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Amid China's economic shift to high-quality development, addressing environmental challenges like greenhouse gas emissions and manufacturing pollution, there is a crucial demand for sustainable and eco-friendly development strategies. This study aims to investigate the impact of innovation efficiency in the high-tech industry on carbon emissions. It seeks to explore regional differences, mechanisms, and the influence of energy consumption structures in achieving sustainable development goals. Utilizing data from 30 provinces spanning 2009 to 2020, the study employs the DEA-Malmquist index model, spatial and temporal classification evaluation, and a panel measurement model to assess the efficiency of innovation and development in high-tech industries and their relationship with carbon emissions. The results indicate several key findings: (1) The overall operational efficiency of high-tech industry innovation and development in China is steadily increasing. However, there are distinct characteristics observed among provinces and cities, reflecting diverse input and output types. (2) High-tech industry innovation efficiency significantly contributes to carbon emission reduction, and there is regional heterogeneity in this impact. The central and western regions exhibit greater effects compared to other provinces and cities. (3) The optimization of the energy structure is identified as a mechanism through which high-tech industry innovation efficiency reduces carbon emissions. Moreover, different intervals of high-tech industry innovation efficiency yield varying effects on carbon emissions. This research underscores the importance of fostering high-tech industry innovation efficiency as a means to reduce carbon emissions. It also identifies key areas for future policy development and resource allocation, emphasizing the support needed for low-carbon technology research and development., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Employing bioinformatics approaches, this investigation pinpointed pivotal differentially expressed genes (DEGs) across the spectrum of Alzheimer's disease (AD), from incipient to severe stages, using the GSE28146 dataset from the GEO repository. Analytical methods included DEG identification via the limma package in R, coupled with GO and KEGG pathway analyses through clusterProfiler, to discern biological processes and pathway involvements. Key findings spotlighted the roles of proteasome subunits PSMB4, PSMB8, PSMC4, and PSMD6 in the early stage, ribosomal proteins RPS3 and RPL11 during moderate AD, and mitochondrial components COX5B, COX6B2, and COX7A2 in severe AD, underscoring their importance in the disease's pathogenesis. Conclusively, these results not only delineate the dynamic genetic shifts accompanying AD progression but also propose critical biomarkers for potential therapeutic targeting, offering a consolidated basis for future AD research and treatment development. This offered a novel idea for analyzing the pathogenesis and development of AD and investigation of targeted drugs., (© 2024. The Author(s), under exclusive licence to Institute of Plant Genetics Polish Academy of Sciences.)

Vascular smooth muscle cells (VSMCs) are involved in restenosis of bypass grafts and cause artery graft occlusion. This study aimed to explore the role of Slit2 in phenotypic switching of VSMCs and its effect on restenosis of vascular conduits. An animal model of vascular graft restenosis (VGR) was produced in SD rats and assessed by echocardiography. The expression of Slit2 and Hif-1α was measured in vivo and in vitro. After Slit2 overexpression, the migration and proliferation of VSMCs were detected in vitro, and the restenosis rates and phenotype of VSMCs were tested in vivo. The arteries of the VGR model presented significant stenosis, and Slit2 was decreased in VSMCs of the VGR model. In vitro, Slit2 overexpression inhibited the migration and proliferation of VSMCs, but Slit2 knockdown promoted migration and proliferation. Hypoxia induced Hif-1α but reduced Slit2, and Hif-1α negatively regulated Slit2 expression. Moreover, Slit2 overexpression weakened the rate of VGR and maintained the patency of artery bypass grafts, which suppressed the phenotypic switching of VSMCs. Slit2 inhibited the synthetic phenotype transformation to inhibit the migration and proliferation of VSMCs and delayed the VGR via Hif-1α., (© 2023. The Author(s).)

Background: Although cardiovascular disease (CVD) has been the major contributor to global mortality and disability especially in undeveloped and developing countries/areas with severer air pollutions, studies are quite limited and evidence is insufficient of short-term main air pollutants exposure on health burden of CVD hospital admissions in those regions particularly through direct costs., Method: Based on an analysis of 30,959 CVD hospital admissions among suburban farmers from 2018 to 2019 through multiple linear regression (MLR), our study evaluated the impact of main air pollutants (PM 2.5 , PM 10 , SO 2 , CO, NO 2 and O 3 ) exposure on number of cases, length of stay (LOS) and costs of CVD hospital admissions in Pingliang, China., Results: Concentration of SO 2 and O 3 rising from a low level was found to lower the costs, LOS and daily cases of CVD hospital admissions and PM 2.5 , PM 10 , CO and NO 2 were found to aggravate the burden. Besides, the NO 2 could put more economic stress on those CVD patients in Pingliang (China) which implies that some improvements could be done on public medical insurance policy and benefit local suburban farmers by strengthening the supports on specific drugs and therapies., Conclusions: More efforts should be made to lower the concentration of air pollution by coordinated control managements even in a low-level scenario. Concentration levels and interactions between main air pollutants may play an important role in air pollution-induced CVD health burden. Future research is needed to explore more evidence in different areas, especially with low-level SO 2 effects., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Cardiovascular disease (CVD), reported to relate with climate change, is the leading cause of global mortality and morbidity. Since the relevant information is quite limited from suburbs and countryside in developing and underdeveloped countries, there are no studies that focused on morbidity through diurnal temperature range (DTR) for these regions. This is the first study to evaluate the short-term effect of DTR on CVD hospital admission in suburban farmers, as well as to identify vulnerable subpopulations. Daily time series data of CVD hospital admissions on suburban farmers of Qingyang, China, and meteorological data from 2011 to 2015 were collected, and a distributed lag non-linear model (DLNM) combined with a quasi-Poisson generalized additive regression model (GAM) was used to examine the exposure-response relationship and delayed effect between DTR and CVD hospital admissions. Stratified analyses by age and gender were performed and extreme DTR effects were examined. Non-linear relation between DTR and CVD hospital admissions was observed, and whether DTR lower or higher than the reference (13 °C, 50 th percentile) had adverse effect while lower DTR have slightly higher impact. Also, both extreme low and extreme high DTR had adverse effect. Besides, adults (age < 65) and males were more vulnerable to the effects of DTR compared with the old (age ≥ 65) and females, respectively. This study provides evidence that not only high DTR but also low DTR had adverse effects on CVD which should be paid attention to. Adults and males were more vulnerable among suburban farmers. The results are inconsistent with the studies from urban and indicate differences between urban and suburban residents. Multiple factors such as occupations, risk awareness, and lifestyles could have a significant influence on CVD morbidity, and further study is needed to explore more evidence., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

A high co-morbidity between Alzheimer's disease (AD) and depression suggests there might be similar mechanisms underlying the course of these diseases. Previous studies have shown that p38MAPK plays a critical role in the pathophysiology of AD and depression. However, little is known about whether SB203580, a selective inhibitor of p38MAPK, may protect against AD-associated cognitive impairments and depression-like behavior, simultaneously. Herein, we have shown, for the first time, that SB203580 may reverse memory impairments and depression-like behavior induced by hippocampal infusion of β-amyloid 1-42 (Aβ 1-42 ), as measured by novel object recognition, Morris water maze, tail-suspension and forced-swimming tests. In addition, phorbol 12-myristate 13-acetate (PMA), a PKC activator which also activates p38MAPK, significantly abolished the effects of SB203580. Moreover, Aβ 1-42 causes increased phosphorylation of p38MAPK and decreased phosphorylation of Ser9-glycogen synthase kinase 3β (GSK3β) and cAMP-response element binding protein (CREB) in the hippocampus of mice, which could be significantly reversed by SB203580. Our results suggest that SB203580 reversed Aβ 1-42 -induced cognitive impairments and depression-like behavior via inhibiting p38MAPK signaling pathway, which not only supports p38MAPK as a therapeutic target for AD-associated cognitive dysfunction and depression-like behavior, but also provides experimental basis for the use of SB203580 in co-morbidity of AD and depression.

Increased osteopontin (OPN) expression in the heart, specifically in myocytes, associates with increased myocyte apoptosis and myocardial dysfunction. Recently, we provided evidence that OPN interacts with CD44 receptor, and induces myocyte apoptosis via the involvement of endoplasmic reticulum stress and mitochondrial death pathways. Here we tested the hypothesis that OPN induces oxidative stress in myocytes and the heart via the involvement of mitochondria and NADPH oxidase-4 (NOX-4). Treatment of adult rat ventricular myocytes (ARVMs) with OPN (20 nM) increased oxidative stress as analyzed by protein carbonylation, and intracellular reactive oxygen species (ROS) levels as analyzed by ROS detection kit and dichlorohydrofluorescein diacetate staining. Pretreatment with NAC (antioxidant), apocynin (NOX inhibitor), MnTBAP (superoxide dismutase mimetic), and mitochondrial KATP channel blockers (glibenclamide and 5-hydroxydecanoate) decreased OPN-stimulated ROS production, cytosolic cytochrome c levels, and apoptosis. OPN increased NOX-4 expression, while decreasing SOD-2 expression. OPN decreased mitochondrial membrane potential as measured by JC-1 staining, and induced mitochondrial abnormalities including swelling and reorganization of cristae as observed using transmission electron microscopy. OPN increased expression of BIK, a pro-apoptotic protein involved in reorganization of mitochondrial cristae. Expression of dominant-negative BIK decreased OPN-stimulated apoptosis. In vivo, OPN expression in cardiac myocyte-specific manner associated with increased protein carbonylation, and expression of NOX-4 and BIK. Thus, OPN induces oxidative stress via the involvement of mitochondria and NOX-4. It may affect mitochondrial morphology and integrity, at least in part, via the involvement of BIK.