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Introduction: A series of significant ecological construction projects in the southern hilly region have brought about substantial changes to the ecological status and comprehensive zoning of the region. Hunan Province, with its strategic significance, was chosen as a representative research subject in the southern hilly region. Methods: We conducted a dynamic evaluation of the ecological status change and comprehensive zoning of Hunan Province from a structure-function perspective by applying the transfer matrix, Theil-Sen, Mann-Kendall, and ecosystem service trade-offs or synergies methods. The research goal was to integrate and harmonize structural complexity and functional diversification, providing valuable insights for optimizing both ecological background and territorial background. Results: The main results are as follows: (1) The structural changes of ecosystems were mainly concentrated in settlement and Cropland ecosystems. While the area of bulti-up ecosystems has increased significantly, from 1.34% in 2000 to 2.72% in 2020. Cropland ecosystems marking a decrease of 1.39%, with a continued conversion of Cropland into construction land ecosystems. (2) Ecosystem function changes have introduced instability. Over time, NPP exhibited an oscillating trend of increase followed by a decrease. Spatially, there was a sharp decline in peripheral building land, and the regions of declining NPP displayed a lateral U-shaped distribution. (3) The overall trend in ecosystem service changes was positive. Quantitatively, GP and CS experienced an ascending-then-decreasing pattern, while HQ showed a weak decline and WY increased annually. At the county scale, there was noticeable spatial heterogeneity. Human socio-economic activities and environmental protection policies exert a significant impact on the ecological conditions within the study area. (4) Regarding the national territory space function partition, urban functional zones have primarily catered to residential functions and were mainly distributed in the Changsha-Zhuzhou-Xiangtan area. Discussion: Ecological functional zones were mainly centered on ecological functions, and most were located in the mountainous areas of western and southern Hunan Province. The agricultural function areas were mainly to serve production functions and were mainly located in the Dongting Lake Plain, the nearshore plain of the mainstream and tributary systems of the rivers of Xiang, Zi, Yuan, and Li. In general, the changes in ecosystem structure and function in the study area reflect changes in ecological conditions. In the future, ecosystem diversity, stability, and sustainability should be improved from an integrated structure-function perspective. [ABSTRACT FROM AUTHOR]

Aims: In patients with renal disease, high serum phosphate shows a relationship with cardiovascular risk. We speculate that high phosphate (HP) impairs arterial vasodilation via the endothelium and explore potential underlying mechanisms. Methods: Isolated vessel relaxation, endothelial function, glomerular filtration rate (GFR), oxidative stress status and protein expression were assessed in HP diet mice. Mitochondrial function and protein expression were assessed in HP‐treated human umbilical vein endothelial cells (HUVECs). Results: High phosphate (1.3%) diet for 12 weeks impaired endothelium‐dependent relaxation in mesenteric arteries, kidney interlobar arteries and afferent arterioles; reduced GFR and the blood pressure responses to acute administration of acetylcholine. The PPARα/LKB1/AMPK/eNOS pathway was attenuated in the endothelium of mesenteric arteries from HP diet mice. The observed vasodilatory impairment of mesenteric arteries was ameliorated by PPARα agonist WY‐14643. The phosphate transporter PiT‐1 knockdown prevented HP‐mediated suppression of eNOS activity by impeding phosphorus influx in HUVECs. Endothelium cytoplasmic and mitochondrial reactive oxygen species (ROS) were increased in HP diet mice. Moreover HP decreased the expression of mitochondrial‐related antioxidant genes. Finally, mitochondrial membrane potential and PGC‐1α expression were reduced by HP treatment in HUVECs, which was partly restored by AMPKα agonist. Conclusions: HP impairs endothelial function by reducing NO bioavailability via decreasing eNOS activity and increasing mitochondrial ROS, in which the AMPK‐related signalling pathways may play a key role. [ABSTRACT FROM AUTHOR]

Aims: Reduced A Disintegrin And Metalloproteinase with a ThromboSpondin type 1 motif member 13 (ADAMTS13) levels are observed in kidney disease. We test whether recombinant human ADAMTS13 (rhADAMTS13) mitigates renal injury in chronic kidney disease (CKD) and the potential mechanisms. Methods: CKD was established 3 months after ischaemia/reperfusion (IR). ADAMTS13 and von Willebrand factor (vWF) levels, renal function and morphological changes were analysed. Afferent arteriolar responses to angiotensin II (Ang II) and acetylcholine (ACh) were measured. Oxidative stress‐related molecules were detected. Results: Higher vWF and lower ADAMTS13 levels were observed in CKD mice, which were markedly attenuated by rhADAMTS13. rhADAMTS13 alleviated renal dysfunction, as documented by decreased blood urea nitrogen (BUN), serum creatinine, kidney injury molecule‐1 (KIM‐1) and neutrophil gelatinase‐associated lipocalin (NGAL) levels in CKD mice. Moreover, rhADAMTS13 attenuated transforming growth factor (TGF)‐β1/Smad3 activation. Plasma vWF: ADAMTS13 ratio showed positive correlations with malondialdehyde (MDA), hydrogen peroxide (H2O2) and proteinuria, and correlated inversely with superoxide dismutase (SOD) and catalase (CAT). Finally, rhADAMTS13 inhibited reactive oxygen species (ROS) levels and improved microvascular functional disorders, accompanied by the inhibition of glycogen synthase kinase (GSK) 3β hyperactivity and upregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2) expression. Conclusions: Acute kidney injury (AKI) reduces the expression of ADAMTS13 that contributes to progressive CKD, microvascular dysfunction, oxidative stress, inhibition of Nrf2 activity and renal histopathological damage. All of which can be alleviated by administration of rhADAMTS13. [ABSTRACT FROM AUTHOR]

Introduction: In the course of immune development, HIV-exposed uninfected (HEU) infants exhibit abnormal immune function and increased infectious morbidity compared to HIV-unexposed uninfected (HUU) infants. Yet the specific functional phenotypes and regulatory mechanisms associated with in-utero HIV and/or ART exposure remain largely obscure., Methods: We utilized flow cytometry and RNA-seq technologies to conduct the immunological and transcriptomic profiling in cord blood from 9 HEU mother-infant pairs and 24 HUU pairs. On top of that, we compared the cord blood dataset with the maternal venous blood dataset to characterize unique effects induced by in-utero HIV and/or ART exposure., Results: Flow cytometry immunophenotyping revealed that the level of B lymphocyte subsets was significantly decreased in HEU cord blood as compared to HUU ( P < 0.001). Expression profiling-based cell abundance assessment, includes CIBERSORT and ssGSEA algorithm, showed a significantly reduced abundance of naive B cells in HEU cord blood (both P < 0.05), supporting the altered composition of B lymphocyte subsets in HEU. Functional enrichment analysis demonstrated suppressed innate immune responses and impaired immune regulatory function of B cells in HEU cord blood. Furthermore, through differential expression analysis, co-expression network analysis using WGCNA, and feature selection analysis using LASSO, we identified a 4-gene signature associated with HEU status. This signature effectively assesses B cell levels in cord blood, enabling discrimination between HEU and HUU infants., Discussion: Our study provides the first comprehensive immunological and transcriptomic characterization of HEU cord blood. Additionally, we establish a 4-gene-based classifier that holds potential for predict immunological abnormalities in HEU infants., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Jin, Zhao, Qi, Tian, Liao, Yang, Li, Zhu, Chen, Shen, Liu and Lu.)

In the pursuit of understanding lattice capacity threshold effects of oxide solid solutions for their supported Ni catalysts, a series of Ca 2+ -doped CeO 2 solid solutions with 10 wt% Ni loading (named Ni/Ca x Ce 1- x O y ) was prepared using a sol-gel method and used for CO 2 methanation. The lattice capacity of Ca 2+ in the lattice of CeO 2 was firstly determined by the XRD extrapolation method, corresponding to a Ca/(Ca + Ce) molar ratio of 11%. When the amount of Ca 2+ in the Ca x Ce 1- x O y supports was close to the CeO 2 lattice capacity for Ca 2+ incorporation, the obtained Ni/Ca 0.1 Ce 0.9 O y catalyst possessed the optimal intrinsic activity for CO 2 methanation. XPS, Raman spectroscopy, EPR and CO 2 -TPD analyses revealed the largest amount of highly active moderate-strength alkaline centers generated by oxygen vacancies. The catalytic reaction mechanisms were revealed using in situ IR analysis. The results clearly demonstrated that the structure and reactivity of the Ni/Ca x Ce 1- x O y catalyst exhibited the lattice capacity threshold effect. The findings offer a new venue for developing highly efficient oxide-supported Ni catalysts for low-temperature CO 2 methanation reaction and enabling efficient catalyst screening.