ERCP has become an important method for diagnosis and treatment of digestive diseases,but the high incidences of post-ERCP complications(PEP),especially for post-ERCP pancreatitis,have limited its application.Prevention of PEP has become a focus of ERCP-related studies.Current drug prevention of PEP is not satisfactory,and there has not been a single drug which can effectively prevent PEP.In contrast,non-pharmacologic preventive techniques such as pancreatic stent placing and guide wire cannulation have been proven to have prominent effects in preventing PEP,which brings new hopes for PEP prevention.This paper reviews the studies on non-pharmacologic prevention of PEP.

With the organic combination of rapid on-site evaluation (ROSE) and interventional pulmonary diagnostic technology, we can build a complete The System of Diagnostic Interventional Pulmonology Based on Rapid on-site Evaluation. With the help of ROSE, changing the ways, methods and modalities of interventional pulmonary diagnostic technology to obtain the target lesions is the core of this system. In this statement, the most commonly used standard operating techniques in The System of Diagnostic Interventional Pulmonology Based on Rapid on-site Evaluation are described in detail, including double-hinge curette operating technique, transbronchial lung biopsy (TBLB) technique, and transbronchial brushing technique.

AIM: To investigate the signaling mechanisms involved in the priming effects of lipopolysaccharide(LPS) on heat killed Staphylococcus aureus(HKSa)-induced nitric oxide(NO) production in macrophages.METHODS: Murine macrophage RAW264.7 was used in the experiment.Griess reagent was used to measure the content of nitrite in culture medium.Real-time PCR and Western blot was utilized to examine the mRNA and protein levels of toll-like receptor 2(TLR2),respectively.Dual luciferase reporter assay was used to assess the transcriptional activity of nuclear factor of activated T cells(NF-AT).RESULTS: The RAW264.7 cells pretreated with LPS for 24 h significantly enhanced NO production induced by HKSa,suggesting that LPS primed the macrophages and increased the reactivity of the cells to HKSa.LPS increased the mRNA and protein levels of TLR2 in a dose-dependent manner in RAW264.7 cells.The RAW264.7 cells pretreated with LPS enhanced NO production induced by peptidoglycan,one of the specific ligand of TLR2.The priming effect of LPS on HKSa-induced NO production was partly blocked by TLR2 neutralizing antibody.LPS significantly enhanced the transcriptional activity of NF-AT,which was inhibited by BAPTA/AM(a cell-permeable cytosolic calcium chelator) and cyclosporine A(CsA,an inhibitor for calcineurin).Both BAPTA/AM and CsA inhibited the priming effect of LPS on HKSa-induced NO production in RAW264.7 cells.CONCLUSION: The present study confirms the priming effect of LPS on the reactivity of RAW264.7 cells to HKSa.Pattern recognition receptor TLR2 and calcium/calcineurin/NF-AT signaling pathway may be involved in the priming process initiated by LPS.

[摘 要] 目的：探究微小RNA-504（miRNA-504）在胃癌（GC）组织中的表达水平及其对GC细胞生物学行为的调控机制。方法：收集2020年6月至2020年12月期间三亚中心医院外科收治的48例胃癌患者的肿瘤组织及癌旁组织标本，qPCR检测组织中miR-504、肿瘤蛋白53诱导型核蛋白1（tumor protein 53-induced nuclear protein 1，TP53INP1）mRNA的水平，WB法检测TP53INP1水平。体外培养人胃癌细胞BGC-823，分为对照组（正常培养的BGC-823细胞）、miR-504 mimic组、mimic-NC组、miR-504 inhibitor组、inhibitor-NC组、miR-504 inhibitor+si-NC组、miR-504 inhibitor+si-TP53INP1组，qPCR检测细胞中miR-504和TP53INP1 mRNA的表达，MTT法、流式细胞术、划痕实验和Transwell侵袭实验分别检测各组细胞的增殖、凋亡、迁移和侵袭能力，WB法检测各组细胞中增殖、迁移和侵袭相关蛋白（Cyclin D1、E-cadherin、MMP-2、MMP-9）以及TP53INP1的表达。双荧光素酶报告基因实验进一步验证miR-504与TP53INP1 mRNA的靶向关系。结果：与癌旁组织相比，胃癌组织中miR-504的表达显著升高（P<0.05），而TP53INP1 mRNA和蛋白表达水平显著降低（P<0.05或P<0.01），miR-504和TP53INP mRNA两者的表达呈负相关（P<0.01）。与对照组相比，miR-504 mimic组BGC-823细胞中miR-504的表达显著升高（P<0.05）、TP53INP1 mRNA和蛋白的表达显著降低（均P<0.05），且细胞增殖率、划痕愈合率、侵袭入Transwell小室下层的细胞数量，Cyclin D1、MMP-2、MMP-9蛋白表达均显著增加，细胞凋亡率和E-cadherin蛋白表达均显著降低（均P<0.05）。转染miR-504 inhibitor能显著下调BGC-823中miR-504的表达、上调TP53INP1 mRNA和蛋白的表达，抑制细胞的增殖、迁移与侵袭能力而促进细胞凋亡（均P<0.05）；而下调TP53INP1的表达可明显减弱miR-504下调对BGC-823细胞增殖、迁移与侵袭的抑制作用（P<0.01）。miR-504高表达能明显抑制野生型TP53INP1质粒的荧光素酶活性（P<0.05）。结论：miR-504在胃癌组织中呈高表达，下调miR-504可抑制胃癌BGC-823细胞的恶性生物学行为而促进其凋亡，其作用机制可能与靶向调控TP53INP1的表达有关。

Adult ; Humans ; Heart Arrest/therapy* ; Cardiopulmonary Resuscitation ; Emergency Service, Hospital ; Out-of-Hospital Cardiac Arrest/therapy* ; Treatment Outcome