro-resilient changes in anxiety- and depression-like behaviors. CONCLUSIONS: SIRT1 coordinates excitatory and inhibitory synaptic genes to regulate GABAergic output tone of D1-MSNs. These findings reveal a novel signaling pathway that has the potential for the development of innovative treatments for affective disorders.

CXCL4:NLRP3-mediated pyroptosis product that regulates cardiac fibrosis.

Severe myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. NOD-like receptor protein 3 (NLRP3) inflammation is involved in the development of myocarditis and is closely related to the form of cell death. Inhibiting pyroptosis mediated by NLRP3 inflammasome can reduce cardiac fibrosis, although its exact mechanism remains unknown. In this study, we induced Viral myocarditis (VMC) via infection of CVB3 to explore the relationship between pyroptosis and fibrosis. Our results showed that intraperitoneal injection of an NLRP3 inhibitor MCC950 or use of NLRP3-/- mice inhibited cardiac pyroptosis mediated by NLRP3 inflammasome in VMC. CXCL4 is a chemokine that has been reported to have pro-inflammatory and pro-fibrotic functions. In VMC, we further found that pyroptosis of Mouse myocardial fibroblasts (MCF) promoted the secretion of CXCL4 by activating Wnt/ß-Catenin signaling. Subsequently, the transcriptome sequencing data showed that CXCL4 could promote cardiac fibrosis by activating PI3K/AKT pathway. In summary, infection of CVB3 induced host oxidative stress to further activate the NLRP3 inflammasome and ultimately lead to heart pyroptosis, in which MCF secreted CXCL4 by activating Wnt/ß-Catenin signaling and CXCL4 participated in cardiac fibrosis by activating PI3K/AKT pathway. Therefore, our findings revealed the role of CXCL4 in VMC and unveiled its underlying mechanism. CXCL4 appears to be a potential target for the treatment of VMC.

[Effects of BMAL2 on Aerobic Glycolysis and Cell Proliferation in Acute Myeloid Leukemia Cells].

OBJECTIVE: To explore the expression of basic helix-loop-helix ARNT like 2 (BMAL2) in acute myeloid leukemia (AML) patients and its correlation with prognosis, and analyze its effects on the aerobic glycolysis and proliferation of AML cells. METHODS: The expressions of BMAL2 in bone marrow mononuclear cells (BMMCs) of AML patients and normal control group were detected by RT-qPCR. The correlation of BMAL2 expression with prognosis of AML patients was analyzed using public database of National Center for Biotechnology Information (NCBI). The interfering in BMAL2 expression of HL-60 and Kasumi-1 cells was performed using lentiviral vector-mediated shRNA. Cell glucose metabolism and proliferation were detected by using glucose uptake experiment, lactate content test, CCK-8 assay and cell colony formation test. RESULTS: The expression level of BMAL2 mRNA in BMMCs of AML patients was significantly higher than normal control group (P < 0.01). The overall survival time of AML patients with high expression of BMAL2 was significantly shorter than those with low expression of BMAL2 (P < 0.05). Knockdown of BMAL2 significantly reduced glucose uptake and lactate production in AML cell line HL-60 and Kasumi-1 cells. The results of RT-PCR and Western blot showed that BMAL2 promoted aerobic glycolysis by enhancing the expression of HIF1A in AML cells, thereby promoting cell proliferation. CONCLUSION: BMAL2 is highly expressed in AML patients, and promotes aerobic glycolysis by enhancing the expression of HIF1A, thereby promoting cell proliferation.

Efficient Homojunction Tin Perovskite Solar Cells Enabled by Gradient Germanium Doping.

P-type self-doping is known to hamper tin-based perovskites for developing high-performance solar cells by increasing the background current density and carrier recombination processes. In this work, we propose a gradient homojunction structure with germanium doping that generates an internal electric field across the perovskite film to deplete the charge carriers. This structure reduces the dark current density of perovskite by over 2 orders of magnitude and trap density by an order of magnitude. The resultant tin-based perovskite solar cells exhibit a higher power conversion efficiency of 13.3% and excellent stability, maintaining 95% and 85% of their initial efficiencies after 250 min of continuous illumination and 3800 h of storage, respectively. We reveal the homojunction formation mechanism using density functional theory calculations and molecular level characterizations. Our work provides a reliable strategy for controlling the spatial energy levels in tin perovskite films and offers insights into designing intriguing lead-free perovskite optoelectronics.

Inhibition of CDK7 mitigates doxorubicin cardiotoxicity and enhances anticancer efficacy.

AIMS: The anthracycline family of anticancer agents such as doxorubicin (DOX) can induce apoptotic death of cardiomyocytes and cause cardiotoxicity. We previously reported that DOX-induced apoptosis is accompanied by cardiomyocyte cell cycle-reentry. Cell cycle progression requires cyclin-dependent kinase 7 (CDK7)-mediated activation of downstream cell cycle CDKs. This study aims to determine whether CDK7 can be targeted for cardioprotection during anthracycline chemotherapy. METHODS AND RESULTS: DOX exposure induced CDK7 activation in mouse heart and isolated cardiomyocytes. Cardiac-specific ablation of Cdk7 attenuated DOX-induced cardiac dysfunction and fibrosis. Treatment with the covalent CDK7 inhibitor THZ1 also protected against DOX-induced cardiomyopathy and apoptosis. DOX treatment induced activation of the proapoptotic CDK2-FOXO1-Bim axis in a CDK7-dependent manner. In response to DOX, endogenous CDK7 directly bound and phosphorylated CDK2 at Thr160 in cardiomyocytes, leading to full CDK2 kinase activation. Importantly, inhibition of CDK7 further suppressed tumor growth when used in combination with DOX in an immunocompetent mouse model of breast cancer. CONCLUSIONS: Activation of CDK7 is necessary for DOX-induced cardiomyocyte apoptosis and cardiomyopathy. Our findings uncover a novel proapoptotic role for CDK7 in cardiomyocytes. Moreover, this study suggests that inhibition of CDK7 attenuates DOX-induced cardiotoxicity, but augments the anticancer efficacy of DOX. Therefore, combined administration of CDK7 inhibitor and DOX may exhibit diminished cardiotoxicity but superior anticancer activity.

High-Efficiency and Stable Colloidal One-Dimensional Core/Shell Nanorod Light-Emitting Diodes.

Anisotropic nanocrystals such as nanorods (NRs) display unique linearly polarized emission, which is expected to break the external quantum efficiency (EQE) limit of quantum dot-based light-emitting diodes (LEDs). However, the progress in achieving a higher EQE using NRs encounters several challenges, primarily involving a low photoluminescence quantum yield (PLQY) of NRs and imbalanced charge injection in NR-LEDs. In this work, we investigated NR-LEDs based on CdSe/CdZnS/ZnS rod-in-rod NRs with a high PLQY and higher linear polarization compared to those of dot-in-rod NRs. The balanced charge injection is achieved using ZnMgO nanoparticles as the electron transport layer and poly-TPD {poly[N,N'-bis(4-butylphenyl)-N,N'-bis(phenyl)benzidine]} as the hole transport layer. Therefore, the NR-LEDs exhibit a maximum EQE of 21.5% and a maximum luminance of >120 000 cd/m2 owing to the high level of in-plane transitions with a dipole moment of 90%. The NR-LEDs also have greatly inhibited droop in EQE under a high current density as well as outstanding operation lifetime and cycle stability.

Bifidobacterium pseudocatenulatum NCU-08 ameliorated senescence via modulation of the AMPK/Sirt1 signaling pathway and gut microbiota in mice.

Aging is a degenerative disease in which organisms and neurological functions decline. Emerging research has underscored the vital role of the gut microbiota in age-related processes. However, the identification of aging-associated core microbiota remains limited. In this investigation, we isolated a strain of B. pseudocatenulatum NCU-08 from the feces of centenarians and assessed its impact on aging using a mouse model induced by D-gal. Our study revealed the exceptional probiotic attributes of B. pseudocatenulatum NCU-08. Administration of B. pseudocatenulatum NCU-08 significantly ameliorated age-related memory impairment, motor dysfunction, and anxiety-like behaviors in aging mice (p < 0.01). Moreover, tissue staining analysis demonstrated that B. pseudocatenulatum NCU-08 reduced the intensity of SA-ß-gal-positive in the hippocampus of aging mice. It also reversed pathological damage and structural abnormalities in brain and intestinal tissue. B. pseudocatenulatum NCU-08 inhibited neuroinflammation induced by TLR4/NF-κB (p < 0.01) and preserved the blood-brain barrier integrity by activating the AMPK/Sirt1 pathway (p < 0.05). Furthermore, it mitigated neuronal apoptosis and oxidative stress by upregulating the PI3K/AKT signaling pathway (p < 0.01) and enhancing the activities of antioxidant enzymes, including GSH-Px (p < 0.01), SOD (p < 0.01), and CAT (p < 0.01). Besides, analysis of 16S rRNA sequencing data demonstrated that treatment with B. pseudocatenulatum NCU-08 restored intestinal microbiota homeostasis after senescence. It enhanced the abundance of beneficial bacteria while suppressing the growth of pathogenic microorganisms. In summary, our study unveiled that this novel strain of B. pseudocatenulatum NCU-08 exerts anti-aging effects through regulating the AMPK/Sirt1 pathway and intestinal microbiota. It holds promise as a functional food for promoting anti-aging effects and offers a novel approach to address aging and associated metabolic disorders.

Predictive factors of psychiatric syndrome in patients with systemic lupus erythematosus.

Introduction: Early detection of neuropsychiatric systemic lupus erythematosus (NPSLE) remains a challenge in clinical settings. Previous studies have found different autoantibodies as markers for NPSLE. This study aimed to describe the distribution of psychiatric syndromes in a group of patients with systemic lupus erythematosus (SLE) and to investigate the association between psychiatric syndromes and specific autoantibodies. Methods: This retrospective study was conducted at a single medical center in China. We reviewed medical records of hospitalized patients with SLE who were consulted by psychiatrists due to potential mental disorders. Results of serum autoantibodies and general laboratory tests were collected. The correlation between clinical variables was examined. Binary logistic regression analyses were used to determine factors related to NPSLE and different psychiatric diagnoses. Results: Among the 171 psychiatric manifestations in 160 patients, 141 (82.4%) were attributed to SLE. Acute confusional state (ACS) had the highest prevalence (57.4%). Anti-cardiolipin (ACL) antibody (X2 = 142.261, p < 0.001) and anti-ß2 glycoprotein I (-ß2GP1) antibody (X2 = 139.818, p < 0.001) varied significantly between groups, with the highest positive rate found in patients with mood disorders (27.3% and 18.2%). SLE disease activity index - 2000 (SLEDAI-2K) score excluding item ACS and item psychosis was a predictor of NPSLE (OR 1.172 [95% CI 1.105 - 1.243]). Conclusions: Disease activity reflected by SLEDAI-2K score is a predictor for NPSLE. Antiphospholipid antibodies are associated with mood disorders in SLE. Further separate investigation of neuropsychiatric disorders is needed in order to better comprehend NPSLE's pathological mechanism.

68Ga-FAPI-04 PET/CT Imaging of Mesenteric Aggressive Fibromatosis.

ABSTRACT: Aggressive fibromatosis is a relatively rare disease. We describe 68Ga-FAPI-04 PET/CT findings in a case of histologically proved mesenteric aggressive fibromatosis. 68Ga-FAPI-04 PET/CT revealed a mass in the mesentery with increased FAPI activity. This case indicates that FAPI PET may be useful for evaluation of aggressive fibromatosis.

Assessment of spilled oil dispersion affected by dispersant: Characteristic, stability, and related mechanism.

Oil dispersion, a crucial process in oil transport, involves the detachment of oil droplets from slicks and their introduction into the water column, influencing subsequent oil migration and transformation. This study examines oil dispersion, considering characteristics, stability, and mechanisms, while evaluating the impact of dispersants and salinity. Results show the significant role of surfactant type in dispersants on oil dispersion characteristics, with anionic surfactants exhibiting higher sensitivity to salinity changes compared to nonionic surfactants. The dispersion efficiency varies with salinity, with anionic surfactants performing better in low salinity (<20‰) and nonionic surfactants showing superior performance at 30-35‰ salinities. Rheological analysis illustrates the breakup and coalescence of oil droplets within the shear rates of breaking waves. An increase in interfacial film rigidity impedes the coalescence of oil droplets, contributing to the dynamic stability of the oil-water hybrid system. The use of GM-2, a nonionic dispersant, results in the formation of a solid-like interface, characterized by increased elastic modulus, notably at 20‰ salinity. However, stable droplet size distribution (DSD) at 35‰ salinity for 60 h suggests droplets can remain dispersed in seawater. The enhancement of stability of oil dispersion is interpreted as the result of two mechanisms: stabilizing DSD and developing the strength of viscoelastic interfacial film. These findings offer insights into oil dispersion dynamics, highlighting the importance of surfactant selection and salinity in governing dispersion behavior, and elucidating mechanisms underlying dispersion stability.

Targeting VDAC: A potential therapeutic approach for mitochondrial dysfunction in Alzheimer's disease.

Mitochondrial dysfunction has been implicated in the pathogenesis of Alzheimer's disease, a neurodegenerative disorder characterized by progressive cognitive decline. Voltage-dependent anion channel (VDAC), a protein located in the outer mitochondrial membrane, plays a critical role in regulating mitochondrial function and cellular energy metabolism. Recent studies have identified VDAC as a potential therapeutic target for Alzheimer's disease. This article aims to provide an overview of the role of VDAC in mitochondrial dysfunction, its association with Alzheimer's disease, and the potential of targeting VDAC for developing novel therapeutic interventions. Understanding the involvement of VDAC in Alzheimer's disease may pave the way for the development of effective treatments that can restore mitochondrial function and halt disease progression.

Long-term exposure to ambient particulate matter is associated with prognosis in people living with HIV/AIDS: Evidence from a longitudinal study.

BACKGROUND: Evidence on the association between particulate matter (PM) exposure and prognosis in people living with HIV/AIDS (PWHA) is scarce. We aim to investigate the associations of long-term exposure to PM with AIDS-related deaths and complications. METHODS: We collected follow-up information on 7444 PWHAs from 2000 to 2021 from the HIV/AIDS Comprehensive Response Information Management System of the Wuhan Center for Disease Control and Prevention. The AIDS-related deaths and complications were assessed by physicians every 3 to 6 months, and the monthly average PM concentrations for each PWHA were extracted from the China High Air Pollutants dataset. We employed time-varying Cox regression models to evaluate the associations of the average cumulative PM exposure concentrations with AIDS-related deaths and complications, as well as the mediating effects of AIDS-related complications in PM-induced AIDS-related deaths. RESULTS: For each 1 µg/m3 increase in PM1, PM2.5, and PM10, the adjusted hazard ratios (HRs) for AIDS-related deaths were 1.021 (1.009, 1.033), 1.012 (1.005, 1.020), and 1.010 (1.005, 1.015), respectively; and the HRs for AIDS-related complications were 1.049 (1.034, 1.064), 1.029 (1.020, 1.038), and 1.031 (1.024, 1.037), respectively. AIDS-related complications mediated 18.38 % and 18.68 % of the association of exposure to PM1 and PM2.5 with AIDS-related deaths, respectively. The association of PM exposure with AIDS-related deaths was more significant in older PWHA. Meanwhile, the association between PM exposure and AIDS-related complications was stronger in PWHA with a BMI ≥ 24 kg/m2. CONCLUSION: Long-term exposure to PM is positively associated with AIDS-related deaths and complications, and AIDS-related complications have mediating effects in PM-induced AIDS-related deaths. Our evidence emphasizes that enhanced protection against PM exposure for PWHAs is an additional mitigation strategy to reduce AIDS-related deaths and complications.

Wireless Gas Sensor Based on the Mesoporous ZnO-SnO2 Heterostructure Enables Ultrasensitive and Rapid Detection of 3-Methylbutyraldehyde.

Achieving ultrasensitive and rapid detection of 3-methylbutyraldehyde is crucial for monitoring chemical intermediate leakage in pharmaceutical and chemical industries as well as diagnosing ventilator-associated pneumonia by monitoring exhaled gas. However, developing a sensitive and rapid method for detecting 3-methylbutyraldehyde poses challenges. Herein, a wireless chemiresistive gas sensor based on a mesoporous ZnO-SnO2 heterostructure is fabricated to enable the ultrasensitive and rapid detection of 3-methylbutyraldehyde for the first time. The mesoporous ZnO-SnO2 heterostructure exhibits a uniform spherical shape (∼79 nm in diameter), a high specific surface area (54.8 m2 g-1), a small crystal size (∼4 nm), and a large pore size (6.7 nm). The gas sensor demonstrates high response (18.98@20 ppm), short response/recovery times (13/13 s), and a low detection limit (0.48 ppm) toward 3-methylbutyraldehyde. Furthermore, a real-time monitoring system is developed utilizing microelectromechanical systems gas sensors. The modification of amorphous ZnO on the mesoporous SnO2 pore wall can effectively increase the chemisorbed oxygen content and the thickness of the electron depletion layer at the gas-solid interface, which facilitates the interface redox reaction and enhances the sensing performance. This work presents an initial example of semiconductor metal oxide gas sensors for efficient detection of 3-methylbutyraldehyde that holds great potential for ensuring safety during chemical production and disease diagnosis.

CXCL4/CXCR3 axis regulates cardiac fibrosis by activating TGF-ß1/Smad2/3 signaling in mouse viral myocarditis.

BACKGROUND: Severe myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. CXCL4 is a chemokine that has been reported to have pro-inflammatory and profibrotic functions. The exact role of CXCL4 in cardiac fibrosis remains unclear. METHODS: Viral myocarditis (VMC) models were induced by intraperitoneal injection of Coxsackie B Type 3 (CVB3). In vivo, CVB3 (100 TCID50) and CVB3-AMG487 (CVB3: 100 TCID50; AMG487: 5 mg/kg) combination were administered in the VMC and VMC+AMG487 groups, respectively. Hematoxylin and eosin staining, severity score, Masson staining, and immunofluorescence staining were performed to measure myocardial morphology in VMC. Enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were performed to quantify inflammatory factors (IL-1ß, IL-6, TNF-α, and CXCL4). Aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase-myocardial band (CK-MB) levels were analyzed by commercial kits. CXCL4, CXCR3B, α-SMA, TGF-ß1, Collagen I, and Collagen III were determined by Western blot and immunofluorescence staining. RESULTS: In vivo, CVB3-AMG487 reduced cardiac injury, α-SMA, Collagen I and Collagen III levels, and collagen deposition in VMC+AMG487 group. Additionally, compared with VMC group, VMC+AMG group decreased the levels of inflammatory factors (IL-1ß, IL-6, and TNF-α). In vitro, CXCL4/CXCR3B axis activation TGF-ß1/Smad2/3 pathway promote mice cardiac fibroblasts differentiation. CONCLUSION: CXCL4 acts as a profibrotic factor in TGF-ß1/Smad2/3 pathway-induced cardiac fibroblast activation and ECM synthesis, and eventually progresses to cardiac fibrosis. Therefore, our findings revealed the role of CXCL4 in VMC and unveiled its underlying mechanism. CXCL4 appears to be a potential target for the treatment of VMC.

Collective self-optimization of binary mixed heterogeneous populations.

To maximize the survival chances of society members, collective self-organization must balance individual interests with promoting the collective welfare. Although situations where group members have equal optimal values are clear, how varying optimal values impacts group dynamics remains unclear. To address this gap, we conducted a self-optimization study of a binary system incorporating communication-enabled active particles with distinct optimal values. We demonstrate that similar particles will spontaneously aggregate and separate from each other to maximize their individual benefits during the process of self-optimization. Our research shows that both types of particles can produce the optimal field values at low density. However, only one type of particle can achieve the optimal field values at medium density. At high densities, neither type of particle is effective in reaching the optimal field values. Interestingly, we observed that during the self-optimization process, the mixture demixed spontaneously under certain circumstances of mixed particles. Particles with higher optimal values developed into larger clusters, while particles with lower optimal values migrated outside of these clusters, resulting in the separation of the mixture. To achieve this separation, suitable noise intensity, particle density, and the significant difference in optimal values were necessary. Our results provide a more profound comprehension of the self-optimization of synthetic or biological agents' communication and provide valuable insight into separating binary species and mixtures.

Recent advances in metal oxide nanozyme-based optical biosensors for food safety assays.

Metal oxide nanozymes are emerging as promising materials for food safety detection, offering several advantages over natural enzymes, including superior stability, cost-effectiveness, large-scale production capability, customisable functionality, design options, and ease of modification. Optical biosensors based on metal oxide nanozymes have significantly accelerated the advancement of analytical research, facilitating the rapid, effortless, efficient, and precise detection and characterisation of contaminants in food. However, few reviews have focused on the application of optical biosensors based on metal oxide nanozymes for food safety detection. In this review, the catalytic mechanisms of the catalase, oxidase, peroxidase, and superoxide dismutase activities of metal oxide nanozymes are characterized. Research developments in optical biosensors based on metal oxide nanozymes, including colorimetric, fluorescent, chemiluminescent, and surface-enhanced Raman scattering biosensors, are comprehensively summarized. The application of metal oxide nanozyme-based biosensors for the detection of nitrites, sulphites, metal ions, pesticides, antibiotics, antioxidants, foodborne pathogens, toxins, and other food contaminants has been highlighted. Furthermore, the challenges and future development prospects of metal oxide nanozymes for sensing applications are discussed. This review offers insights and inspiration for further investigations on optical biosensors based on metal oxide nanozymes for food safety detection.

A stronger association of mental disorders with smaller particulate matter and a modifying effect of air temperature.

Mental disorders (MDs) can be triggered by adverse weather conditions and particulate matter (PM) such as PM2.5 and PM10 (aerodynamic diameter ≤2.5 µm and ≤10 µm). However, there is a dearth of evidence on the role of smaller PM (e.g. PM1, aerodynamic diameter ≤1 µm) and the potential modifying effects of weather conditions. We aimed to collect daily data on emergency department visits and hospitalisations for schizophrenia-, mood-, and stress-related disorders in a densely populated Chinese city (Hefei) between 2016 and 2019. A time-stratified case-crossover analysis was used to examine the short-term association of MDs with PM1, PM2.5, and PM10. The potential modifying effects of air temperature conditions (cold and warm days) were also explored. The three size-fractioned PMs were all associated with an increased risk of MDs; however, the association differed between emergency department visit and hospitalisation. Specifically, PM1 was primarily associated with an increased risk of emergency department visit, whereas PM2.5 was primarily associated with an increased risk of hospitalisation, and PM10 was associated with an increased risk of both emergency department visit and hospitalisation. The PM-MD association appeared to be greatest (although not significant) for PM1 (odds ratio range: 1.014-1.055), followed by PM2.5 (odds ratio range: 1.001-1.009) and PM10 (odds ratio range: 1.001-1.006). Furthermore, the PM-MD association was observed on cold days; notably, the association between PM and schizophrenia-related disorders was significant on both cold and warm days. Our results suggest that the smaller the PM, the greater the risk of MDs, and that the PM-MD association could be determined by air temperature conditions.