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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]

Dipeptidyl peptidase 4 (DPP4) is a serine protease widely distributed in membrane-bound and soluble forms in various tissues and organs throughout the body. DPP4 plays a role in inflammation, immune regulation, cell growth, migration and differentiation. The role of DPP4 in tumors has garnered increasing attention. Previous research has demonstrated that DPP4 contributes to the promotion of cancer in most cancers, and it may play a specific biological function through the variation in tumor cell types and expression forms. However, the expression of DDP4 in different tumor types and its specific mechanism remains unclear. In this review, we describe the structure of DPP4, summarize the recent research progress of its expression and potential mechanisms in common tumors, and discuss the development prospects of DPP4 inhibitors in tumor therapy. Although current research emphasizes the potential of DPP4 as a drug target, the incomplete understanding of its regulatory mechanisms impedes the discovery and development of new therapies against it. Further research on DPP4-related tumors is anticipated to promote its clinical application as a potential therapeutic target. [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]

The multistep dynamic process of metastasis is the primary cause of breast cancer deaths. C‐terminal Eps15‐homology domain‐containing protein 1 (EHD1), a translocator associated with endocytic recycling, has been implicated in various oncogenic processes. However, the precise molecular mechanisms of EHD1‐induced breast cancer metastases remain largely unexplored. Here we found that the upregulation of EHD1 in breast cancer was positively associated with distant lymph node metastasis in patients. Meanwhile, EHD1 promoted epithelial‐mesenchymal transition (EMT), invasion, and metastasis of breast cancer cells in both two‐dimensional (2D) and three‐dimensional (3D) culture models in vitro, as well as in vivo. Remarkably, EHD1 can activate the AKT–mTOR pathway to upregulate the protein expression of hypoxia‐inducible factor 2α (HIF2α) under normoxic conditions and subsequently enhance the invasive and metastatic breast cancer. Our findings indicated EHD1 as a new regulator of HIF2α and a potential therapeutic target for inhibiting breast cancer metastasis. [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]