Risk factors analysis of endoscopy and TIPS in the treatment of secondary esophagogastric varicose bleeding with cirrhosis.

Objective: To analyse the risk factors of secondary hemorrhage and survival rate in cirrhotic patients with esophagogastric variceal rupture and to compare the efficacy and safety of endoscopic hemostasis and TIPS (transjugular intrahepatic portosystemic shunt). Methods: A total of 120 patients with secondary bleeding after endoscopic treatment of esophagogastric varicose bleeding with cirrhosis in our hospital during the past 3 years were retrospectively analysed. There were 65 males and 55 females, ranging in age from 49 to 74 years old, with an average of (59.5 ± 8.4) years old. The etiology, degree of varicose veins, bleeding location, hemostasis method, Infection, ascites, portal vein thrombosis or cancer thrombus, albumin, platelets, prothrombin activity, Child Pugh (Child-Pugh classification is a diagnostic criterion for liver reserve function) grade were compared in each group. The risk factors of treatment failure and analyse the survival time was analysed. Results: There were statistically significant differences in varicosis degree, infection, ascites, portal vein thrombosis or cancer thrombus, child Pugh grade, albumin and prothrombin activity between the failed Endoscopy group and the successful hemostasis group (P< 0.05). There were statistically significant differences in child Pugh grade, albumin and prothrombin activity between the failed TIPS treatment group and successful hemostasis group (P< 0.05). There was no significant difference in 1-year survival between the endoscopy group and the TIPS group. Conclusion: Severe varicose veins, infection, ascites, portal vein thrombosis or cancer thrombus, child pugh classification, albumin, and prothrombin activity were the major risk factors for failed secondary endoscopic therapy, child Pugh classification, albumin and prothrombin activity were the main risk factors for failure TIPS treatment. There is no significant difference in long-term survival between the two methods.

MiR-10b-3p alleviates cerebral ischemia/reperfusion injury by targeting Krüppel-like factor 5 (KLF5).

Although miR-10b-3p has been identified to be involved in cerebral ischemia injury, its impact and specific mechanism in cerebral ischemia injury remain unclear. The effects of Mir-10b-3p were investigated by establishing rat and cell models of ischemia/reperfusion (I/R) injury. Oxygen-glucose deprivation/reperfusion (OGD/R) was performed on pheochromocytoma-12 (PC12) cells. MiR-10b-3p expression levels in brain tissues and PC12 cells were detected by qRT-PCR. The impacts of miR-10b-3p on neurological deficits, infarct volume, inflammatory factor expression, in vivo brain water content, cell viability, and cell apoptosis were assessed. The relationship between miR-10b-3p and KLF5 was determined by TargetScan and luciferase reporter assay. The rescue experiments were performed to confirm the role of this axis in cerebral ischemia injury. Mir-10b-3p levels in rat brain tissue and PC12 cells were significantly decreased after I/R injury. MiR-10b-3p overexpression obviously reduced neurological deficits, infarct volume, brain water content, inflammatory factors expression, and neuronal apoptosis in the brain of ischemia-stroked rats. Meanwhile, miR-10b-3p upregulation also inhibited cell viability and apoptosis of OGD/R-induced PC12 cells. Besides, KLF5 was identified as a target of miR-10b-3p, and rescue experiments revealed that KLF5 was involved in the regulation of miR-10b-3p in ischemic injury. Our results demonstrated that miR-10b-3p had the neuroprotective effects against ischemia injury by targeting KLF5 and provided a potential underlying target for ischemic stroke treatment.

Dexmedetomidine exerts a protective effect on ischemic brain injury by inhibiting the P2X7R/NLRP3/Caspase-1 signaling pathway.

Dexmedetomidine (Dex) has been suggested to exert a protective function in ischemic brain injury. In this study, we aimed to elucidate the intrinsic mechanisms of Dex in regulating microglia pyroptosis in ischemic brain injury via the purinergic 2X7 receptor (P2X7R)/NLRP3/Caspase-1 signaling pathway. First, permanent middle cerebral artery occlusion (p-MCAO) rat model was established, followed by the measurement of behavioral deficit, neuronal injury, the volume of brain edema and the infarct size. Dex treatment was suggested to alleviate the neurological deficits in p-MCAO rats and reduce the brain water content and infarct size. Additionally, rat microglia were cultured in vitro and a model of oxygen and glucose (OGD) was established. Microglia cell activity and ultrastructure were detected. Dex could increase cell activity and reduce LDH activity, partially reversing the changes in cell morphology. Furthermore, the activation of P2X7R/NLRP3/Caspase-1 pathway was tested. The obtained findings indicated Dex suppressed microglial pyroptosis by inhibiting the P2X7R/NLRP3/Caspase-1 pathway. Inhibition of P2X7R or NLRP3 could inhibit Caspase-1 p10 expression, improve cell activity, and reduce LDH activity. The same result was verified in vivo experiments. This study indicated that Dex inhibited microglia pyroptosis by blocking the P2X7R/NLRP3/Caspase-1 pathway, thus playing a protective role against ischemic brain injury.

Response of transpiration to rain pulses for two tree species in a semiarid plantation.

Responses of transpiration (Ec) to rain pulses are presented for two semiarid tree species in a stand of Pinus tabulaeformis and Robinia pseudoacacia. Our objectives are to investigate (1) the environmental control over the stand transpiration after rainfall by analyzing the effect of vapor pressure deficit (VPD), soil water condition, and rainfall on the post-rainfall Ec development and recovery rate, and (2) the species responses to rain pulses and implications on vegetation coverage under a changing rainfall regime. Results showed that the sensitivity of canopy conductance (Gc) to VPD varied under different incident radiation and soil water conditions, and the two species exhibited the same hydraulic control (-dG c/dlnVPD to Gcref ratio) over transpiration. Strengthened physiological control and low sapwood area of the stand contributed to low Ec. VPD after rainfall significantly influenced the magnitude and time series of post-rainfall stand Ec. The fluctuation of post-rainfall VPD in comparison with the pre-rainfall influenced the Ec recovery. Further, the stand Ec was significantly related to monthly rainfall, but the recovery was independent of the rainfall event size. Ec enhanced with cumulative soil moisture change (ΔVWC) within each dry-wet cycle, yet still was limited in large rainfall months. The two species had different response patterns of post-rainfall Ec recovery. Ec recovery of P. tabulaeformis was influenced by the pre- and post-rainfall VPD differences and the duration of rainless interval. R. pseudoacacia showed a larger immediate post-rainfall Ec increase than P. tabulaeformis did. We, therefore, concluded that concentrated rainfall events do not trigger significant increase of transpiration unless large events penetrate the deep soil and the species differences of Ec in response to pulses of rain may shape the composition of semiarid woodlands under future rainfall regimes.