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Background Patients with acute ischemic stroke (AIS) and cancer are at exceptionally high risk for recurrent thromboembolism (RTE), which includes venous thromboembolism (VTE) and arterial thromboembolism (ATE). Yet contemporary data from Chinese patients remain scarce. Methods In this retrospective, observational study conducted at Tianjin First Central Hospital (June 2023-December 2024), consecutive adults with AIS and cancer were enrolled. The primary outcomes during 6 months follow-up were recurrent VTE།composite VTE (symptomatic and incidental VTE requiring treatment), recurrent stroke [cerebral infarction, transient ischemic attack (TIA), and systemic embolism (SE)], and bleeding (major bleeding and clinically significant non-major bleeding). Multivariable logistic regression was used to identify independent predictors of each endpoint. Results Among 218 eligible patients, 49 (22.5%) had baseline VTE, of whom 45 (91.8%) were asymptomatic. Baseline VTE was independently predicted by cryptogenic stroke subtype (OR 2.70; 95% CI 1.101–6.621; P  = 0.030) and D-dimer > 1.2 µg/mL (OR 3.619; 95% CI 1.505–8.703; P  = 0.004). During follow-up, 25 patients (11.5%) experienced composite VTE, 71 patients (32.6%) experienced recurrent stroke, and 21 patients (9.6%) experienced bleeding. Multivariable analysis revealed that D-dimer > 1.2 µg/mL independently predicted recurrent VTE (OR 3.501; 95% CI 1.012–12.112; P  = 0.048), whereas cancer metastasis portended recurrent stroke (OR 3.155; 95% CI 1.423–6.995; P  = 0.005), and anticoagulant therapy was associated with an increased bleeding risk (OR 9.458; 95% CI 1.158–77.267; P  = 0.036). Conclusions In this Chinese cohort of patients with acute ischemic stroke (AIS) and cancer, routine screening revealed venous thromboembolism (VTE) in roughly one-fifth of participants at baseline, most of whom were asymptomatic. Exploratory multivariable analyses indicated that cryptogenic stroke subtype and D-dimer > 1.2 µg/mL were associated with prevalent VTE, while D-dimer > 1.2 µg/mL also predicted recurrent VTE. These findings suggested that D-dimer guided VTE screening might be considered at the time of stroke presentation, even in the absence of symptoms. Cancer metastasis showed an association with recurrent stroke, whereas anticoagulant therapy was linked to a higher bleeding risk.

Background To explore the correlation between the volume of putamen and brain cognitive impairment in patients with HIV and to predict the feasibility of early-stage HIV brain cognitive impairment through radiomics. Method Retrospective selection of 90 patients with HIV infection, including 36 asymptomatic neurocognitive impairment (ANI) patients and 54 pre-clinical ANI patients in Beijing YouAn Hospital. All patients received comprehensive neuropsychological assessment and MRI scanning. 3D Slicer software was used to acquire volume of interest (VOI) and radiomics features. Clinical variables and volume of putamen were compared between patients with ANI and pre-clinical ANI. The Kruskal Wallis test was used to analysis multiple comparisons between groups. The relationship between cognitive scores and VOI was compared using linear regression. For radiomics, principal component analysis (PCA) was used to reduce model overfitting and calculations and then a support vector machine (SVM) was used to build a binary classification model. For model performance evaluation, we used an accuracy, sensitivity, specificity and receiver operating characteristic curve (ROC). Result There were no significant differences in clinical variables between ANI group and pre-clinical-ANI group ( P >0.05). The volume of bilateral putamen was significantly different between AHI group and pre-clinical group ( P <0.05), but there was only a trend in the left putamen between ANI-treatment group and pre-clinical treatment group( P  = 0.063). Reduced cognitive scores in Verbal Fluency, Attention/Working Memory, Executive Functioning, memory and Speed of Information Processing were negatively correlated with the increased VOI ( P <0.05), but the correlation was relatively low. In diagnosing the ANI from pre-clinical ANI, the mean area under the ROC curves (AUC) were 0.85 ± 0.22, the mean sensitivity and specificity were 63.12 ± 5.51 and 94.25% ± 3.08%. Conclusion The volumes of putamen in patients with ANI may be larger than patients with pre-clinical ANI, the change of the volume of the putamen may have a certain process; there is a relationship between putamen and cognitive impairment, but the exact mechanism is unclear. Radiomics may be a useful tool for predicting early stage HAND in patients with HIV.

A multiple variable model is developed for a multiple-effect low temperature desalination system. Multiple-effect water desalination has been used in industry for decades due to its high efficiency and high quality of fresh water production. Here, its dynamical process is modeled based on the mass and heat conservation laws and then expressed in terms of a state space equation, enabling people to carry out analysis and design controllers.

EVO is a natural alkaloid that reportedly has potential value in regulating gastrointestinal motility, but this conclusion remains controversial, and the molecular mechanism is unclear. In this study, we aimed to explore the effect of short-chain fatty acids on rat colonic hypermotility induced by water avoidance stress and the underlying mechanism. We constructed a hypermotile rat model by chronic water avoidance stress, and Western blot was used to detect the protein level of nNOS in colon tissue. The organ bath and multichannel physiological signal acquisition systems were used to examine the spontaneous contractions of smooth muscle strips. The whole-cell patch-clamp technique was used to investigate L-type voltage-dependent calcium and BK channel currents in colonic smooth muscle cells. EVO inhibited the spontaneous contractions of colonic smooth muscle strips in a dose-dependent manner. Moreover, EVO decreased the fecal output induced by chronic water avoidance stress. TTX did not block the inhibitory effect of EVO on spontaneous colon contractions, while L-NNA, a selective nNOS synthase inhibitor, did partially abolish this inhibitory effect. The protein expression of nNOS in the colon tissues of rats administered EVO was significantly increased compared to that in control rats. EVO reversibly inhibited the L-type calcium channel current without changing the steady-state activation or inactivation in colonic smooth muscle cells. EVO significantly inhibited the BK current but did not change the shape of the I-V curves. EVO inhibits gastrointestinal motility by inhibiting L-type calcium and BK channels in colonic smooth muscle cells and indirectly interacting with nNOS.

Aim： In the penumbra after focal cerebral ischemia, an increase of protease Omi is linked to a decrease of Hsl-associated protein X-1 （Hax-1）, a protein belonging to the Bcl-2 family. In this study we investigated the mechanisms underlying the regulation of Hax-1 by protease Omi in cerebral ischemia/reperfusion （I/R） injury. Methods： Mouse neuroblastoma N2a cells were subjected to oxygen-glucose deprivation and reoxygenation （OGD/R）; cell viability was assessed with MTT assay. Mice underwent 2-h middle cerebral artery occlusion （MCAO） and reperfusion, and the infarct volume was determined with TTC staining. The expression of Omi and Hax-1 was detected using immunoblot and immunofluorescence assays. The mitochondrial membrane potential was measured using TMRM staining. Results： In the brains of MCAO mice, the protein level of Omi was significantly increased, while the protein level of Hax-1 was decreased. Similar changes were observed in OGD/R-treated N2a cells, but the mRNA level of Hax-1 was not changed. Furthermore, in OGD/R-treated N2a cells, knockdown of Omi significantly increased Hax-1 protein level. Immunofluorescence assay showed that Omi and Hax-1 were co-localized in mitochondria of N2a cells. OGD/R caused marked mitochondrial damage and apoptosis in N2a cells, while inhibition of Omi protease activity with UCF-101 （10 pmol/L） or overexpression of Hax-1 could restore the mitochondrial membrane potential and attenuate cell apoptosis. Moreover, pretreatment of MCAO mice with UCF-101 （7.15 mg/kg, ip） could restore Hax-1 expression, inhibit caspase activation, and significantly reduce the infarct volume. Conclusion： Protease Omi impairs mitochondrial function by cleaving Hax-1, which induces apoptosis in OGD/R-treated N2a cells and causes I/R injury in MCAO mice.

Heart failure (HF) represents one of the leading causes of cardiovascular diseases with high rates of hospitalization, morbidity and mortality worldwide. Ample evidence has consolidated a crucial role for mitochondrial injury in the progression of HF. It is well established that mitochondrial Ca 2+ participates in the regulation of a wide variety of biological processes, including oxidative phosphorylation, ATP synthesis, reactive oxygen species (ROS) generation, mitochondrial dynamics and mitophagy. Nonetheless, mitochondrial Ca 2+ overload stimulates mitochondrial permeability transition pore (mPTP) opening and mitochondrial swelling, resulting in mitochondrial injury, apoptosis, cardiac remodeling, and ultimately development of HF. Moreover, mitochondria possess a series of Ca 2+ transport influx and efflux channels, to buffer Ca 2+ in the cytoplasm. Interaction at mitochondria-associated endoplasmic reticulum membranes (MAMs) may also participate in the regulation of mitochondrial Ca 2+ homeostasis and plays an essential role in the progression of HF. Here, we provide an overview of regulation of mitochondrial Ca 2+ homeostasis in maintenance of cardiac function, in an effort to identify novel therapeutic strategies for the management of HF.

A study was conducted to identify the differences in the decompositions of leaf litter, lignin and carbohydrate between coniferous forest and broadleaf forest at 20℃ and 30℃ in Huangshan Mountain, Anhui Province, China. Results showed that at 20℃ mass loss of leaf litter driven by microbial decomposers was higher in broadleaf forest than that in coniferous forest, whereas the difference in mass loss of leaf litter was not significant at 30℃. The temperature increase did not affect the mass loss of leaf litter for coniferous forest treatment, but significantly reduced the decomposition rate for broadleaf forest treatment. The functional decomposers of microorganism in broadleaf forest produced a higher lignin decomposition rate at 20℃, compared to that in coniferous forest, but the difference in lignin decomposition was not found between two forest types at 30℃. Improved temperature increased the lignin decomposition for both broadleaf and coniferous forest. Additionally, the functional group of microorganism from broadleaf forest showed marginally higher carbohydrate loss than that from coniferous forest at both temperatures. Temperature increase reduced the carbohydrate decomposition for broadleaf forest, while only a little reduce was found for coniferous forest. Remarkable differences occurred in responses between most enzymes （Phenoloxidase, peroxidase, !5-glucosidase and endocellulase） and decomposition rate of leaf litter to forest type and temperature, although there exist strong relationships between measured enzyme activities and decomposition rate in most cases. The reason is that more than one enzyme contribute to the mass loss of leaf litter and organic chemical components. In conclusion, at a community scale the coniferous and broadleaf forests differed in their temperature-decomposition relationships.

In Arabidopsis, the salt overly sensitive (SOS) pathway, consisting of calcineurin B-like protein 4 (CBL4/SOS3), CBL-interacting protein kinase 24 (CIPK24/SOS2) and SOS1, has been well defined as a crucial mechanism to control cellular ion homoeostasis by extruding Na+ to the extracellular space, thus conferring salt tolerance in plants. CBL10 also plays a critical role in salt tolerance possibly by the activation of Na+ compartmentation into the vacuole. However, the functional relationship of the SOS and CBL10-regulated processes remains unclear. Here, we analyzed the genetic interaction between CBL4 and CBL10 and found that the cbl4 cbl10 double mutant was dramatically more sensitive to salt as compared to the cbl4 and cbl10 single mutants, suggesting that CBL4 and CBL10 each directs a different salt-tolerance pathway. Furthermore, the cbl4 cbl10 and cipk24 cbl10 double mutants were more sensitive than the cipk24 single mutant, suggesting that CBL10 directs a process involving CIPK24 and other partners different from the SOS pathway. Although the cbl4 cbl10, cipk24 cbl10, and sos1 cbl10 double mutants showed comparable salt-sensitive phenotype to sos1 at the whole plant level, they all accumulated much lower Na+ as compared to sos1 under high salt conditions, suggesting that CBL10 regulates additional unknown transport processes that play distinct roles from the SOS1 in Na+ homeostasis.

The primary processed product of Panax ginseng C.A. Meyer ( P. ginseng ) is red ginseng. As technology advances, new products of red ginseng have arisen. Red ginseng products, e.g., traditional red ginseng, sun ginseng, black ginseng, fermented red ginseng, and puffed red ginseng, are commonly used in herbal medicine. Ginsenosides are the major secondary metabolites of P. ginseng . The constituents of P. ginseng are significantly changed during processing, and several pharmacological activities of red ginseng products are dramatically increased compared to white ginseng. In this paper, we aimed to review the ginsenosides and pharmacological activities of various red ginseng products, the transformation law of ginsenosides in processing, and some clinical trials of red ginseng products. This article will help to highlight the diverse pharmacological properties of red ginseng products and aid in the future development of red ginseng industrialization.

Dual-atom catalysts, combining single-atom catalysts and metal alloys, are promising electrocatalysts for CO2 reduction but are limited by sluggish CO2 reduction kinetics and ill-defined dual-atom sites. Here, we develop a catalyst of Ni dual-atom sites via in situ conversion of nanoparticles into dual atoms. We achieve efficient electrocatalytic CO2 reduction on Ni dual-atom catalysts with a CO partial current density up to ~1 A cm−2 and turnover frequency of 77,500 h−1 at >99% Faradaic efficiency. In situ X-ray absorption and theoretical calculations reveal that during the catalytic process the Ni dual-atom sites trigger the adsorption of hydroxyl (OHad), forming electron-rich active centres that endow a moderate reaction kinetic barrier of *COOH formation and *CO desorption. The resultant catalytic microenvironment enables expedited kinetics compared with either the kinetics of bare dual-atom sites or OHad regulated single-atom sites.Dual-atom catalysts are promising for CO2 reduction reactions; however, sluggish kinetics limit practical applications. Now, a Ni dual-atom catalyst has been synthesized, realizing efficient electrocatalytic CO2 reduction with a CO partial current density of ~1 A cm2 at >99% Faradaic efficiency.