Systemic injury plays a central role in severe acute pancreatitis (SAP). Retrograde biliopancreatic duct infusion of sodium taurocholate (NaT) is commonly used to establish SAP animal models. To better characterize the systemic injury in this model, SAP was induced in Sprague-Dawley rats by NaT administration (3.5 or 5%), followed by sacrifice at 3, 6, 9, 12, 24, 48 and 72 h. Normal saline was used as a control in Sham-operated rats. The mortality rate, ascites volume, and serum and ascitic fluid amylase and lipase activities were assessed. Multiple organ dysfunction, including dysfunction of the pancreas, lung, ileum, liver, and kidney, was investigated using hematoxylin and eosin staining. The interleukin (IL)-1β, IL-6, and tumor necrosis factor-α levels in the ascitic fluid, serum, and ileum tissues were evaluated using an enzyme-linked immunosorbent assay (ELISA). Tight junction proteins, zonula occludens-1 (ZO-1) and occludin, in ileum tissues were studied using immunofluorescence. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine (CRE) and urea levels were measured using an automatic biochemical analyzer. The results of the present study indicated that both 3.5 and 5% NaT could induce a stable elevation of pancreatitis indices, with histopathological injury of the pancreas, lungs and ileum (5% NaT). The ascitic fluid levels of IL-6 and IL-1β were increased in the 5% NaT group. ALT and AST levels increased temporarily and recovered in 72 h, without a significant increase in CRE and urea levels or apparent hepatic and renal pathological injury. In conclusion, rats with NaT-induced SAP have characteristics of necrotizing hemorrhagic pancreatitis with multiple organ injuries, including inflammatory lung injury, ischemic intestinal injury and slight liver and kidney injuries.

To stabilize the power out and reduce the dynamic loads in the over‐rated state, the pitch system is key for regulating pitch angle to the desired one obtained from the command layer. Here, actuator failure of the pitch system is considered and a neural adaptive fault‐tolerant control strategy with a rate function is proposed. More specifically, a non‐linear model of the pitch system considering time‐varying parameter uncertainties and unknown disturbances is established firstly. Then, the neural network is used to counteract the external disturbance and system uncertainty. The rate function with adjustable parameters is designed to transform the error, which makes the tracking error decrease at a fast rate and converge to a small zero domain, and realize the control goal of accurate and fast tracking the desired pitch angle of the pitch system. A co‐simulation is developed, and the merits of the proposed method are verified.

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Persistent Helicobacter pylori infection causes a variety of gastrointestinal diseases and even gastric cancer. H. pylori invades gastric epithelial cells to survive and proliferate, which is one of the key factors in persistent colonization. A Published study has confirmed that cells can eliminate intracellular H. pylori through xenophagy to maintain intracellular balance. However, a growing body of evidences indicate that H. pylori can inhibit xenophagy by miRNA through regulating the expression of key autophagy-related genes. Through western blot analysis, mRFP-GFP-LC3 transfection assay, and transmission electron microscopy, we found that H. pylori infection obstructed autophagy flux degradation stage in GES-1 cell lines. Gentamicin protection assay confirmed that inhibit xenophagy is benefit for intracellular H. pylori survive. miR-30c-1-3p and miR-30c-5p were upregulated in GES-1 cell lines after infecting with H. pylori, resulting in the negative regulation on xenophagy. Further studies through bioinformatics analysis and dual-luciferase reporter assays confirmed that ATG14 and ULK1 were the target genes of miR-30c-1-3p and that ATG12 was the target gene of miR-30c-5p. The overexpression of miR-30c-1-3p and miR-30c-5p reduces the expression of ATG14, ULK1, and ATG12 at mRNA level and also decreased intracellular H. pylori elimination in GES-1 cells. The above results suggested that the inhibition on xenophagy by miR-30c-1-3p and miR-30c-5p through ATG14, ULK1, and ATG12 targeting benefitted intracellular H. pylori in the evasion of xenophagy clearance.

Selection and peer-review under responsibility of the scientific committee of the 13 th Int. Conf. on Applied Energy (ICAE2021).