急性肾损伤(acute kidney injury,AKI)指短时间内肾功能持续减退的临床综合征.据统计,术后患者中AKI发病率达25％;且预后欠佳,AKI病死率为28％～90％,是临床上的急危重症[1,2].围手术期AKI的发病率逐年升高是当今临床亟待解决的问题,构建AKI风险预测模型,准确评估其发生风险是近年临床预警研究领域热点,良好的预测模型对AKI风险患者具有高达80％的识别率,仅使用患者住院时长、体质量指数、白细胞计数最大值等24个重要指标进行预测时仍有良好性能[3],本文就AKI预测模型的研究进展综述如下.

脓毒症是由于机体对感染的反应失控导致的危及生命的器官功能障碍 [1]，脓毒性休克则是经充分的液体复苏后仍需血管活性药物维持循环稳定，并伴有高乳酸血症。由于有效循环血量不足，机体的组织、器官缺血缺氧，出现各种代谢功能紊乱，甚至可引起多器官功能衰竭，造成不可逆的损伤甚至死亡 [2,3]。脓毒症及脓毒性休克是重症监护室（intensive care unit, ICU）患者中导致危重症和死亡的首要原因 [4,5]，其造成的循环衰竭和代谢紊乱足以显著增加患者的病死率，同时患者通常会遗留长期的躯体和心理障碍，从而造成严重的医疗健康和社会经济负担 [6]，所以早期识别和及时诊治脓毒症和脓毒性休克非常重要。

连续性肾脏替代治疗目前在重症监护室中的应用较为广泛,不仅可以用来治疗慢性肾脏功能衰竭的患者,还可以用来维持患者血流动力学稳定.连续性肾脏替代治疗过程中心脏并发症的发生比较常见 [1-2],然而之前对于左心室的研讨较多,右心室相对较少,超声作为一项无创检查,可以为患者提供较好的帮助,应用超声评价连续性肾脏替代治疗对患者右心室的影响进行相应综述.

目的 应用迷你容量负荷试验结合重症超声颈总动脉峰值流速度变异率(ΔVpeakCA)指导ICU机械通气的脓毒性休克患者进行液体复苏,评价其容量管理的应用价值.方法 2017年6月至2018年12月华北理工大学附属医院经有创机械通气治疗的脓毒性休克患者68例,随机分为超声引导治疗组(Ⅰ组)和常规治疗组(Ⅱ组).Ⅰ组予以迷你容量负荷试验,并在超声引导下获取ΔVpeakCA,用以评估容量状态、指导液体复苏.Ⅱ组予以常规液体复苏治疗.比较两组患者治疗前后不同时间点循环、灌注,以及液体平衡情况、血管活性药物的应用、成功拔管时间、ICU停留时间、尿量恢复时间等.结果 最终纳入研究61例,其中Ⅰ组33例,Ⅱ组28例.两组患者一般临床资料比较无统计学差异(P均＞0.05);两组患者在复苏后各时间点平均动脉压(MAP)、中心静脉压(CVP)、pH、脉搏灌注指数(PI)、中心静脉血氧饱和度(ScvO2％)、呼吸频蟀(RR)、心率(HR)、乳酸、中心静脉-动脉血二氧化碳分压差(PCV-aCO2)均较复苏前明显好转(P均＜0.05).虽然Ⅱ组MAP、CVP经液体复苏后于部分时间显著优于Ⅰ组(P均＜0.05),但Ⅰ组乳酸、RR、PI及复苏净平衡液体量、去甲肾上腺素应用时间及剂量、成功拔除气管插管时间、ICU停留时间、尿量达到≥0.5 ml·kg-1·h-1的时间均优于Ⅱ组(P均＜0.05).结论 重症超声联合迷你容量负荷试验可对ICU机械通气的脓毒性休克患者的容量状态进行精细管理,优化血流动力学,降低ICU患者的医疗成本.

BACKGROUND:Hepatocellular carcinoma (HCC) is the most common primary liver cancer and accounts for over 90% of all primary liver cancers. Increasing evidence suggests that microRNAs (miRNAs) mediate signaling pathways by gene expression regulation.METHODS:In this study, we evaluated the role of miR-29a-3p in HCC progression. MiR-29a-3p was found significantly down-regulated in HCC tissues compared to adjacent non-tumor tissues. Meantime, PTEN expression was up-regulated in HCC tissues. Moreover, NF-κB activity was decreased following PTEN up-regulation.RESULTS:In vitro assays in the HCC cell line BEL7402 demonstrated that miR-29a-3p suppresses cell proliferation.CONCLUSIONS:miR-29a-3p participates in the HCC progression by regulation of NF-κB pathway via targeting PTEN.

目的 探讨Padua评分对预测重症患者发生静脉血栓栓塞症(VTE)风险的有效性.方法 采用病例对照的方法 进行回顾性研究,选取华北理工大学附属医院重症医学科(ICU)患者中确诊的78例VTE患者(VTE组)及同时期同科室随机抽取的96例未患VTE患者(非VTE组).依据Padua评分对两组患者进行评分和危险分层.比较两组评分结果 以及危险等级之间的关系,采用多因素Logistic回归模型分析危险因素与VTE发生之间的关系.结果 VTE组Padua评分与非VTE组比较,差异有统计学意义(P<0.05),VTE组高于非VTE组,高评分等级组患者发生VTE的风险是低评分等级组的7.66倍.以ICU住院患者的相关因素作为自变量进行Logistic回归分析发现:卧床≥3 d是ICU住院患者发生VTE的最高级别的危险因素.结论 Pauda评分可较好地评估ICU患者VTE发病的危险程度.

Objective To explore the protective mechanisms of hydrogen-rich saline on renal ischemiareperfusion injury.Methods Mice were divided in to 3 groups:control (sham operation),ischemia-reperfusion (IR) and ischemia-reperfusion+ hydrogen-rich saline (HRS).Mice in IR+ HRS group were administrated HRS by intravenous injection 3days and 1min before operation and 4 times in the following 2hours after operation.Mice in control and IR group were administrated normal saline as the same volume and frequency with IR + HRS group.Mice were sacrificed 24 hours after operation,creatinine and urea nitrogen in serum were detected by biochemical analyzer,MDA and SOD level were detected by spectrophotometer,expression of Bcl-xl,Bcl2,Bak,Bax,Cleaved Caspase-3 proteins level were detected by western blot.Results Compared to IR group,creatinine,urea nitrogen,MDA level decreased significantly after HRS consumption.SOD enzyme activity increased significantly after HRS consumption.HRS treatment down-regulates expression of Bak,Bax and Cleaved Caspase-3 protein level,and up-regulates expression of Bcl2,and Bcl-xl protein level.Conclusion HRS eliminates ROS and elevates antioxidant activity in renal after IR,besides,HRS also regulate apoptosis signal pathway to protect IR injury in renal.

Background/Aims: Erinacine, which is extracted from the medicinal mushroom Hericium erinaceus, is known to play anticancer roles in human cancers. The following study aims to investigate the role of erinacine in the opening of the mitochondrial permeability transition pore (MPTP) in hepatocellular carcinoma (HCC) through the PI3K/Akt/GSK-3β signaling pathway and highlights the applicability of erinacine in HCC treatments. Methods: HCC and paracancerous tissues were obtained from 85 HCC patients who’ve undergone surgical resection. Immunohistochemistry was adopted to detect positive expression of PI3K, Akt, and GSK-3β. Treatment of HepG-2 with LY294002 (an inhibitor of the PI3K/Akt/GSK-3β signaling pathway) and different concentration of erinacine was performed to determine the involvement of LY294002 in erinacine action. The expressions of PI3K, Akt, GSK-3β, CyclinD1, Vimentin, β-catenin, Bcl-2, E-cadherin, Bax, and caspase-9 were determined by RT-qPCR and Western blot analysis. Cell viability, colony formation rate, migration, invasion, cycle, and apoptosis were detected by MTT, colony formation, wound healing assay, Transwell assay, and flow cytometry, respectively. The size and weight of xenograft tumors were observed in nude mice. Mitochondrial membrane potential in HepG-2 was determined using laser scanning confocal microscopy following JC-1 staining. Mitochondrial Ca2+ indicator Rhod-2, AM was used to detect the changes of mitochondrial Ca2+, while western blot analysis was employed to detect the presence levels of cytochrome C (cyt-C). Results: The results revealed that PI3K, Akt, and GSK-3β were up-regulated in HCC tissues. Erinacine or LY294002 led to a decrease in mitochondrial membrane potential, increase in intracellular mitochondrial Ca2+, and the release of cyt-C in mitochondria. In addition, Erinacine was found to decrease the mitochondrial membrane potential, expression of PI3K, Akt, GSK-3β, CyclinD1, Vimentin, β-catenin, and Bcl-2, cell proliferation, colony formation ability, migration, invasion, and xenograft tumor size, while E-cadherin, Bax, and caspase-9 expression, and cell apoptosis were elevated in a dose-dependent manner. Erinacine also stimulated the effects of LY294002 on the HCC. Following the addition of 500 μM Erinacine and MPTP opening inhibitor CsA, we found that the mitochondrial membrane potential level increased, while mitochondrial Ca2+ and Cyt-C decreased from the mitochondria. Conclusion: The results from the study demonstrated that erinacine induced MPTP opening, facilitates the release of cyt-C, and inhibited cell proliferation, migration, and invasion, while it promotes apoptosis by inactivating the PI3K/Akt/GSK-3β signaling pathway, preventing the progression of HCC.

Objective To test the validity of identifying the risk of deep venous thrombosis (DVT) in chronic obstructive pulmonary disease (COPD) inpatients with Padua risk assessment model.Methods In a retrospective case-control study,sixty chronic obstructive pulmonary disease inpatients with DVT and one hundred and twenty chronic obstructive pulmonary disease inpatients extracted randomly during the same period and the same subjects without DVT admitted to the Intensive Care Unit(ICU) in author's hospital from January 2015 to January 2017 were conducted in the Padua risk assessment model.The risk of VTE was assessed according to the Padua risk assessment model and the relationship of the scores and the dangerous levels between the two groups were compared.The association between the dangerous levels and DVT were analyzed with univariate logistic regression model.Receiver operating characteristic (ROC) curve was plotted to calculate the area under the curve (AUC).Results The average score of Padua risk scores (3.53 ± 2.34) in the DVT group was significantly higher than that in the control group (1.20 ± 1.49) (t =8.132,P＜0.001).Padua-4 model and Padua-3 model were analyzed by univariate logistic regression.Patients whose score was more than 4 were associated with 11.811-fold increased risk of DVT (P ＜0.001),and the patients whose score was more than 3 were associated with 7.000-fold increased risk of DVT (P＜0.001).The AUC was higher in Padua-3 model (0.708) than Padua-4 model (0.667) (P＜0.001).Conclusion The Padua-3 model is more effective for stratification of low and high risk of DVT in patients with chronic obstructive pulmonary disease than the Padua-4 model.

The aim of the present study was to investigate the effects of cytomegalovirus (CMV) infection on the prognosis of inflammatory bowel disease (IBD). Various databases were searched using a combination of keywords associated with CMV infection and IBD. Subsequent to the selection of relevant studies in line with strict inclusion and exclusion criteria, a meta-analysis was conducted using the Stata 12.0 software. A total of 195 studies were initially retrieved, including 28 studies in Chinese and 167 in English. Following the exclusion of unsuitable studies, 7 cohort studies with 374 IBD patients were included in the meta-analysis. The results of the present study identified significant differences between patients with and without CMV infection regarding the disease duration of IBD [standardized mean difference, -0.81; 95% confidence interval (CI), -1.19 to -0.43; P<0.001], the efficacy of corticosteroid therapy [relative risk (RR), 1.24; 95% CI, 1.02-1.49; P=0.029], the colectomy rate (RR, 2.13; 95% CI, 1.03-4.40; P=0.042) and the incidence of severe IBD (RR, 1.32; 95% CI, 1.04-1.67; P=0.022). Considering the IBD onset area, patients with CMV infection may have higher susceptibility to pancolitis (RR, 1.31; 95% CI; 1.01-1.72; P=0.045); however, no difference in susceptibility to left-sided IBD was observed between patients with or without CMV infection (RR, 0.97; 95% CI, 0.72-1.30; P=0.828). In conclusion, CMV infection may be associated with the disease duration, efficacy of corticosteroid therapy, colectomy rate, severe IBD incidence and disease location of IBD; thus, the presence of CMV infection may be considered as an important biomarker for determining the prognosis of IBD.

目的：探讨肝细胞生长因子（Hepatocyte growth factor ，HGF）对内质网应激参与的急性肝损伤的保护作用。方法 BALB／c 小鼠随机分为正常组、模型组、治疗组，采用50％浓度的 CCl4植物油溶液2ml／kg 腹腔注射小鼠建立 CCl4急性肝损伤模。治疗组以尾静脉注射法为每只小鼠注入20μg 将 HGF 质粒（pCMV － HGF），经8h 处理后再次给予50％浓度的 CCl4植物油溶液2ml／kg 腹腔注射，正常对照组和模型组注射等量的含 p CDNA3的质粒（20μg／只）生理盐水。分别于造模前和造模后各48h 取小鼠血样（眼眶）及同一小鼠肝组织。以 ELISA 法检测小鼠血清丙氨酸转氨酶（ALT ）、天门冬氨酸转氨酶（AST ）的水平，蛋白免疫印迹法定量检测肝细胞 GRP78的蛋白表达情况。结果与模型组比较，HGF 显著降低CCl4肝损伤小鼠 ALT 、AST 水平，同时 HGF 能抑制肝组织中 GRP78蛋白表达。结论肝细胞生长因子可能是通过抑制内质网应激介导的肝细胞凋亡，进而发挥肝保护作用。