Fasting glucose and its association with 20-year all-cause and cause-specific mortality in Chinese general population

ObjectiveThe aim of this study was to explore the relationship between fasting glucose levels and all-cause and cause-specific mortality in Chinese population.MethodsThe role of fasting blood glucose levels as a predictor of all-cause and cause-specific mortality was estimated in 9930 participants from four Chinese general populations with a 20-year follow-up. Multivariate Cox proportional hazard models were used to identify the relationship between fasting glucose and mortality.ResultsThere were 1471 deaths after a median follow-up of 20.2 years (a total of 187,374 person-years), including 310 cardiovascular deaths, 581 cancer deaths, and 580 other-cause deaths. After adjustment for age, sex, urban or rural, northern or southern of China, types of work, education level, physical exercise, smoking status, drinking status, body mass index, systolic blood pressure, and serum total cholesterol at baseline, the hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality in the fasting blood glucose categories of <60, 60–69, 70–79, 90–99, 100–109, 110–125, and ≥126 mg/dl were 1.38 (1.04–1.84), 1.20 (1.01–1.43), 1.18 (1.03–1.36), 1.18 (0.99–1.41), 1.48 (1.16–1.88), 1.17 (0.84–1.62), and 2.23 (1.72–2.90), respectively, in contrast to the reference group (80–89 mg/dl). The HRs and 95% CIs for cardiovascular disease mortality in these groups were 2.58 (1.44–4.61), 1.41 (0.95–2.10), 1.56 (1.15–2.11), 1.29 (0.88–1.89), 1.36 (0.78–2.37), 1.05 (0.52–2.11), and 2.73 (1.64–4.56), respectively.ConclusionsBoth low and high fasting glucose were significantly associated with increased risk of all-cause and cardiovascular mortality in Chinese general population.     

黄芪汤加减治疗急性加重期慢性阻塞性肺疾病疗效研究

摘 要 目的:探讨黄芪汤加减治疗慢性阻塞性肺疾病急性加重期（AECOPD）的临床疗效。方法:采用随机数字表法将166例AECOPD患者随机分为常规组和观察组各83例。常规组采用常规西医方法治疗，观察组在常规组的基础上给予黄芪汤加减治疗。观察两组治疗前后第1秒用力呼气量（FEV1）、用力肺活量（FVC）、FEV1占FVC的百分比（FEV1/FVC％）、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）、肿瘤坏死因子 α（TNF α）、白细胞介素 1β（IL 1β）、白细胞介素 6（IL 6）水平。结果:两组治疗后FEV1、FEV1/FVC、PaO2水平与治疗前相比较均显著升高（P＜0.05），且观察组与同期常规组相比较均显著升高（P＜0.05）；两组治疗后PaCO2、TNF α、IL 1β、IL 6水平与治疗前相比较均显著降低（P＜0.05），且观察组与同期常规组相比较均显著降低（P＜0.05）。结论:黄芪汤加减治疗AECOPD可降低患者炎症反应水平，改善动脉血气和肺功能，提高治疗效果，值得临床应用。     

双氢青蒿素诱导肿瘤细胞铁死亡及其机制研究

目的阐明双氢青蒿素(DHA)诱导肿瘤细胞铁死亡的作用及其机制。方法利用3,3′,5,5′-四甲基联苯胺(TMB)检测DHA与FeSO_4体外芬顿样(Fenton)反应生成氧自由基(·OH)的能力;MTT法检测DHA对人肝癌HepG2细胞的毒性(包括FeSO_4与去铁胺预处理组)。MTT法考察谷胱甘肽(GSH)与铁死亡抑制剂(Fer-1)对DHA细胞毒性的影响;采用DCFH-DA染料考察DHA(包括FeSO_4预处理组)诱导的细胞内活性氧的生成能力;采用C11-BODIPY581/591与DiO分别考察DHA(包括FeSO_4预处理组)对细胞内脂质过氧化物生成能力以及细胞膜结构的影响;利用谷胱甘肽过氧化物酶4(GPX-4)试剂盒测定DHA(包括FeSO_4预处理组)对HepG2细胞内GPX-4活性的影响。结果 Fe~(2+)能够催化DHA发生芬顿样反应并生成·OH;DHA的半数抑制浓度(IC_(50))为(39.96±8.78)μmol/L,FeSO_4与去铁胺分别能够增加或者降低DHA的细胞毒性;DHA处理后细胞内活性氧含量与脂质过氧化物含量升高,细胞形态变大,细胞膜呈散点状分布并呈现解离状态。FeSO_4预处理组与DHA组相比较进一步增加细胞内活性氧含量与脂质过氧化物含量,并且细胞膜形态完全破坏。FeSO_4能够增强DHA对GPX-4活性的抑制作用。结论 DHA通过芬顿样反应升高细胞内活性氧而最终诱导肿瘤细胞铁死亡。另外,外源性铁可以加速DHA发生芬顿样反应进而加速肿瘤细胞铁死亡的发生与发展。     

Physiological changes in the hemolymph of juvenile shrimp Litopenaeus vannamei to sublethal nitrite and nitrate stress in low-salinity waters

Juveniles of the shrimp Litopenaeus vannamei (3.3 ± 0.4 g) were exposed separately to nitrite (0.0, 1.1, 2.6, and 5.3 mg/L nitrogen as nitrite [NO₂⁻-N]) and nitrate (0, 90, 225 and 400 mg/L nitrogen as nitrate [NO₃⁻-N]) concentrations equivalent to 0, 10, 25, and 50% of the LC₅₀-96 h value of NO₂⁻-N and NO₃⁻-N in low salinity water (3 g/L). Shrimps responded to nitrite and nitrate according to changes in oxyhemocyanin, glucose, lactate and ion levels in the hemolymph after 6, 12, 24, and 48 h of exposure. Oxyhemocyanin levels decreased with increasing nitrite and nitrate levels and were higher at 50% exposure to the contaminants. Compared to the control, glucose and lactate increased significantly at 50% exposure to nitrite and nitrate, particularly at 12 and 24 h. Na⁺ in the hemolymph changed with nitrite and nitrate, while K⁺ only changed ˜with nitrite.     

镇心省睡益智方及其精油对AD模型小鼠学习记忆的影响

目的:观察镇心省睡益智方水提液及其精油对β淀粉样前体蛋白基因/早老素基因(APP/PS1)双转基因小鼠学习记忆的影响并探讨其可能机制。方法:采用APP/PS1双转基因痴呆小鼠及同月龄相同遗传背景C57BL/6JNju小鼠2种小鼠。C57BL/6JNju小鼠作为正常组,APP/PS1双转基因痴呆小鼠随机分为模型组,镇心省睡益智方精油低、高质量浓度组(12.13,48.50 mg·L~(-1)),镇心省睡益智方水提液组(0.46 g·kg~(-1)),每组12只。每天给药1次,连续给药22 d。给药结束后采用跳台实验、Morris水迷宫实验对小鼠行为学能力进行检测,采用尼氏染色观察海马CA1区神经元变化,采用硫磺素(Th S)染色观察海马DG区老年斑(SP)沉积,采用免疫组化法检测小鼠脑组织中葡萄糖转运蛋白1(GLUT1),胰岛素受体底物-1(IRS-1)的表达,采用酶联免疫吸附测定(ELISA)检测小鼠海马组织中乙酰胆碱(ACH),γ-氨基丁酸(GABA),谷氨酸(GLU)含量的变化。结果:与正常组比较,模型组小鼠跳台实验潜伏期显著缩短,错误次数显著增加(P0.01),Morris水迷宫实验定位航行逃避潜伏期明显延长(P0.05,P0.01),海马CA1区神经元出现缺失,DG区出现明显的老年斑沉积(P0.05),ACH,GLUT1含量均显著下降(P0.01),GABA,GLU水平及IRS-1的表达均显著升高(P0.01);与模型组比较,各给药组均可显著延长小鼠跳台实验潜伏期、减少跳台错误次数(P0.01),明显降低定位航行小鼠逃避潜伏期(P0.05,P0.01),可一定程度保护小鼠海马CA1区神经元,减少DG区老年斑沉积(P0.05,P0.01),明显增加小鼠脑组织中ACH,GLUT1表达(P0.05,P0.01),显著降低GABA,GLU水平及IRS-1的表达(P0.01)。结论:镇心省睡益智方水提液及其精油能够改善APP/PS1小鼠的学习记忆行为,保护神经元,增加脑组织GLUT1的表达,减少脑组织IRS-1的表达,减少老年斑沉积,升高ACH含量,降低GABA,GLU含量,可能是其防治阿尔茨海默症的机制。     

基于“脾胰同源”应用养阴益气活血法减少血糖波动干预糖尿病大血管病变的研究

目的探讨基于"脾胰同源"应用养阴益气活血法观察参芪复方对糖尿病血糖波动的影响。方法建立由高脂饲料喂养的糖尿病大血管并发症大鼠模型,实验分为空白组,模型组,参芪复方组,西药西格列汀组,各组灌胃8周。实验期间观察动物一般状况,在灌胃的第4周每周1次测定1日内5个时间点的血糖情况,并计算MBG、SDBG、LABG值。灌胃8周后处死GK大鼠,检测各组血脂水平、CRP、血清胰岛素、血清胰高血糖素、血清GLP-1,对腹主动脉及胰腺组织进行HE染色后进行病理形态学观察。结果参芪组一般状况优于模型组,血糖波动方面,每日平均血糖标准差(SDBG)和最大血糖波动幅度(LAGE)值优于模型组。甘油三酯(TG)、胆固醇(TC)以及C反应蛋白(CRP)较模型组降低,但与西药组无统计学意义。胰岛素(INS)与胰高血糖素(GC)与模型组相比,无统计学意义;而GLP-1较模型组有显著的差异(P<0.01)。病理方面,参芪组腹主动脉和胰腺切片优于模型组和西药组。结论应用参芪复方可以改善糖尿病大血管病变GK大鼠的一般状态,提高GLP-1的浓度,控制血糖的波动幅度;且可以改善脂代谢紊乱,降低CRP,减轻模型GK大鼠血管内皮损伤,延缓糖尿病大血管病变的进展。     

益气活血通络汤治疗原发性高血压合并糖耐量减低临床研究

目的:观察中药益气活血通络汤治疗高血压合并糖耐量减低的临床疗效。方法:将64例高血压合并糖尿病患者,随机分为2组各32例,对照组口服硝苯地平片治疗;观察组加用中药益气活血通络汤,以治疗前后收缩压(SBP)、舒张压(DBP)、三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、血糖、胰岛素、胰岛素敏感性指数(ISI)、胰岛素抵抗指数(HOMA-IR)为观察指标。结果:治疗3个月后,观察组疗效优于对照组(Z=-1.998,P<0.05)。与治疗前比较,2组经治疗后SBP、DBP、TC、TG、LDL-C均下降,HDL-C上升,差异有统计学意义(P<0.05);观察组治疗后SBP、DBP、TC、TG、LDL-C、HDL-C与对照组治疗后比较,差异有统计学意义(P<0.05)。与治疗前比较,2组经治疗后空腹和餐后2 h血糖、胰岛素、HOMA-IR均下降,ISI上升,差异有统计学意义(P<0.05);且经治疗后,观察组上述所有指标改善情况均优于对照组,差异有统计学意义(P<0.05)。2组患者在3个月的治疗期间中均未出现严重不良反应。结论:中药益气活血通络汤治疗高血压合并糖耐量降低疗效较好且安全性高,能显著降低血压,改善血脂。     

The relationships among monocyte subsets,miRNAs and inflammatory cytokines in patients with acute myocardial infarction

Background

Acute myocardial infarction (AMI) causes irreversible myocardial damage and release of inflammatory mediators, including cytokines, chemokines and miRNAs. We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI.