目的 探讨血清热休克蛋白70(HSP70)水平与急性一氧化碳中毒后迟发性脑病(DEACMP)的相关性.方法 选择2015年1月～2017年12月收治的187例急性一氧化碳中毒(ACMP)患者为研究对象,根据是否发生迟发性脑病分为DEACMP组和ACMP组,另选100例同期健康志愿者作为对照组.采用酶联免疫吸附试验法(ELISA)检测各组受试者血清中HSP70的水平.采用多因素Logistic回归分析法分析ACMP患者发生迟发性脑病的影响因素,绘制ROC曲线评价血清HSP70对ACMP患者发生迟发性脑病的预测价值.结果 三组研究对象在性别、体重指数、高血压、糖尿病、颅内病变、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、血尿素氮(BUN)、肌酐(Cr)、肌酸激酶(CK)、肌酸激酶同工酶MB(CK-MB)和肌钙蛋白I(cTnI)方面差异无统计学意义(P>0.05).相比较于ACMP组,DEACMP组年龄明显较高,DEACMP组昏迷时间和接触CO时间均显著增长,差异具有统计学意义(χ2=3.747～10.533,均P<0.05).DEACMP组和ACMP组血清中HSP70的水平均显著高于对照组,差异具有统计学意义(χ2=3.443,P<0.05),且DEACMP组血清中HSP70的水平显著高于ACMP组(P<0.05).血清HSP70和接触CO时间是ACMP患者发生迟发性脑病的危险因素.血清HSP70预测ACMP患者发生迟发性脑病的cut-off值为32.9ng/ml,其相应的敏感度和特异度分别为0.827和0.709.结论 ACMP患者中毒早期血清HSP70水平显著增高,有可能成为预测ACMP患者发生迟发性脑病的新指标.

Objective To investigate the mechanism of miR-451 regulating the resistance of gastric cancer to 5-Fu by down-regulating the expression of MRP. Methods Real-time quantitative PCR was used to detect the relative expression of miR-451 in 20 pairs of human gastric cancer tissues and adjacent tissues and gastric cancer cell lines. The expression of miR-451 in the resistance group and non-resistant group were detected. We constructed gastric cancer cell line with stable plent-miR-451 overexpression, and the overexpression efficiency of miR-451 in gastric cancer cell line was detected by real-time quantitative PCR. The proliferation activity of the cells was detected by CCK8. The miR-451 target gene was analyzed by bioinformatics method and verified by luciferase assay. The effect of miR-451 on the mRNA and protein of targeted gene MRP were detected by real-time quantitative PCR and Western blot. Results The expression of miR-451 in normal tissues was higher than that in cancer tissues, and miR-451 expression in the non-resistant gastric cancer tissues was higher than that in the drug-resistant gastric cancer tissues. The overexpression of miR-451 reduced the resistance of gastric cancer cells to 5-Fu treatment (P=0.0006). Bioinformatics analysis showed that MRP was the target gene of miR-451. Luciferase assay also confirmed that MRP was a potential target gene of miR-451. miR-451 overexpression decreased the mRNA and protein of the drug resistance gene MRP (P=0.00069). Conclusion Overexpression of miR451 could down-regulate MRP expression, which reduces the resistance of tumor cells to 5-Fu.

Aberrant activation of Wnt/β‑catenin signaling is observed in >90% of colorectal cancer cases. microRNAs (miRNAs) regulate the expression of key genes in Wnt/β‑catenin signaling. As a result, abnormal expression of miRNAs regulates the activation of Wnt/β‑catenin signaling in several types of cancer. In the current study, it was demonstrated that miR‑501‑3p was overexpressed in colorectal tumor tissues compared to the adjacent normal tissues. Downregulation of miR‑501‑3p inhibited cell proliferation and sphere formation, while it induced cell cycle arrest at the G1 phase in colorectal cancer cells. Bioinformatics analysis results predicted that adenomatous polyposis coli (APC), a negative regulator of Wnt/β‑catenin signaling, was a potential target gene of miR‑501‑3p. Inhibition of miR‑501‑3p increased APC expression in colorectal cancer cells. Additionally, β‑catenin was destabilized following miR‑501‑3p inhibition; immunofluorescence analysis revealed that β‑catenin translocated from nucleus to cytoplasm. In addition, cyclin D1 and c‑Myc, two well‑characterized target genes of Wnt/β‑catenin signaling, were downregulated following miR‑501‑3p inhibition. Transfection of APC small interfering RNA re‑activated β‑catenin and stimulated the expression of cyclin D1 and c‑Myc. Furthermore, silencing of APC reversed the miR‑501‑3p inhibitor‑induced cell cycle disruption, and the inhibition of cell proliferation and sphere formation in colorectal cancer cells. In conclusion, the present study identified miR‑501‑3p as a novel regulator of Wnt/β‑catenin signaling in colorectal cancer cells via targeting APC, suggesting that miR‑501‑3p may act as a novel oncogenic miRNA in colorectal cancer.

Objective To explore the influence of cyanidin-3-O-glucoside (C3G) on the proliferation of colorectal cancer cells and its mechanism. Methods In vitro binding and in vitro kinase assay were used to detect the binding ability of C3G and T-LAK cell-originated protein kinase (TOPK) and its effect on TOPK activity. Soft AGAR test was used to detect the effect of C3G on the clonal ability of colon cancer cells. The cytotoxicity of C3G was determined by MTS assay. E. coli BL21 was used to express GST-histone H3 fusion protein. The effect of C3G on the clonogenesis of colon cancer cells with silenced TOPK was examined by lentivirus infection. The phosphorylation of histone H3 by C3G in HCT116 cells was determined by Western blotting. A mouse model of xenograft was established to study the phosphorylation level of histone H3 by immunohistochemical staining. Results C3G was directly bound to TOPK in vitro and inhibited TOPK activity. C3G inhibited the proliferation and clone formation of colon cancer cells in a concentration-dependent manner. Silencing TOPK decreased the sensitivity of colon cancer cells to C3G. C3G inhibited the phosphorylation of histone H3 downstream of TOPK in a time- and concentration-dependent manner. In addition, C3G inhibited tumor growth in mice with xenograft tumors from colon cancer tissues of a patient. Conclusion C3G can inhibit colorectal cancer growth by targeting TOPK.

Retraction This article has been retracted at the request of Author 'Serine hydroxymethyl transferase 2 regulates the AMPK/mTOR pathway and induces autophagy to promote chemotherapy resistance in colon cancer cells' by Liu F, Liu Y, Gao H, Wang L. The above article, published online on Apr 2019, in Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, 35(4):344-350; 356, has been retracted by agreement with all authors. The authors of the paper wish to retract the paper due to the discovery of error in the processing of the raw data. They apologize for any inconvenience this may have caused. Reference Liu F, Liu Y, Gao H, Wang L. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, 2019 Apr;35(4):344-350; 356.PMID: 31167694. Retraction of Serine hydroxymethyl transferase 2 regulates the AMPK/mTOR pathway and induces autophagy to promote chemotherapy resistance in colon cancer cells. [Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2019].

Background Growing evidence has implicated the important role of the long non-coding RNAs (lncRNAs) in gastric cancer progression. In this study, we examined the expression of lncRNA zinc finger E-box-binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in gastric cancer tissues and elucidated the molecular mechanisms underlying ZEB2-AS1-mediated gastric cancer progression. Methods Quantitative real-time PCR measured the gene expression level; CCK-8, colony formation and cell invasion assays determined gastric cancer cell proliferation, growth and invasion, respectively; the xenograft nude mice model was used to determine in vivo tumor growth; Bioinformatics analysis and luciferase reporter assay determined the downstream targets of ZEB2-AS1 and miR-143-5p. The expression of ZEB2-AS1 was upregulated in gastric cancer cell lines. Results Knockdown of ZEB2-AS1 suppressed gastric cancer cell proliferation, growth and invasion, and also suppressed in vivo tumor growth in the nude mice. Overexpression of ZEB2-AS1 potentiated gastric cancer cell proliferation, growth and invasion. Bioinformatics analysis and luciferase reporter assay showed that miR-143-5p was a direct target of ZEB2-AS1 and was negatively regulated by ZEB2-AS1. Furthermore, hypoxia-inducible factor-1α (HIF-1α) was found to be a target of miR-143-5p and was negatively regulated by miR-143-5p. The rescue in vitro assays showed that the effects of ZEB2-AS1 overexpression on gastric cancer cell proliferation, growth and invasion was mediated via miR-143-5p/HIF-1α. ZEB2-AS1 and HIF-1α was upregulated in gastric cancer tissues, while miR-143-5p was down-regulated; and ZEB2-AS1 expression level was inversely correlated with miR-143-5p expression level, and positively correlated with HIF-1α mRNA expression level; while miR-143-5p expression level was inversely correlated with HIF-1α expression level. High ZEB2-AS1 expression level was correlated with poor differentiation, lymph node metastasis and distant metastasis. Conclusion Collectively, our results indicated that ZEB2-AS1 was up-regulated in gastric cancer tissues and cells and promoted cell proliferation and metastasis through miR-143-5p/HIF-1α pathway, which may provide a promising target for treatment of gastric cancer.

Objective To investigate the mechanism of serine hydroxymethyl transferase 2 (SHMT2) inducing autophagy and promoting chemotherapy resistance in colon cancer cells. Methods TCGA database and real-time quantitative PCR were used to analyze the level of SHMT2 mRNA in colon cancer tissues. Western blot analysis and immunohistochemistry were used to detect the expression and distribution of SHMT2 in colon cancer tissues. Western blot analysis was performed to detect the SHMT2 protein levels of SW480, SW620, HCT116, CACO2, RKO, HCT8, HT15 and HT29 cells. After over-expression of SHMT2 in CACO2 colon cancer cells, MTT assay was used to detect cell viability, and annexin V-FITC/PI double labeling was used to detect the apoptosis of colon cancer cells induced by 5-fluorouracil (5-Fu). The autophagosomes of colon cancer cells were observed by transmission electron microscopy. The protein levels of LC3 II/I, P62, cleaved PARP (c-PARP), and cleaved caspase-3 (c-caspase-3) were examined by Western blot analysis. Signaling Phospho-Antibody Array and Western blot analysis were applied to analyze the phosphorylation level of AMPK/mTOR. Results SHMT2 was highly expressed in colon cancer tissues and cells. Over-expression of SHMT2 significantly increased cell viability and the ratio of LC3 II/ LC3 I. It was found that the phosphorylation level of AMPK was raised and the phosphorylation level of mTOR was reduced after the over-expression of SHMT2. Conclusion SHMT2 may induce autophagy by promoting AMPK phosphorylation and directly or indirectly inhibiting mTOR activity, thus leading to chemotherapy-induced apoptosis tolerance and resistance to chemotherapeutics.

目的 探讨热休克蛋白(HSP)70基因多态性与脓毒症患者病情严重程度及预后的相关性.方法 选取2014年1月至2017年1月我院住院治疗的182例脓毒症患者纳入研究,分为脓毒症组(n=40)和脓毒性休克组(n=142),再根据患者发病28 d后转归情况各自分为存活和死亡两个亚组,采用聚合酶链反应-直接测序法检测HSP70-1+190G/C、HSP70-2+ 1267A/G和HSP70-hom+ 2437T/C位点多态性.结果 脓毒症组和脓毒症休克组HSP70-2+ 1267A/G位点等位基因分布频率差异有统计学意义(P＜0.05),HSP70-1+190G/C和HSP70-hom+2437T/C位点基因型和等位基因分布频率差异无统计学意义(均P＜0.05).携带HSP70-2+1267A/G位点AA基因型患者急性生理学与慢性健康状况Ⅱ(APACHE Ⅱ)评分和序贯器官衰竭(SOFA)评分均显著高于AG基因型和GG基因型携带者(均P＜0.05).HSP70-1+190G/C和HSP70-hom+ 2437T/C位点不同基因型患者APACHEⅡ评分和SOFA评分差异均无统计学意义(均P＞0.05).在脓毒症组,存活亚组和死亡亚组各位点基因型和等位基因分布频率差异均无统计学意义(P均＞0.05);在脓毒性休克组,存活亚组和死亡亚组HSP70-2+1267A/G位点等位基因分布频率差异有统计学意义(P＜0.05),HSP70-1+190G/C和HSP70-hom+ 2437T/C位点基因型和等位基因分布频率差异均无统计学意义(P均＞0.05).结论 HSP70基因多态性可能与脓毒症患者病情严重程度和预后相关.

目的:探讨热休克蛋白(HSP) 70基因多态性与慢性心力衰竭(CHF)患者预后的相关性.方法:将408例CHF患者纳入研究,根据随访2年内是否发生心血管事件将患者分为事件组与非事件组,采用聚合酶链反应-限制性内切酶分析法检测HSP70-1基因+190G/C、HSP70-2基因+1267A/G和HSP70-hom基因+2437T/C多态性,并收集患者临床资料进行分组及统计学分析.结果:事件组与非事件组患者年龄(t=2.392,P=0.017),脑钠肽(BNP)水平(t=3.922,P=0.000),NYHA分级(x2=5.100,P=0.024),左室舒张末期内径(LVEDD) (t=2.872,P=0.004)、右室舒张末期内径(RVEDD)(t=2.232,P=0.026)、左室射血分数(LVEF)超声测值(t=4.338,P=0.000)等参数比较均差异有统计学意义.2组HSP70-2基因+1267A/G位点基因型和等位基因分布频率比较差异均有统计学意义(x2 =8.480,P=0.014;x2=7.643,P=0.006),在隐性基因模型下HSP70-2基因+1267A/G位点基因多态性与CHF患者发生心血管事件相关(x2=9.877,P=0.002);HSP70-1基因+ 190G/C和HSP70-hom基因+2437T/C位点基因型和等位基因分布频率均差异无统计学意义(均P＞0.05),且在显性基因模型和隐性基因模型下两位点基因多态性均与CHF患者发生心血管事件无关(均P＞0.05).Logistics多因素回归分析结果显示HSP70-2基因+1267A/G位点GG基因型是CHF患者发生心血管事件的危险因素(OR=1.362;95％CI 1.046～2.701;P=0.003).结论:HSP70-2基因+1267A/G多态性与CHF患者预后相关,GG基因型可增加CHF患者发生心血管事件的风险.HSP70-1基因+190G/C和HSP70-hom基因+2437T/C多态性可能与CHF患者预后关联不大.

糖尿病已成为21世纪严重危害人类健康的疾病之一，其中2型糖尿病占较大比重（type 2 diabetes mellitus，T2DM），主要体现在各种慢性并发症，如糖尿病神经病变、糖尿病肾病、糖尿病视网膜病变等，有着高致残率和致死率，直接影响了人们日常生活。慢性假性肠梗阻（chronic intestinal pseudo-obstruc-tion，CIPO）是由于肠道神经病变和（或）肌病引起的肠道运动障碍性疾病，临床上表现为反复发作或持续存在的肠梗阻，但缺乏机械性肠梗阻的诊断依据。成人CIPO常继发于系统性疾病（如结缔组织病）和内分泌疾病（如糖尿病、神经系统疾病、肿瘤和病毒感染等），无明确病因的CIPO称为慢性特发性假性肠梗阻（chronic idiopathic intestinal pseudo-obstruc-tion，CIIP）[1]。近年来国内已有2型糖尿病合并CIPO的报道[2]，本研究对12例患者临床资料进行回顾性分析，分析其共有特征，以便在今后的工作中对该类疾病提高认识，减少误诊、漏诊，减轻患者不必要的医疗负担。

目的 探讨苦寒类中药大黄对大鼠应激性溃疡的作用及其可能机制. 方法 用水浸束缚应激法(WIRS)复制大鼠应激性溃疡模型.将30只大鼠随机分为正常对照组、模型组、大黄组.大黄组提前7d给予大黄灌胃,应激6h后处死大鼠,光镜下观察胃黏膜损伤程度并计数各组溃疡指数(UI)的变化,放射免疫分析方法检测血浆及胃黏膜匀浆表皮生长因子(EGF)的含量. 结果 水浸束缚应激6h后大鼠出现急性胃黏膜损害;大黄组较模型组及正常对照组血浆及胃黏膜EGF含量显著增高(P＜0.05);大黄组较模型组UI明显下降(P＜0.05). 结论 大黄参与了应激性溃疡的保护作用,其作用可能与EGF有关.

目的：探讨溶血磷脂酸（LPA）、同型半胱氨酸（HCY）、D-二聚体（D-D）对急性冠状动脉综合征（ACS）的预警作用。方法：102例ACS患者分为急性心肌梗死（AMI）组50例和不稳定型心绞痛（UAP）组52例,另选健康体检者53例作为对照组。所有入选者采静脉血进行LPA、HCY、D-D测定;计算单独检测、两两联合检测以及同时检测LPA、HCY和D-D预警ACS的敏感度和特异度,并相互比较。结果：AMI组和UAP组血清LPA、HCY、D-D水平均明显高于对照组（均P〈0.01）;AMI组血清LPA、HCY、D-D水平较UAP组升高（均P〈0.05）;ACS组LPA、HCY、D-D的检测阳性率分别是42.16%、61.76%、46.08%,对照组分别是3.78%、1.89%、1.89%,两组比较有统计学差异（P〈0.01）;单独检测LPA、HCY、D-D灵敏度分别为42.16%、61.76%、46.08%,特异度分别为96.23%、98.11%、98.11%;两两联合检测的灵敏度分别为69.61%、70.59%、59.80%,特异度分别为94.34%、96.23%、96.23%;3个指标联合检测的灵敏度为76.47%,特异度为94.34%。结论：LPA、HCY、D-D水平与ACS的发生、发展有着密切的关系,联合检测三指标可以显著提高ACS的早期诊断率,对ACS的预警作用最强。

目的:探讨溶血磷脂酸(LPA)、同型半胱氨酸(HCY)、D-二聚体(D-D)对急性冠状动脉综合征(ACS)的预警作用.方法:102例ACS患者分为急性心肌梗死(AMI)组50例和不稳定型心绞痛(UAP)组52例,另选健康体检者53例作为对照组.所有入选者采静脉血进行LPA、HCY、D-D测定;计算单独检测、两两联合检测以及同时检测LPA、HCY和D-D预警ACS的敏感度和特异度,并相互比较.结果:AMI组和UAP组血清LPA、HCY、D-D水平均明显高于对照组(均P＜0.01);AMI组血清LPA、HCY、D-D水平较UAP组升高(均P＜ 0.05);ACS组LPA、HCY、D-D的检测阳性率分别是42.16％、61.76％、46.08％,对照组分别是3.78％、1.89％、1.89％,两组比较有统计学差异(P＜0.01);单独检测LPA、HCY、D-D灵敏度分别为42.16％、61.76％、46.08％,特异度分别为96.23％、98.11％、98.11％;两两联合检测的灵敏度分别为69.61％、70.59％、59.80％,特异度分别为94.34％、96.23％、96.23％;3个指标联合检测的灵敏度为76.47％,特异度为94.34％.结论:LPA、HCY、D-D水平与ACS的发生、发展有着密切的关系,联合检测三指标可以显著提高ACS的早期诊断率,对ACS的预警作用最强.

目的:研究雌激素及其拮抗剂对人胃腺癌SGC-7901细胞系血管内皮细胞生长因子(VEGF)表达的影响.方法:用雌二醇及其拮抗剂三苯氧胺(tamoxifen)处理体外培养的胃癌细胞系SGC-7901,在相差显微镜下观察细胞形态的变化;用四甲基偶氮唑蓝(MTT)比色法测定细胞增殖;用双抗体夹心酶联免疫吸附试验(ELISA)和免疫细胞化学SABC法测定细胞培养上清液和细胞质中VEGF蛋白含量.结果:胃癌细胞经雌二醇处理,培养液中VEGF浓度明显高于对照组(P＜0.05);而雌二醇加三苯氧胺联合处理胃癌细胞,VEGF浓度有回降,比雌二醇处理组下降.结论:提示雌激素参与调节胃癌细胞VEGF的表达浓度,三苯氧胺有抑制VEGF表达的作用.

Objective To explore the correlation of D-dimer with coronary artery lesions in patients with acute coronary syndrome (ACS). Methods Sixty patients with ACS were enrolled in this study,including 30 patients with acute myocardial infarction(AMI) and 30 patients with unstable angina pectoris( UAP) . Thirty healthy subjects were chosen as controls. The peripheral venous blood were taken in all patients to detect the level of D-dimer. The lesions of coronary arteries were assessed by Gensini score. The relation of serum D-dimer with Gensini score was analyzed in ACS patients. Results The level of D-dimer was higher in ACS group( inclding AMI and UAP)than that in control group(P<0. 01). Gensini score was significantly higher in AMI group than in UAP group(P<0. 01). The level of D-dimer was positively related with Gensini score in ACS patients(r=0. 586,P<0. 01). Conclusion Level of D-dimer in patients with ACS may be closely related to the atherosclerostic lesions of coronary arteries.

目的探讨溶血磷脂酸（LPA）、高敏C反应蛋白（hs-CRP）在急性冠脉综合征（ACS）患者中的表达及意义。方法选择60例ACS患者分为急性心肌梗死（AMI）组30例和不稳定型心绞痛（UAP）组30例,另选30例健康体检者作为对照组。所有入选者抽静脉血测定LPA、hs-CRP水平,对ACS患者的冠脉病变进行Gensini评分。比较各组间LPA、hs-CRP水平的差异,分析LPA、hs-CRP与Gensini评分的相关性,分析LPA与hs-CRP的相关性。结果 ACS组LPA、hs-CRP水平明显高于对照组（P＜0.01）,AMI组LPA、hs-CRP水平较UAP组升高（P＜0.01）,AMI组比UAP组Gensini评分高（P＜0.01）;ACS组LPA、hsCRP水平与Gensini评分呈正相关（r分别为0.83、0.79,P＜0.01）,LPA与hs-CRP水平呈正相关（r=0.85,P＜0.01）。结论LPA、hs-CRP在ACS患者中表达升高,二者联合检测对ACS患者预测、诊断、判断预后具有重要的临床价值。

目的:分析重组人脑利钠肽对急性左心衰竭患者的临床疗效.方法:选择100 例急性左心衰竭患者,随机分为对照组与治疗组,每组50 例,在常规治疗基础上应用重组人脑利钠肽,对比两组患者治疗效果.结果:研究组症状缓解时间和住院时间均低于对照组,治疗总有效率高于对照组,差异有统计学意义(P＜0.05 ).研究组治疗前后NT-proBNP 水平与治疗前和对照组相比差异有统计学意义(P＜0.05),LVEF 变化情况不显著,差异无统计学意义(P＞0.05 ).结论:重组人脑利钠肽能够有效改善急性左心衰竭患者的临床症状与体征,缩短治疗时间,效果较好.

目的研究曲美他嗪治疗慢性心力衰竭(CHF)患者心功能及N-末端脑钠肽前体(NT-proBNP)、超敏C反应蛋白(hs-CRP)的影响。方法将80例CHF患者，随机分成观察组（50例）和对照组（30例），对照组采用常规抗心衰治疗，观察组在常规抗心衰治疗同时加用曲美他嗪。对比两组患者治疗前后血清NT-proBNP、hs-CRP的差异及心功能的改善情况。结果观察组总有效率明显高于对照组，两组血清 NT-proBNP、hs-CRP 的表达均下降，但观察组的下降值明显高于对照组。结论曲美他嗪能明显改善患者心功能，同时下调患者血清 NT-proBNP、hs-CRP的浓度。

总结62例经尿道等离子汽化电切术后膀胱痉挛的预防及护理。预防护理重点为做好心理护理,给予腹部、背部、足部按摩,加强体位护理,及时调节膀胱冲洗液温度和冲洗速度,同时保持引流通畅。一旦发生膀胱痉挛,及时观察和评价,并按膀胱痉挛程度给予相应护理,缓解患者症状。