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Impermeability is a feature of fully encapsulated chemical protective ensembles (FCPE), which can affect people's sweat and affect their clothing's thermal-wet comfort. This study investigated the dynamics of upper-body sweat distribution in young males wearing FCPE and explored variations in sweat rate intra-region and inter-time for 10 young and healthy male college students. The study was carried in a climatic chamber (environment temperature 35 °C, relative humidity 60%) with participants exercising on a treadmill at 4 km/h, 5%. Sweat was collected using a 35-pad set of absorbent pads that were changed every 5 min during the course of the experiment. A total of 7-pad sets were collected with an average sweat rate of 389, 631, 920, 1137, 1100, 1211, and 1105 g m−2 h−1, respectively. The medial upper back, lateral lower back, medial upper chest, medial mid-back, and lateral top back had the highest sweat rates, with average values of 1406, 1278, 1198, 1181 and 1139 g m−2 h−1, respectively. The waist (with average values of 557, 370, 596, and 332 g m−2 h−1, respectively) and bottom zones (373, 398, 661, and 849 g m−2 h−1, respectively) had the lowest sweat rates. The above data showed that the role of FCPE in promoting body perspiration. The upper body may be split into three zones of sweat rates based on the distribution result allowing for the design of more comfortable clothing. The study includes the fundamental physiological data as well as the design recommendations for advanced personal protective equipment. [ABSTRACT FROM AUTHOR]

Background/Aims: Although the adriamycin-induced nephropathy model is frequently employed in the study of nephrotic syndrome and focal segmental glomerulosclerosis, the accompanying myocardial damage has always been a cause for concern. Therefore, there is a great need to study cardiorenal communication in this model. Methods: An adriamycin-induced nephropathy model was established via tail vein injection. The levels of the biochemical indicators serum albumin, serum globulin, serum total protein, serum cholesterol, serum creatinine (SCr), urinary protein, and urinary creatinine (UCr) were measured, and histopathological changes in the heart and kidneys were assessed using hematoxylin-eosin staining. Metabolomic changes in the heart, blood, and kidneys were analyzed using the metabolomics method based on ultra-performance liquid chromatography Q-Exactive Orbitrap mass spectrometry. Results: Compared with the control group, the model group showed significant decreases in serum protein and total protein levels, albumin/globulin ratio, and creatinine clearance rate as well as significant increases in serum cholesterol, SCr, urinary protein, and UCr levels. Significant pathological changes were observed in the renal pathology sections in the model group, including diffusely merged glomerular epithelial cells, inflammatory infiltration, and vacuolated glomerular cells. Additionally, thickened myocardial fibers, swollen nuclei, inflammatory infiltration, and partial myocardial necrosis could be seen in the cardiac pathology sections in the model group. Based on multivariate statistical analysis, a total of 20 differential metabolites associated with 15 metabolic pathways were identified in the heart, 7 differential metabolites with 7 metabolic pathways were identified in the blood, and 16 differential metabolites with 21 metabolic pathways were identified in the kidney. Moreover, 6 common metabolic pathways shared by the heart and kidney were identified: arginine and proline metabolism; arginine biosynthesis; glutathione metabolism; alanine, aspartate, and glutamate metabolism; beta-alanine metabolism; and histidine metabolism. Among these metabolic pathways, alanine, aspartate, and glutamate metabolism was shared by the heart, blood, and kidney. Succinic acid was found to be the key regulatory metabolite in cardiorenal metabolic communication. Conclusion: Six metabolic pathways were found to be involved in cardiorenal metabolic communication in an adriamycin-induced nephropathy model, in which alanine, aspartate, and glutamate metabolism may be the metabolic link between the heart and kidney in the development and maintenance of oxidative stress and inflammation. Succinic acid may serve as a key regulatory metabolic switch or marker of cardiac and renal co-injury, as shown in an adriamycin-induced nephropathy model. [ABSTRACT FROM AUTHOR]

Viruses have evolved multiple strategies to manipulate their host's translational machinery for the synthesis of viral proteins. A common viral target is the alpha subunit of eukaryotic initiation factor 2 (eIF2α). In this study, we show that global protein synthesis was increased but the eIF2α phosphorylation level was markedly decreased in porcine kidney 15 (PK15) cells infected with pseudorabies virus (PRV), a swine herpesvirus. An increase in the eIF2α phosphorylation level by salubrinal treatment or transfection of constructs expressing wild-type eIF2α or an eIF2α phosphomimetic [eIF2α(S51D)] attenuated global protein synthesis and suppressed PRV replication. To explore the mechanism involved in the inhibition of eIF2α phosphorylation during PRV infection, we examined the phosphorylation status of protein kinase R-like endoplasmic reticulum kinase (PERK) and double-stranded RNA-dependent protein kinase R (PKR), two kinases that regulate eIF2α phosphorylation during infection with numerous viruses. We found that the level of neither phosphorylated (p)-PERK nor p-PKR was altered in PRV-infected cells or the lungs of infected mice. However, the expression of growth arrest and DNA damage-inducible protein 34 (GADD34), which promotes eIF2α dephosphorylation by recruiting protein phosphatase 1 (PP1), was significantly induced both in vivo and in vitro. Knockdown of GADD34 and inhibition of PP1 activity by okadaic acid treatment led to increased eIF2α phosphorylation but significantly suppressed global protein synthesis and inhibited PRV replication. Collectively, these results demonstrated that PRV induces GADD34 expression to promote eIF2α dephosphorylation, thereby maintaining de novo protein synthesis and facilitating viral replication. [ABSTRACT FROM AUTHOR]

The optimal spatial layout for a radar wind profiler (RWP) network in rainfall forecasting, especially over complex terrain, remains uncertain. This study explores the benefits of assimilating vertical wind measurements from various RWP network layouts into convective-scale numerical weather prediction (NWP) through observing system simulation experiments (OSSEs). Synthetic RWP data were assimilated into the Weather Research and Forecasting (WRF) model using the National Severe Storms Laboratory three-dimensional variational data assimilation (DA) system for three southwest (SW)-type heavy rainfall events in the Beijing-Tianjin-Hebei region. Four types of DA experiments were conducted and compared: a control experiment (CTL) that assimilates data solely from the operational RWP network, and three additional experiments incorporating foothill (FH), ridge (RD), and combined foothill-ridge (FH_RD) RWP network layouts. A detailed examination of the 21 July 2023 case reveals that the FH_RD experiment generally exhibits more skillful storm forecasts in terms of areal coverage, storm mode, and orientation, benifiting from refined mesoscale wind analysis. Particularly, in the RD experiment, RWP data assimilation notably reduces wind errors and enhances mesoscale dynamics near the Taihang Mountains upstream of Beijing, crucial for convective initiation (CI). Aggregated score metrics across all cases also indicate that both FH and RD experiments offer substantial added value over the operational network alone. Further sensitivity experiments on vertical resolution and maximum detection height indicate that the RWP system configuration with the highest detection height achieves the best performance, while lower detection height degrades forecast quality. These findings highlight the importance of strategic RWP network placement along the Taihang Mountains' ridge and foothill for short-term quantitative precipitation forecast in the Beijing-Tianjin-Hebei region. [ABSTRACT FROM AUTHOR]

Background: Glioma is a common primary central nervous system tumour, and therapeutic drugs that can effectively improve the survival rate of patients in the clinic are lacking. Bufalin is effective in treating various tumours, but the mechanism by which it promotes the apoptosis of glioma cells is unclear. The aim of this study was to investigate the drug targets of bufalin in glioma cells and to clarify the apoptotic mechanism. Methods: Cell viability and proliferation were evaluated by CCK-8 and colony formation assays. Then, the cell cycle and apoptosis, intracellular ion homeostasis, oxidative stress levels and mitochondrial damage were assessed after bufalin treatment. DARTS-PAGE technology was employed and LC–MS/MS was performed to explore the drug targets of bufalin in U251 cells. Molecular docking and western blotting were performed to identify potential targets. siRNA targeting Annexin A2 and the DRP1 protein inhibitor Mdivi-1 were used to confirm the targets of bufalin. Results: Bufalin upregulated the expression of cytochrome C, cleaved caspase 3, p-Chk1 and p-p53 proteins to induce U251 cell apoptosis and cycle arrest in the S phase. Bufalin also induced oxidative stress in U251 cells, destroyed intracellular ion homeostasis, and caused mitochondrial damage. The expression of mitochondrial division-/fusion-related proteins in U251 cells was abnormal, the Annexin A2 and DRP1 proteins were translocated from the cytoplasm to mitochondria, and the MFN2 protein was released from mitochondria into the cytoplasm after bufalin treatment, disrupting the mitochondrial division/fusion balance in U251 cells. Conclusions: Our research indicated that bufalin can cause Annexin A2 and DRP1 oligomerization on the surface of mitochondria and disrupt the mitochondrial division/fusion balance to induce U251 cell apoptosis. [ABSTRACT FROM AUTHOR]

Cancer is one of the diseases that threatens human health and is a leading cause of mortality worldwide. High levels of reactive oxygen species (ROS) have been observed in cancer tissues compared with normal tissues in vivo, and it is not yet known how this influences chemotherapeutic drug action. Cationic porphyrin 5,10,15,20-tetra-(N-methyl-4-pyridyl) porphyrin (TMPyP4) is a photosensitizer used in photodynamic therapy (PDT) and a telomerase inhibitor used in the treatment of telomerase-positive cancer. Here, we investigated the anticancer activity of TMPyP4 in A549 and PANC cells cultured in H2O2. The results showed that compared to TMPyP4 alone, the combination of TMPyP4 and H2O2 exhibited sensitization effects on cell viability and colony formation inhibition and apoptosis in A549 and PANC cells, but had no effect in human normal MIHA cells. Mechanistically, the combination of TMPyP4 and H2O2 activates high ROS and mitochondrial membrane potential in A549 and PANC cells, resulting in intense DNA damage and DNA damage responses. Consequently, compared to TMPyP4 alone, TMPyP4 and H2O2 combined treatment upregulates the expression of BAX, cleaved caspase 3, and p-JNK and downregulates the expression of Bcl-2 in A549 and PANC cells. Taken together, these data suggested that H2O2 enhanced the anticancer activity of TMPyP4-mediated ROS-dependent DNA damage and related apoptotic protein regulation, revealing that the high ROS tumor microenvironment plays an important role in chemotherapeutic drug action. [ABSTRACT FROM AUTHOR]