高甘油三酯血症性急性胰腺炎（hypertriglyceridemia-induced acute pancreatitis, HTG-AP）因"诱因隐匿、淀粉酶升高不明显、发病年轻化、合并症多、病情进展快、易重症化"给临床救治带来困难。快速降低甘油三酯水平是逆转病情进展和治疗的关键。本文报道病因隐匿的急性胰腺炎（acute pancreatitis, AP）治疗成功案例1例，旨在对HTG-AP早期识别和病因治疗提供临床经验。

目的 探讨利用国际顶级医学学术期刊及其官网资源对高年资住培医生临床思维培训的应用效果.方法 2021 年 8-9 月,随机选择西安交通大学第二附属医院 15 名三年级住院医师规范化培训(简称"住培")医生,对其进行每周 1 节临床病案推理及临床思维培训课.该课程由 8 名西安交通大学第二附属医院急诊科授课老师授课.8 名授课教师随机分为对照组(n=4)和试验组(n=4),对照组临床教学病例来源于本住培基地临床病例,试验组临床教学病例来源于国际顶级医学学术期刊报道或其官网有关医学教育内容.2 名评委随堂听课.每堂课程结束后对住培医生、评委、授课教师进行问卷调查,对问卷结果进行分析.结果 在病案新颖性、认知启发性、临床思维提升、科研启发、临床病案质量、学员随堂临床思维发散程度及病案对授课教师自我认知的提高方面,试验组均优于对照组,差异有统计学意义(P＜0.05).结论 利用国际顶级医学学术期刊及其官网资源对高年资住培医生进行临床思维培训,能够提高住培教学质量,使得教学内容国际化,达到教学相长的效果.

目的 分析急性呼吸衰竭(ARF)患者发生胃肠功能障碍的危险因素并构建预测模型.方法 选择2018 年8 月—2022 年8 月西安交通大学第二附属医院急诊科收治的老年ARF患者 452 例,采用急性胃肠功能障碍(AGI)评分评估患者胃肠道功能并分为无障碍组136 例和障碍组316 例.收集患者临床资料,采用二元Logistic回归分析老年ARF患者发生胃肠功能障碍的危险因素,基于危险因素构建老年ARF患者发生胃肠功能障碍的预测模型.Hosmer-Lemeshow(H-L)检验、受试者工作特征曲线(ROC)检验预测模型的校准度和区分度.结果 AGI分级 1 级136 例,2 级152 例,3 级101 例,4 级63 例,共316 例发生胃肠道功能障碍,胃肠道功能障碍发生率为69.91%.2 组年龄、ARF病因、腹腔感染、营养支持、ICU住院时间、APACHEⅡ评分、SOFA评分、PCT、CRP、DAO、D-乳酸、IFABP等比较差异有统计学意义(P<0.05).年龄大、脓毒症、SOFA评分高、D-乳酸高、IFABP高是老年ARF患者发生胃肠功能障碍的危险因素[OR(95%CI)=2.273(1.480～3.491)、2.175(1.467～3.225)、1.900(1.294～2.790)、1.540(1.173～2.023)、1.489(1.158～1.913)].预测模型预测老年ARF患者发生胃肠功能障碍的曲线下面积为 0.840(95%CI 0.803～0.873,P<0.05),H-L检验P =0.109.根据回归系数计算危险因素的预测得分,其最佳临界值为 2 分,曲线下面积为0.848(95%CI 0.811～0.880,P<0.05).结论 年龄大、脓毒症、SOFA评分高、D-乳酸高、IFABP高是老年ARF患者胃肠道功能障碍的危险因素,据此建立预测模型具有较好的预测效能.

重症急性胰腺炎（severe acute pancreatitis, SAP）约占急性胰腺炎（acute pancreatitis, AP）的15%~20% [1]，不仅起病急、病情进展快，而且易并发胰外重要脏器损伤甚至发生多脏器功能障碍，致使患者的病死率高达15%~30% [2]。

目的 对SCD个案报道文献回顾性研究,为SCD的预防、诊断、治疗提供理论依据.方法 在PubMed数据库中检索脊髓亚急性联合变性相关词条,获取2019年3月2日-1990年1月1日发表文章526篇,最终255个案纳入研究.结果 SCD常见病因为维生素B12缺乏(128例)、吸入N2O(70例)、铜缺乏(31例).该病多见于中年人(44.5±19.9)岁,病程相对较长(36.5±85.1)w.患者以肢体感觉减退最常见(73.3％),其次为共济障碍(61.6％),四肢运动系统也可受累(35.3％).自主神经系统、颅神经、意识障碍、认知障碍少见.SCD患者常合并巨细胞性贫血(72.5％)和高同型半胱氨酸血症(80.9％).脊髓MR可见后索异常信号影(82.9％),以颈髓最多见.结论 维生素B12缺乏是成人SCD最常见病因,青年人应该注意N2O滥用可能.患者多表现为周围神经系统损害表现,以感觉系统受损多见,脊髓MR后索异常信号影对诊断具有特异性.大部分SCD患者经治疗后预后良好.

高脂血症是我国急性胰腺炎(AP)的第二大病因,其中高甘油三酯血症性急性胰腺炎(HTG?AP)是主要类型.由于HTG?AP的病因、发病机制特殊,因此其临床特征与其他病因所致AP并不相同,致使该病易被漏诊且易于重症化,导致患者病情进展迅速、病死率高,即使治愈后也容易复发.目前缺少针对HTG?AP的可操作性高的专家共识/指南,本文围绕笔者等近期执笔的《高甘油三酯血症性急性胰腺炎诊治急诊专家共识》,并结合最新研究进展以及AP诊治的相关专家共识/指南,就HTG?AP的诊断、病因治疗、常规治疗及预防等方面进行探讨.

目的 探讨品管圈(QCC)在急性缺血性脑卒中(AIS)患者中的应用效果.方法 选取2019年1月至2019年6月我院急诊抢救室收治的30例AIS静脉溶栓患者,设为对照组(采用常规流程治疗),将2019年7月至2019年12月收治的30例AIS静脉溶栓患者设为观察组(成立QCC小组,采用QCC优化流程救治).比较两组的应用效果.结果 观察组的入院至评估患者、入院至获得影像学检查、取药-溶栓、DNT用时均短于对照组(P<0.05).观察组的溶栓有效率和DNT达标率均高于对照组(P<0.05).结论 开展QCC活动可提高AIS患者静脉溶栓DNT达标率,同时提升了医护人员应用QC手法解决临床实际问题的能力.

Accumulating evidence has suggested that Glypican-5 (GPC5) is a tumor suppressor gene in many types of cancers. However, whether GPC5 is involved in glioma remains unknown. This study was designed to explore the expression, biological function and regulatory mechanism of GPC5 in glioma. Our results demonstrated that GPC5 expression was significantly decreased in multiple glioma cell lines. Gain-of-function experiments showed that the ectopic expression of GPC5 markedly inhibited the proliferation, invasion and Wnt/β-catenin signaling of glioma cell lines. GPC5 was identified as a target gene of microRNA-301b (miR-301b). Further data showed that miR-301b expression was significantly up-regulated in glioma tissues and cell lines. In addition, miR-301b expression was inversely correlated with GPC5 expression in clinical glioma tissues. The overexpression of miR-301b promoted the proliferation, invasion and Wnt/β-catenin signaling of glioma cell lines, whereas the inhibition of miR-301b showed the opposite effect. However, the silencing of GPC5 significantly reversed the antitumor effect of miR-301b inhibition. Overall, our results revealed a tumor suppressive role of GPC5 in glioma and suggested that GPC5 expression was regulated by miR-301b. Our study indicates that the inhibition of miR-301b represses the proliferation and invasion of glioma cells by up-regulating GPC5 expression.

目的 探讨屎肠球菌的万古霉素替考拉宁A型抗性蛋白/D-丙氨酸-D-丙氨酸连接酶(Vancomycin Teicoplanin A-type resistance protein D-alanine-D-alanine ligase,VanA)调控人正常结直肠黏膜细胞FHC凋亡的机制.方法 在人正常结直肠黏膜细胞FHC中使用屎肠球菌感染,Annxin-V染色检测细胞凋亡情况.使用屎肠球菌的VanA蛋白刺激,检测FHC细胞凋亡情况、ROS水平以及ROS标志蛋白MDA、GSH和SOD的表达水平.ROS抑制Acetylcysteine处理VanA刺激的FHC细胞后,检测细胞凋亡相关蛋白的表达水平.结果 屎肠球菌与人正常结直肠黏膜细胞FHC共培养后,人正常结直肠黏膜细胞FHC的凋亡水平明显升高(t=2.876,P=0.045 2),并且VanA蛋白能促进FHC凋亡水平(t=5.579,P=0.005 1),同时细胞凋亡相关蛋白CLEAVED-CAS9、BAK的表达量上升,BCL-2的表达量下降.屎肠球菌的VanA蛋白刺激后,发现正常结直肠黏膜细胞FHC的ROS水平上升(t=10.190,P=0.000 5),ROS标志蛋白MDA (t=4.315,P=0.012 5)和SOD (t=5.751,P=0.004 5)的表达水平上升,GSH(t=5.225,P=0.006 4)的表达水平下降,但是,ROS抑制剂Acetylcysteine能够抑制这种现象.结论 屎肠球菌的VanA通过提高细胞内ROS水平来促进人正常结直肠黏膜细胞FHC凋亡.

Renal ischemia-reperfusion (I/R) injury is a common but severe scientific problem. Luteolin has great anti-inflammatory and antioxidant effects. In this study, we studied the effect of luteolin on renal I/R injury in rats. Intragastric administration of luteolin or saline was performed in Sprague-Dawley rats before (40 mg/kg for three days) and after (one day) renal I/R modeling. Kidney and blood samples were harvested to detect the severity of renal injury 24 hours after operation. The results showed that luteolin-treated rats exhibited milder histomorphological changes with lower scores of renal histological lesions; lower blood urea nitrogen and creatinine levels; lower renal malondialdehyde (MDA), 8-oxo-deoxyguanosine (8-OHdG), and myeloperoxidase (MPO) levels; and higher superoxide dismutase (SOD) and catalase (CAT) activities in the kidney. Luteolin attenuated the increased levels of serum and renal tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, renal high mobility group box-1 (HMGB1), and nuclear factor kappa β (NF-κB) expression levels in I/R rats. Furthermore, luteolin treatment significantly reduced renal cell apoptosis and endoplasmic reticulum (ER) stress caused by renal I/R injury. In conclusion, luteolin improved renal function in I/R rats by reducing oxidative stress, neutrophil infiltration, inflammation, renal cell apoptosis, and expression of HMGB1 and NF-κB, and ER stress.

BACKGROUND Postsurgical peritoneal adhesions (PPAs) are pathologic fibrous bands within the peritoneal cavity. The aim of this study was to investigate the protective effect of hydrogen-rich saline (HRS) on PPAs formation in mice. MATERIAL AND METHODS Adhesions were induced in mice using the cecum rubbing model. The mice were allocated into 4 groups: control sham group without cecum rubbing; PPA group with saline applied intraperitoneally (i.p.) daily after cecum rubbing; PPA+HRS (5) group with 5 ml/kg of HRS applied i.p. daily after cecum rubbing; and PPA+HRS (10) group with 10 ml/kg of HRS applied i.p. daily after cecum rubbing. On the 1st, 3rd, and 7th days after the operation, mice were killed and pathological adhesion bands were quantified to detect the effect of HRS on PPAs formation. RESULTS HRS did not affect PPAs formation on the 1st day, but did make a significant reduction on the 3rd and 7th days. A significant increase of t-PA and decrease of TGF-b1 and PAI-1 in the peritoneal fluids were observed in the HRS-treated groups. The levels of MDA and MPO in the HRS-treated groups were significantly lower than those in the PPA group. TNF-α and IL-6 levels in HRS-treated groups significantly decreased compared with those in the PPA group on postoperative day 3 and 7. Moreover, HRS decreased the mRNA levels of pro-inflammatory cytokines and TGF-β1 expression in the postsurgical adhesion bands. CONCLUSIONS These results showed that HRS had therapeutic potential for preventing PPAs formation, possibly through balancing the expression of TGF-β1, t-PA, and PAI-1, and inhibiting oxidative stress and inflammation.