This investigation devotes to the kinetics of the reduction of (MnO) with carbon-saturated liquid iron. The experiment condition involves high content realm of both ("I. MnO)
ObjectiveThe objective of this study is to investigate the association between the incidence of pancreatic fistula after pancreaticoduodenectomy (PD) and the degree of pancreatic fibrosis.MethodBetween January 2013 and December 2016, the analysis of the clinical data of 529 cases of pancreaticoduodenectomy patients of our hospital was performed in a retrospective fashion. The univariate analysis and multivariate analysis were done using the Pearson chi-squared test and binary logistic regression analysis model; correlations were analyzed by Spearman rank correlation analysis. The value of the degree of pancreatic fibrosis to predict the incidence of pancreatic fistula after pancreaticoduodenectomy was evaluated by the area under the receiver operating characteristic (ROC) curve.ResultsThe total incidence of pancreatic fistula after pancreaticoduodenectomy was 28.5% (151/529). Univariate analysis and multivariate analysis showed that BMI ≥ 25 kg/m2, pancreatic duct size ≤ 3 mm, pancreatic CT value< 30, the soft texture of the pancreas (judged during the operation), and the percent of fibrosis of pancreatic lobule ≤ 25% are prognostic factors of pancreatic fistula after pancreaticoduodenectomy (P < 0.05); the pancreatic CT value and the percent of fibrosis of pancreatic lobule in pancreatic fistula group were both lower than those in non-pancreatic fistula group (P < 0.05). Results indicated that there is a negative correlation between the severity of pancreatic fistula and the pancreatic CT value or the percent of fibrosis of pancreatic lobule (r = − 0.297, − 0.342, respectively). The areas under the ROC curve of the percent of fibrosis of pancreatic lobule and the pancreatic CT value were 0.756 and 0.728, respectively.ConclusionThe degree of pancreatic fibrosis is a prognostic factor which can influence the pancreatic texture and the incidence of pancreatic fistula after pancreaticoduodenectomy. The pancreatic CT value can be used as a quantitative index of the degree of pancreatic fibrosis to predict the incidence of pancreatic fistula after pancreaticoduodenectomy.
Chronic cerebral hypoperfusion is believed to cause white matter lesions (WMLs), leading to cognitive impairment. Previous studies have shown that inflammation and apoptosis of oligodendrocytes (OLs) are involved in the pathogenesis of WMLs, but effective treatments have not been studied. In this study, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), a chloride (Cl−) channel blocker, was injected into chronic cerebral ischemia-hypoxia rat models at different time points. Our results showed that DIDS significantly reduced the elevated mRNA levels and protein expression of chloride channel 2 (ClC-2) in neonatal rats induced by ischemia-hypoxia. Meanwhile, DIDS application significantly decreased the concentrations of reactive oxygen species (ROS); and the mRNA levels of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha TNF-α in neonatal rats with hypoxic-ischemic damage. Myelin staining was weaker in neonatal rats with hypoxic-ischemic damage compared to normal controls in corpus callosum and other white matter, which was ameliorated by DIDS. Furthermore, the elevated number of caspase-3 and neural/glial antigen 2 (NG-2) double-labeled positive cells was attenuated by DIDS after ischemia anoxic injury. Administration of DIDS soon after injury alleviated damage to OLs much more effectively in white matter. In conclusion, our study suggests that early application of DIDS after ischemia-hypoxia injury may partially protect developing OLs.
BackgroundBladder cancer (BCa) is one of the most frequent malignant tumors globally, with a significant morbidity and mortality rate. Gene expression dysregulation has been proven to play a critical role in tumorigenesis. Ras-related C3 botulinum toxin substrate3 (RAC3), which is overexpressed in several malignancies and promotes tumor progression, has been identified as an oncogene. However, RAC3 has important but not fully understood biological functions in cancer. Our research aims to reveal the new functions and potential mechanisms of RAC3 involved in BCa progression.MethodsWe explored the expression level of RAC3 and its relationship with prognosis by publicly accessible BCa datasets, while the correlation of RAC3 expression with clinicopathological variables of patients was analyzed. In vitro and in vivo proliferation, migration, autophagy, and other phenotypic changes were examined by constructing knockdown(KD)/overexpression(OE) RAC3 cells and their association with PI3K/AKT/mTOR pathway was explored by adding autophagy-related compounds.ResultsCompared with non-tumor samples, RAC3 was highly expressed in BCa and negatively correlated with prognosis. KD/OE RAC3 inhibited/promoted the proliferation and migration of BCa cells. Knockdown RAC3 caused cell cycle arrest and decreased adhesion without affecting apoptosis. Inhibition of RAC3 activates PI3K/AKT/mTOR mediated autophagy and inhibits proliferation and migration of BCa cells in vivo and in vitro. Autophagy inhibitor 3MA can partially rescue the metastasis and proliferation inhibition effect caused by RAC3 inhibition. Inhibit/activate mTOR enhanced/impaired autophagy, resulting in shRAC3-mediated migration defect exacerbated/rescued.ConclusionRAC3 is highly expressed in BCa. It is associated with advanced clinicopathological variables and poor prognosis. Knockdown RAC3 exerts an antitumor effect by enhancing PI3K/AKT/mTOR mediated autophagy. Targeting RAC3 and autophagy simultaneously is a potential therapeutic strategy for inhibiting BCa progression and prolonging survival.
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