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Objective To explore the relationship and predictive function of blood urea nitrogen (BUN) level in association with major adverse cardiovascular event(MACE) subsequent to percutaneous coronary intervention(PCI) among patients diagnosed with acute coronary syndrome (ACS). Methods Between April 2017 and November 2017, ACS patients undergoing their initial PCI at the Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University were recruited. Following a 36-month follow-up period, 487 patients were included as 114 subjects experiencing MACE and 373 subjects without MACE. The Cox proportional hazards regression model was utilized to assess the risk ratio of MACE and its 95% confidence interval (CI) concerning BUN levels and ACS post-PCI. Additionally, the area under the receiver operating characteristic (ROC) curve (AUC) was applied to assess the predictive effect of BUN. Results After adjusting for confounding variables, Cox proportional hazards regression analysis revealed that the risk of MACE was approximately four times higher in the high BUN level group compared to the low BUN level group (OR=4.722,95% CI 1.716-12.993). Upon inclusion of BUN in both the basic prediction model and SCORE model for cardiovascular event risk, there was a significant increase in the AUC area (P＜ 0.001). Conclusions BUN levels can independently predict the risk of MACE following PCI in ACS patients, irrespective of traditional risk factors.

Soil multifunctionality is essential for the enhancement of soil carbon sequestration, but disturbances such as thinning practices can influence soil microbial activity and carbon cycling. Microbial residues, particularly microbial residue carbon (MRC), are important contributors to soil organic carbon (SOC), but the effects of thinning intensity on MRC accumulation remain poorly understood. This study evaluated the impact of four thinning treatments—control (CK, 0%), light-intensity thinning (LIT, 20%), medium-intensity thinning (MIT, 30%), and high-intensity thinning (HIT, 45%)—on soil multifunctionality in Chinese fir plantations five years after thinning. Soil nutrient provision, microbial biomass, enzyme activity, and microbial residue carbon were assessed. The results showed that thinning intensity significantly affected soil nutrient provision and microbial biomass, with MIT and HIT showing higher nutrient levels than CK and LIT. Specifically, MIT's and HIT's total nutrient provision increased by 0.04 and 0.15 compared to that of CK. Enzyme activity was highest in LIT (+0.89), followed by MIT (+0.07), with HIT showing a decline (−0.84). Microbial biomass, including bacterial PLFAs (B-PLFAs), fungal PLFAs (F-PLFAs), microbial biomass carbon (MBC), and nitrogen (MBN), was highest in CK and MIT, and lowest in HIT, with MIT showing a 0.13 increase compared to CK. Microbial residue carbon (MRC) accumulation was positively correlated with soil organic carbon (SOC), total nitrogen (TN), available nitrogen (AN), and easily oxidized organic carbon (EOC). The highest MRC content in the 0–20 cm soil layer was observed in MIT and CK (10.46 and 11.66 g/kg, respectively), while the MRC in LIT and HIT was significantly lower, reduced by 24% and 12%, respectively. These findings highlight the significant role of thinning intensity in microbial activity and carbon cycling. Medium-intensity thinning (MIT, 30%) was identified as the most effective approach for promoting microbial biomass and enhancing carbon cycling in Chinese fir forest soils, making it an optimal approach for forest management aimed at increasing soil carbon sequestration. [ABSTRACT FROM AUTHOR]

Tumor-derived exosomes bind to organ resident cells, activating S100 molecules during the remodeling of the local immune microenvironment. However, little is known regarding how organ resident cell S100A10 mediates cancer metastatic progression. Here, we provided evidence that S100A10 plays an important role in regulating the lung immune microenvironment and cancer metastasis. S100A10-deficient mice reduced cancer metastasis in the lung. Furthermore, the activation of S100A10 within lung fibroblasts via tumor-derived exosomes increased the expression of CXCL1 and CXCL8 chemokines, accompanied by the myeloid-derived suppressor cells (MDSCs) recruitment. S100A10 inhibitors such as 1-Substituted-4-Aroyl-3-hydroxy-5-Phenyl-1 H-5-pyrrol-2(5 H)-ones inhibit lung metastasis in vivo. Our findings highlight the crucial role of S100A10 in driving MDSC recruitment in order to remodel the lung immune microenvironment and provide potential therapeutic targets to block cancer metastasis to the lung. [ABSTRACT FROM AUTHOR]

Karst ecosystems are characterized by the dissolution of soluble rocks, displaying distinctive landscape features such as rugged peaks, steep slopes, and deep valleys. Afforestation is an effective approach for improving soil quality in rocky desertification areas because plants have evolved unique adaptations to thrive in such environments. However, the effects of tree species composition and cultivation patterns on the soil quality, microbial diversity, stability, and functions in rocky desertification areas remain unclear. In this work, four study plots including three types of forests—pure Pinus massoniana plantations, Toona sinensis plantations, mixed coniferous and broadleaf plantations (Pinus massoniana–Betula luminifera forests), and unforested area as the control—were established in a karst desertification area in the Hunan province of China. Soil properties including soil bulk density, soil organic carbon, total nitrogen, total phosphate, soil ammonium nitrogen, nitrate, available phosphate, soil pH, and soil microbial diversity were investigated in the study area. The results showed that the forests significantly increased the soil organic carbon, total nitrogen, and ammonium nitrogen compared to the unforested area. The microbial diversity indicators in mixed forests were significantly higher than those in the Pinus massoniana forests. The dominant bacteria phyla included Proteobacteria, Acidobacteria, and Actinobacteria, while fungi species such as Ascomycota and Basidiomycota were identified in all study plots. In addition, the AVD index evaluation revealed that the mixed forests enhanced the stability of the soil microbial communities compared to the monoculture plantations and unforested plots in rocky desertification areas. The research results indicated that, among the various forest types, the mixed forest was the most effective choice for afforestation in terms of improving the soil quality by changing the soil's physiological properties in rocky desertification areas. Our study provided guidance and insights for afforestation technology and the optimal allocation of different tree species in the cultivation and management of plantation forests in rocky desertification regions. [ABSTRACT FROM AUTHOR]

Multiple cancers have been reported to be associated with angiogenesis and are sensitive to anti‐angiogenic therapies. Vascular normalization, by restoring proper tumor perfusion and oxygenation, could limit tumor cell invasiveness and improve the effectiveness of anticancer treatments. However, the underlying anticancer mechanisms of antiangiogenic drugs are still unknown. Metformin (MET) and simvastatin (SVA), two metabolic‐related drugs, have been shown to play important roles in modulating the hypoxic tumor microenvironment and angiogenesis. Whether the combination of MET and SVA could exert a more effective antitumor effect than individual treatments has not been examined. The antitumor effect of the synergism of SVA and MET was detected in mouse models, breast cancer patient‐derived organoids, and multiple tumor cell lines compared with untreated, SVA, or MET alone. RNA sequencing revealed that the combination of MET and SVA (but not MET or SVA alone) inhibited the expression of endothelin 1 (ET‐1), an important regulator of angiogenesis and the hypoxia‐related pathway. We demonstrate that the MET and SVA combination showed synergistic effects on inhibiting tumor cell proliferation, promoting apoptosis, alleviating hypoxia, decreasing angiogenesis, and increasing vessel normalization compared with the use of a single agent alone. The MET and SVA combination suppressed ET‐1‐induced hypoxia‐inducible factor 1α expression by increasing prolyl hydroxylase 2 (PHD2) expression. Furthermore, the MET and SVA combination showed a more potent anticancer effect compared with bosentan. Together, our findings suggest the potential application of the MET and SVA combination in antitumor therapy. [ABSTRACT FROM AUTHOR]

Electrocatalytic CO2 reduction reaction (CO2RR) is one of the most effective methods to convert CO2 into useful fuels. Introducing defects into metal nanostructures can effectively improve the catalytic activity and selectivity towards CO2RR. This review provides the recent progress on the use of metal nanomaterials with defects towards electrochemical CO2RR and defects engineering methods. Accompanying these ideas, we introduce the structure of defects characterized by electron microscopy techniques as the characterization and analysis of defects are relatively difficult. Subsequently, we present the intrinsic mechanism of how the defects affect CO2RR performance. Finally, to promote a wide and deep study in this field, the perspectives and challenges concerning defects engineering in metal nanomaterials towards CO2RR are put forward. [ABSTRACT FROM AUTHOR]

Introduction Bisphenols are a group of chemicals with two hydroxyphenyl functionalities in the structure (Liao and Kannan 2013). Bisphenols are widely used in the manufacturing industry, with bisphenol A (BPA) [...], BACKGROUND: Bisphenol S (BPS) has increasingly been used as a substitute for bisphenol A (BPA) in some 'BPA-free' consumer goods and in thermal papers. Wide human exposure to BPS has been reported; however, the biological and potential toxic effects of BPS are poorly understood. OBJECTIVE: In this study, we sought to elucidate the sex-specific rapid effect of BPS in rat hearts and its underlying mechanism. METHODS: We examined the rapid effects of BPS in rat hearts using electrophysiology, confocal and conventional fluorescence imaging, and immunoblotting. Treatment was administered via acute perfusion of excised hearts or isolated cardiac myocytes. RESULTS: In female rat hearts acutely exposed to [10.sup.-9] M BPS, the heart rate was increased; in the presence of catecholamine-induced stress, the frequency of ventricular arrhythmia events was markedly increased. BPS-exposed hearts showed increased incidence of arrhythmogenic-triggered activities in female ventricular myocytes and altered myocyte [Ca.sup.2+] handling, particularly spontaneous [Ca.sup.2+] release from the sarcoplasmic reticulum. The dose responses of BPS actions were inverted U-shaped. The impact of BPS on myocyte [Ca.sup.2+] handling was mediated by estrogen receptor β signaling and by rapid increases in the phosphorylation of key [Ca.sup.2+] handling proteins, including ryanodine receptor and phospholamban. The proarrhythmic effects of BPS were female specific; male rat hearts were not affected by BPS at the organ, myocyte, or protein levels. CONCLUSION: Rapid exposure to low-dose BPS showed proarrhythmic impact on female rat hearts; these effects at the organ, cellular, and molecular levels are remarkably similar to those reported for BPA. Evaluation of the bioactivity and safety of BPS and other BPA analogs is necessary before they are used as BPA alternatives in consumer products. http://dx.doi.org/10.1289/ehp.l408679

INTRODUCTION Bisphenol A (BPA; CAS 80-05-7) is one of the highest production volume chemicals worldwide, with annual production exceeding 3 million metric tons. BPA is used in the production of [...], BACKGROUND: The need for mechanistic understanding of nonmonotonic dose responses has been identified as one of the major data gaps in the study of bisphenol A (BPA). Previously we reported that acute exposure to BPA promotes arrhythmogenesis in female hearts through alteration of myocyte [Ca.sup.2+] handling, and that the dose response of BPA was inverted U-shaped. OBJECTIVE: We sought to define the cellular mechanism underlying the nonmonotonic dose response of BPA in the heart. METHODS: We examined rapid effects of BPA in female rat ventricular myocytes using video-edge detection, confocal and conventional fluorescence imaging, and patch clamp. RESULTS: The rapid effects of BPA in cardiac myocytes, as measured by multiple end points, including development of arrhythmic activities, myocyte mechanics, and [Ca.sup.2+] transient, were characterized by nonmonotonic dose responses. Interestingly, the effects of BPA on individual processes of myocyte [Ca.sup.2+] handling were monotonic. Over the concentration range of [10.sup.-12] to [10.sup.-6] M, BPA progressively increased sarcoplasmic reticulum (SR) [Ca.sup.2+] release and [Ca.sup.2+] reuptake and inhibited the L-type [Ca.sup.2+] current ([I.sub.CaL]). These effects on myocyte [Ca.sup.2+] handling were mediated by estrogen receptor (ER)β signaling. The nonmonotonic dose responses of BPA can be accounted for by the combined effects of progressively increased SR [Ca.sup.2+] reuptake/release and decreased [Ca.sup.2+] influx through [I.sub.CaL]. CONCLUSION: The rapid effects of BPA on female rat cardiac myocytes are characterized by nonmonotonic dose responses as measured by multiple end points. The nonmonotonic dose response was produced by ERβ-mediated monotonic effects on multiple cellular [Ca.sup.2+] handling processes. This represents a distinct mechanism underlying the nonmonotonicity of BPA's actions. http://dx.doi.org/10.1289/ehp.1307491

Background: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality globally. Hypercholesterolemia accelerates atherosclerotic development and is an independent modifiable risk factor for ASCVD. Reducing cholesterol levels is effective in preventing ASCVD. Acetyl-L-carnitine (ALC) is an endogenous molecule that plays a primary role in energy metabolism; however, its effect on cholesterol metabolism remains unclear., Methods: We collected plasma samples and clinical data from 494 individuals with hyperlipidemia. Targeted metabolomics were used to measure plasma ALC levels and explore the association of ALC with clinical cholesterol levels. Additionally, we explored the effects of ALC in cholesterol levels and cholesterol metabolism in a murine hypercholesterolemia model. An LDLR -/- mouse-based atherosclerotic model was established to investigate the roles of ALC on atherosclerotic progression., Results: Plasma ALC concentrations were significantly negatively correlated with plasma total cholesterol (TC) levels ( r  = -0.43, p  < 0.0001) and low-density lipoprotein cholesterol (LDL-C; r  = -0.53, p  < 0.0001). Incorporating ALC into the diet significantly reduced plasma TC and LDL-C levels, downregulated genes involved in cholesterol synthesis, such as sterol regulatory element-binding protein 2 (SREBP2) and 3-hydroxy-3-methyl-glutaryl-CoA reductase, and upregulated low-density lipoprotein receptor expression. ALC supplementation substantially lowered plasma TC levels and inhibited atherosclerosis in LDLR -/- mice., Conclusion: ALC reduced atherosclerotic plaque formation by lowering plasma cholesterol levels via suppression of SREBP2-mediated cholesterol synthesis, thus suggesting that ALC is a potential therapeutic target for ASCVD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as potential conflicts of interest., (Copyright © 2024 Xing, Du, Li, Wang, Zhang, Gao, Han, Sun, Sun, Du, Hu, Yu and Qin.)