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Background: Cerebral venous thrombosis (CVT) is a rare but serious condition that can lead to significant morbidity and mortality. Virchow's triad elucidates the role of blood hypercoagulability, blood flow dynamics, and endothelial damage in the pathogenesis of CVT. Cerebral venous congestion (CVC) increases the risk of cerebral venous sinus thrombosis and can lead to recurrent episodes and residual symptoms. However, the precise mechanism by which blood congestion leads to thrombosis remains unclear. Our objective was to investigate the cellular and molecular alterations linked to CVC through analysis of the pathological morphology of venous sinus endothelial cells and transcriptomic profiling. Results: This study demonstrated a remarkable correlation between CVC and the phenotypic transformation of endothelial cells from an anticoagulant to a procoagulant state. The findings revealed that cerebral venous stasis results in tortuous dilatation of the venous sinuses, with slow blood flow and elevated pressure in the sinuses and damaged endothelial cells of the retroglenoid and internal jugular vein ligation (JVL) rat model. Mechanistically, analysis of transcriptomic results of cerebral venous sinus endothelial cells showed significant activation of platelet activation, complement and coagulation cascades pathway in the JVL rats. Furthermore, the expression of von Willebrand factor (vWF) and coagulation factor VIII (F8) in the complement and coagulation cascades and Fgg and F2 in the platelet activation was increased in the cerebral venous sinuses of JVL rats than in sham rats, suggesting that endothelial cell injury in the venous sinus induced by CVC has a prothrombotic effect. In addition, endothelial cell damage accelerates coagulation and promotes platelet activation. Significantly, the concentrations of vWF, F2 and F8 in venous sinus blood of patients with internal jugular vein stenosis were higher than in their peripheral blood. Conclusion: Collectively, our data suggest that CVC can induce endothelial cell damage, which then exhibits a procoagulant phenotype and ultimately increases the risk of CVT. This research contributes to our understanding of the pathophysiology of CVC associated with procoagulant factors and reexamines the components of Virchow's triad in the context of CVC. [ABSTRACT FROM AUTHOR]

Immune checkpoint blockade (ICB) therapy for tumors has arisen in growing interest. However, the low response rate of tumors to ICB is mainly attributed to the inhibitory infiltration of immune cells in the tumor microenvironment (TME). Despite the promising benefits of ICB, the therapeutic effects of antibodies are dependent on a high dose and long‐term usage in the clinic, thereby leading to immune‐related adverse effects. Accordingly, ICB combined with nano‐delivery systems could be used to overcome T cell exhaustion, which reduces the side effects and the usage of antibodies with higher response rates in patients. In this review, the authors aim to overcome T cell exhaustion in TME via immune checkpoint modulation with nano‐delivery systems for enhanced immunotherapy. Several strategies are summarized to combine ICB and nano‐delivery systems to further enhance immunotherapy: a) expressing immune checkpoint on the surface of nano‐delivery systems; b) loading immune checkpoint inhibitors into nano‐delivery systems; c) loading gene‐editing technology into nano‐delivery systems; and d) nano‐delivery systems mediated immune checkpoint modulation. Taken together, ICB combined with nano‐delivery systems might be a promising strategy to overcome T cell exhaustion in TME for enhanced immunotherapy. [ABSTRACT FROM AUTHOR]

Considering the mismatch in the supply of and demand for the industrial process wastes, we investigate when the interfirm waste utilisation can be both economically and environmentally superior to the no waste utilisation. The Nash bargaining approach is employed to resolve the incentive misalignment problem. Our analysis suggests that the conversion strategy changes from over-conversion, to full conversion, and then to partial conversion with increasing waste trading price. Furthermore, an increase in the waste disposal fee contributes to the diversion of wastes from the landfill but may result in worse environmental consequences especially for wastes with a slight reduction in the production impact compared to raw materials. This implies that policy makers should charge the waste disposal fee based on waste types and focus on increasing that for wastes with higher disposal and lower production impacts. Finally, at the lower waste trading price, the interfirm waste utilisation is always a win-win strategy. While at the higher waste trading price, it is a win-win strategy for products with a substantial reduction in the production impact when producing with wastes. Otherwise, it is a win-win strategy for products with a lower production impact relative to the raw material usage and waste disposal impacts. [ABSTRACT FROM AUTHOR]

Obesity has become a major disease that endangers human health. Studies have shown that dietary interventions can reduce the prevalence of obesity and diabetes. Resistant starch (RS) exerts anti-obesity effects, alleviates metabolic syndrome, and maintains intestinal health. However, different RS types have different physical and chemical properties. Current research on RS has focused mainly on RS types 2, 3, and 4, with few studies on RS1. Therefore, this study aimed to investigate the effect of RS1 on obesity and gut microbiota structure in mice. In this study, we investigated the effect of potato RS type 1 (PRS1) on obesity and inflammation. Mouse weights, as well as their food intake, blood glucose, and lipid indexes, were assessed, and inflammatory factors were measured in the blood and tissues of the mice. We also analyzed the expression levels of related genes using PCR, with 16S rRNA sequencing used to study intestinal microbiota changes in the mice. Finally, the level of short-chain fatty acids was determined. The results indicated that PRS1 promoted host obesity and weight gain and increased blood glucose and inflammatory cytokine levels by altering the gut microbiota structure. [ABSTRACT FROM AUTHOR]