Hypoxia induces immunosuppression, metastasis and drug resistance in pancreatic cancers.

Pancreatic cancer is one of the common malignant tumors of the digestive system and is known as the "king of cancers". It is extremely difficult to diagnose at an early stage, the disease progresses rapidly, and the effect of chemotherapy and radiotherapy is poor, so the prognosis of pancreatic cancer patients is very poor. Numerous studies have suggested that hypoxia is closely related to the development and progression of pancreatic cancer. Inadequate blood supply and desmoplasia in the microenvironment of pancreatic cancer can result in its extreme hypoxia. This hypoxic microenvironment can further contribute to angiogenesis and desmoplasia. Hypoxia is mediated by the complex hypoxia inducible factor (HIF) signaling pathway and plays an important role in the formation of a highly immunosuppressive microenvironment and the metastasis of pancreatic cancer. Further work on the hypoxic microenvironment will help clarify the specific mechanisms of the role of hypoxia in pancreatic cancer and provide a basis for the realization of hypoxia-targeted therapeutic and diagnostic strategies.

Selective Ethanol Oxidation Reaction at the Rh-SnO2 Interface.

Direct ethanol fuel cells (DEFCs) are regarded as an attractive power source with high energy density, bio-renewability, and convenient storage and transportation. However, the anodic reaction of DEFCs, that is, the ethanol oxidation reaction (EOR), suffers from poor efficiency due to the low selectivity to CO2 (C1 pathway) and high selectivity to CH3 COOH (C2 pathway). In this study, the selective EOR to CO2 can be achieved at the Rh-SnO2 interface in SnO2 -Rh nanosheets (NSs). The optimized catalyst of 0.2SnO2 -Rh NSs/C exhibits excellent alkaline EOR performance with a mass activity of 213.2 mA mgRh -1 and a Faraday efficiency of 72.8% for the C1 pathway, which are 1.7 and 1.9 times higher than those of Rh NSs/C. Mechanism studies indicate that the strong synergy at the Rh-SnO2 interface significantly promotes the breaking of CC bond of C2 H5 OH to form CO2 , and facilitates oxidation of the poisonous intermediates (* CO and * CH3 ) to suppress the deactivation of the catalyst. This work not only provides a highly selective, active, and stable catalyst for the EOR, but also promotes fundamental research for the design of efficient catalysts via interface modification.

Simvastatin Alleviates Intestinal Ischemia/Reperfusion Injury by Modulating Omi/HtrA2 Signaling Pathways.

PURPOSE: The objective of this research was to survey the therapeutic action of simvastatin (Sim) on intestinal ischemia/reperfusion injury (II/RI) by modulating Omi/HtrA2 signaling pathways. METHODS: Sprague Dawley rats were pretreated with 40 mg/kg Sim and then subjected to 1 hour of ischemia and 3 hours of reperfusion. The blood and intestinal tissues were collected, pathologic injury was observed, the contents of serum tumor necrosis factor-α and interleukin-6 (IL-6) were estimated, and superoxide dismutase, methane dicarboxylic aldehyde, and cysteinyl aspartate specific proteinase-3 (caspase-3) levels, as well as the expressions of Omi/HtrA2 and caspase-3, were measured in the intestinal tissues. RESULTS: Sim preconditioning mitigated the damnification of intestinal tissues by decreasing oxidative stress, inflammatory damage, and apoptosis and downregulating the expression of Omi/HtrA2 compared to the ischemia/reperfusion group, while Sim+Ucf-101 significantly augmented this effect. CONCLUSION: These results suggest that Sim may alleviate intestinal ischemia/reperfusion injury by modulating Omi/HtrA2 signaling pathways.