目的 综合评价我国空巢老人抑郁患病率,并分析不同分层因素下空巢老人的抑郁患病率.方法 检索中国(CNKI)学术文献总库、万方数据库、维普(VIP)数据库、PubMed数据库、Science Direct数据库,收集发表年限为2000年至2012年的有关中国空巢老人抑郁患病率的文献,对纳入的文献提取资料后进行Meta分析.结果 共纳入18篇文献,Meta分析结果显示,总合并抑郁患病率为40.4％ (95％ CI:28.6％～52.2％);轻度和中重度抑郁患病率分别为43.2％和9.3％;女性和男性抑郁患病率分别为32.1％和27.0％;60岁、70岁、80岁以上空巢老人抑郁患病率分别为28.9％、21.5％和24.5％;独居和偶居空巢老人抑郁患病率分别为47.9％和36.0％.结论 我国空巢老人抑郁患病率较高,不同分层间抑郁患病率差别较大.

目的 研究纳米二氧化钛染毒对大鼠脑皮层细胞内钙离了浓度([Ca2+]i)和钙蛋白酶1(calpain 1)表达的影响.方法 将50只健康SPF级雄性Wistar大鼠随机分为5组,分别为对照(蒸馏水)组和低(62.5 mg/kg)、中(125 mg/kg)和高(250mg/kg)剂量纳米二氧化钛染毒组及微米二氧化钛(250 mg/kg)染毒组,每组10只.采用灌胃方式进行染毒,每天1次,连续染毒60 d,测定大鼠脑皮层细胞内[Ca2+]和calpain 1的表达水平.结果 与对照组比较,仅高剂量纳米二氧化钛染毒组大鼠脑皮层细胞内[Ca2+]i升高,差异有统计学意义(P＜0.05);而低、中剂量纳米二氧化钛及微米二氧化钛染毒组大鼠脑皮层细胞内[Ca2+]i略有升高趋势,但差异均无统计学意义(P≥0.05).且随着纳米二氧化钛染毒剂量的升高,大鼠脑皮层细胞内[Ca2+]呈上升趋势.与对照组比较,纳米二氧化钛及微米二氧化钛染毒组大鼠腋皮层组织calpain 1表达水平略有升高趋势,但差异均无统计学意义(P≥0.05).结论 在本实验剂量下,纳米二氧化钛染毒可导致大鼠脑皮层细胞内[Ca2+]i升高,但并未影响calpain 1的表达.

为评价我国东部沿海水域中抗生素的生态学危害,通过检索国内外数据库获得7篇文献,并计算水域中各抗生素的风险商值(risk quotients,RQ)。结果显示,渤海湾、海河和珠江流域抗生素RQ值总体较高,大于关注水平(level of concern,LOCs)的抗生素RQ值的比例分别为70%,55.6%,67.5%。其中,渤海湾中氧氟沙星RQ值最高,为451.3,其次为海河的红霉素,RQ值为215;莱州湾、黄浦江、九龙江和北部湾抗生素RQ值均较低。提示渤海湾、海河和珠江流域抗生素残留生态危害严重。

目的 观察二十二碳六烯酸(DHA)对1-溴丙烷(1-BP)致大鼠学习能力损伤的拮抗作用.方法 将48只健康成年SPF级雄性Wistar大鼠随机分为4组,即对照(玉米油)组、1-BP染毒组和低、高剂量DHA干预组,每组12只.1-BP染毒组和低、高剂量DHA干预组每天灌胃染毒800 mg/kg的1-BP;4 h后,低、高剂量DHA干预组分别灌胃染毒250、500mg/kg的DHA,每日1次,连续11d.染毒第8～11天采用Morris水迷宫试验中的定位导航试验检测大鼠的学习能力.染毒结束后,检测大脑皮层匀浆中还原型谷胱甘肽(GSH)、丙二醛(MDA)含量及谷胱甘肽还原酶(GR)活力.采用Westernblotting方法检测大脑皮层脑红蛋白(neuroglobin,Ngb)的表达.结果 与对照组比较,1-BP染毒组大鼠游泳总路程和逃避潜伏期延长(P＜0.05);与1-BP染毒组相比,各剂量DHA干预组大鼠的游泳路程和逃避潜伏期缩短(P＜0.05).与对照组比较,1-BP染毒组大鼠大脑皮层匀浆中GSH含量及GR活力均下降,而1-BP染毒组MDA含量及高剂量DHA干预组GSH含量均升高(P＜0.05);与1-BP染毒组比较,各剂量DHA干预组大鼠大脑皮层匀浆中GSH含量及GR活力均升高,MDA含量均下降(P＜0.05).与对照组比较,1-BP染毒组和低剂量DHA干预组大鼠大脑皮层匀浆中Ngb蛋白的表达水平均下降,而高剂量DHA干预组Ngb蛋白的表达水平升高(P＜0.05);与1-BP染毒组比较,各剂量DHA干预组大鼠大脑皮层匀浆中Ngb蛋白的表达水平均升高(P＜0.05).结论 DHA能够减轻1-BP导致的大鼠中枢神经系统氧化应激反应及由此引起的学习能力损伤,激活GR活力、增强Ngb表达可能是DHA的保护机制之一.

为探讨土壤抗生素测定中回收率变异的原因,采用超声萃取-液相色谱-质谱法测定土壤中抗生素,观察样品前处理过程各个环节的抗生素损失和土壤有机质去除对回收率的影响.结果显示,前处理中添加土壤样品后,回收率下降,下降幅度为氟喹诺酮类(48％～52％)＞四环素类(15％～27％)＞磺胺类(5％～14％).去除土壤样品中有机质后,磺胺类的回收率无明显变化,氟喹诺酮类的回收率下降(4％～7％)而四环素类的回收率上升(9％～13％)(P＜0.05).提示土壤中粘土矿物对氟喹诺酮类有较强吸附,土壤中的有机质和粘土矿物对四环素类均有较强吸附作用,使其回收率较低,而对磺胺类的影响不明显.

Objective To investigate the relationship between Chinese children and pregnant mothers' pesticides exposure and childhood leukemia.Methods Databases were searched and 12 relevant published articles were got finally.Meta analysis was performed after extract data of included literatures.Results Children and pregnant mothers' pesticides exposure could increase the risk of childhood leukemia(OR =2.28,95% CI:2.01-2.59).Area,sources of control groups,sample size,investigation time and contact mode were set as the grouping factors,the results showed that each group of children and pregnant mothers exposed to pesticides could increase the risk of childhood leukemia.Conclusion Children and pregnant mothers pesticides exposure is a risk factor for childhood leukemia.

Objective To study the influence of nano-titanium dioxide on the cerebral cortex structure and level of oxidative stress in rats.Methods A total of 50 SPF Wistar rats were randomly divided into five groups:control group(distilled water),three nano-titanium dioxide groups(62.5,125 and 250 mg/kg body weight) and ordinary particle size group(250 mg/kg body weight).Titanium dioxide was given to rats by oral gavage,once a day for 60 consecutive days.The levels of T-SOD,MDA,GSH-Px and T-AOC in cortex were determined.The cerebral cortex pathological slices were prepared to observe the structural changes of the cerebral cortex.Results Compared with the control group,the level of T-SOD decreased significantly in 250 mg/kg group(P<0.05),the level of MDA increased significantly in 250 mg/kg group and 125 mg/kg group(P<0.05).Pathological examination showed cell swelling,nuclear condensation,fragmentation and chromatolysis in nano-titanium exposed groups.No significant damages were observed in the cerebral cortex in ordinary particle size group.Conclusion Nano-titanium dioxide exposure may cause damage of cerebral cortex tissues and increase the level of peroxide in rats.

目的 研究纳米二氧化钛对大鼠体内氧化应激水平及大鼠海马组织结构的影响.方法 将32只健康SPF级雄性Wistar大鼠随机分为4组,分别为对照(蒸馏水)组和低(250 mg/kg)、中(500 mg/kg)、高(1 000 mg/kg)剂量纳米二氧化钛组,每组8只.采用灌胃方式进行染毒,每天1次,连续染毒14d.分别在染毒第3、7、14天测定大鼠血浆中总超氧化物歧化酶(T-SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力、总抗氧化能力(T-AOC)及丙二醛(MDA)含量;实验结束后,观察海马组织结构的变化.结果 与对照组比较,第3、7、14天高剂量纳米二氧化钛组血浆中T-SOD、GSH-Px活力和T-AOC均明显降低,MDA含量均明显升高;中剂量纳米二氧化钛组T-SOD活力在第3、14天明显降低,GSH-Px活力在第14天明显降低,T-AOC在第3天明显降低,MDA含量在第7、14天明显升高,差异均有统计学意义(P＜0.05);而低剂量纳米二氧化钛组以上4个指标均无显著改变.在各剂量纳米二氧化钛染毒组内,仅低、中剂量组第14天T-SOD活力显著低于第3天,差异均有统计学意义(P＜0.05).各染毒组海马区神经细胞出现不同程度的病理改变,如染色质溶解、核固缩、细胞密度降低等现象,中、高剂量组可见神经细胞坏死形成的空泡状区域.结论 本实验条件下,纳米二氧化钛染毒可引起体内氧化应激反应增强,并可导致大鼠海马组织结构损伤.

Objective To study the antagonistic effect of vitamin E(VE) on acute liver injury induced by N,N-dimethylformamide(DMF).Methods A total of 30 healthy SPF male KM mice were randomly divided into five groups:normal control group,VE(10 mg/kg) control group,DMF poisoning model group,low dose(5 mg/kg) and high dose(10 mg/kg) VE-protected groups.VE control group,low dose and high dose VE-protected groups were treated with VE solution through gavage.Simultaneously,normal control group and DMF poisoning model group were given corn oil.The gavage volume was 2.5 ml/kg,once a day,for five consecutive days.0.5 h after the last VE-gavage,DMF poisoning model group and each VE-protected group were given 2 g/kg DMF one time.Simultaneously,normal control group and VE control group were given distilled water one time.The gavage volume was 5 ml/kg.24 h after DMF poisoning,the activities of serum ALT,AST,XOD and the contents of hepar GSH,MDA were detected.Results Compared with the DMF poisoning model group,the activities of serum ALT,AST,XOD in VE-protected groups decreased significantly(P<0.05),the content of hepar GSH increased significantly(P<0.05),and the content of hepar MDA decreased significantly(P<0.05).Conclusion VE may have effective antagonism on the liver injury induced by DMF.