Mitochondrial-mediated apoptosis in neural stem cells exposed to manganese.

Manganese is an essential nutrient for humans that has to be maintained at proper levels for normal brain functioning. However, manganese also acts as a toxicant to the brain, and several studies have linked exposure to excessive manganese to neurotoxicity in adults. A recent report has suggested that ingesting high doses of manganese via drinking water can impede intellectual functions in children. It is known that during development, the nervous system is particularly vulnerable to different types of injuries and toxicants. Neural stem cells (NSCs) play an essential role in both the developing nervous system and the adult brain where the capacity for self-renewal may be important. In the present study, we have used NSCs to investigate the molecular mechanisms involved in manganese developmental neurotoxicity. The results show that primary cultures of rat embryonic cortical NSCs as well as the murine-derived multipotent NSC line C17.2 undergo apoptotic cell death via a mitochondrial-mediated pathway in response to manganese. Exposed cells exhibit typical apoptotic features, such as chromatin condensation and cell shrinkage, mitochondrial cytochrome c release, activation of caspase-3, and caspase-specific cleavage of the endogenous substrate poly (ADP-ribose) polymerase. In addition, our data also show that reactive oxygen species formation plays a role in the onset of manganese toxicity in NSCs.     

地塞米松误用于水痘患者致多器官衰竭死亡

15岁女童,因出疹2天并发热(T38.4℃)静脉滴注地塞米松(量不详)。次日,皮疹加重并出现出血性疱疹,伴腰痛;第3天出现头痛、恶心、呕吐,查WBC19.65×109/L,RBC3.65×1012/L,Hb123g/L,PLT46×109/L,ALT4247U/L,AST4719U/L,LDH1209U/L,CK612U/L。入院后患者精神恍惚,全腹压痛,双肾区叩痛;HR130次/min,BP86/60mmHg;WBC17.4×109/L,L0.32;RBC2.56×1012/L,Hb93g/L,PLT27×109/L;尿潜血( );PO211.76mmHg,PCO22.5mmHg;2周内有与水痘患者密切接触史,诊断为水痘,水痘脑炎,多器官功能损害,感染性休克,弥漫性血管内凝血,代谢性酸中毒。给予升压、扩容、止血、纠正酸中毒、抗感染等治疗,但患者出现呕血,口腔、鼻腔持续出血,无尿,血压下降,深度昏迷,入院12h死亡。     

碘普罗胺370致过敏性休克死亡

1名44岁女性静脉曲张患者,行增强CT检查前,给予碘普罗胺370100ml,0.9%氯化钠注射液40ml,地塞米松10mg,高压注射器静脉团注,速度约为2.5ml/s。注入完毕,患者即出现意识丧失,呼吸、心跳停止。立即给予心肺复苏、气管插管、抗休克药物等抢救,2h多后患者死亡。尸检报告提示多器官组织嗜酸性粒细胞浸润,肺水肿,喉头、会厌水肿。     

绍兴市省外流动人口5岁以下儿童死亡分析

[目的]了解绍兴市省外流动人口5岁以下儿奄死亡情况,为制定干预措施提供依据. [方法]对绍兴市2007年97例省外流动人口5岁以下儿童死亡率、死亡原因、死前保健服务与本地户口死亡儿童进行比较. [结果]省外流动人口新生儿死亡率、婴儿死亡率、5岁以下儿童死亡率均高于本地户口儿童;流动人口儿童死亡原因主要为早产和低出生体重、溺水、出生窒息、意外窒息和交通意外,分类死因以新生儿疾病、意外和中毒为主;死亡儿童住院出生比率低于本地户口儿童,死亡末治疗比率高于本地户口儿童,差异有显著性. [结论]省外流动人口5岁以下儿童死亡率高于本地户口儿童,主要死因为早产和低出生体重、意外死亡,流动人口保健服务利用低于本地户口儿童.     

氟罗沙星静脉滴注过程中患者突然死亡

1例40岁女性患者，因患急性肾盂肾炎，先给予头孢噻肟钠2g溶入0．9％氯化钠注射液250ml静脉滴注，未见不良反应。其后给予氟罗沙星0．4g＋5％葡萄糖注射液500ml静脉滴注。在输入氟罗沙星注射液约250ml时，出现寒战，查BP100／70mmHg，HR84次／min。停止输液，给予异丙嗪肌内注射、地塞米松静脉推注。约17min后患者突然四肢抽搐，血压未测及，心脏停搏，随后呼吸停止。经持续抢救无效死亡。     

抗癫(癎)药物对戊四氮点燃大鼠癫(癎)发作及生命影响的研究

目的:研究抗癫癎药物(AEDs)对戊四氮(PTZ)点燃大鼠发作的控制与生存的影响。方法:选用健康雄性成年SD大鼠70只,随机分为7组,每组10只。随机选取1组作为正常对照组(NS组),其余6组用PTZ点燃,制备大鼠癫癎模型;致癎后随机选取1组作为癫癎对照组(PTZ组),其余5组分别给予卡马西平(CBZ组)、苯妥英钠(PHT组)、丙戊酸钠(VPA组)、托吡酯(TPM组)及拉莫三嗪(LTG组)控制癫癎发作。2周后观察大鼠的癫癎发作控制率和病死率。结果:PHT组有4只(4/10)持续发作,TPM组有3只(3/10)持续发作,其他3组控制良好,癫癎未再发作。PTZ组和TPM组各死亡1只(1/10),LTG组死亡2只(2/10)。结论:PHT、TPM对PTZ点燃的癫癎发作控制不良;TPM、LTG可导致大鼠死亡。     

启东市居民30年预期寿命分析

[目的]分析启东市居民1975—2004年预期寿命的变化趋势,了解启东居民的健康水平。[方法]寿命表的编制采用蒋庆琅(C.L.Chiang)法,使用SPSS 11.0软件编程并进行统计分析。[结果]1975—2004年启东市居民的平均寿命由71.5岁增加到78.8岁,提高了7.3岁。从1995年以后随着婴儿死亡率的下降,预期寿命提高明显;各时期女性的预期寿命均明显高于男性(7岁左右)。[结论]启东市居民预期寿命的提高体现了启东居民健康水平的提高和经济发展和卫生事业的进步。     

永昌县2003～2007年5岁以下儿童死亡原因监测分析

目的探讨甘肃省永昌县5岁以下儿童死亡病因、死亡率及动态变化状况,为制定干预策略提供科学依据。方法对2003~2007年甘肃省永昌县5岁以下儿童死亡监测资料汇总、整理并进行回顾性分析。结果2003~2007年5岁以下儿童死亡率为16.65‰。前5位死因分别为早产和低出生体重、出生窒息、肺炎、先天异常和意外伤害。年龄构成显示新生儿死亡占83.60%,婴儿死亡占93.10%,1~4岁儿童死亡占6.90%。结论应提高保健服务质量,降低新生儿死亡率。     

1991～2005年济南市历下区居民死因分析

[目的]了解济南市历下区居民的死亡水平、死亡的变化趋势以及死因模式的变化。[方法]运用死亡率、标准化死亡率、死因别死亡率、死因构成、期望寿命等指标对1991-2005年历下区居民死因监测资料进行统计分析。[结果]1991~2005年历下区居民年均粗死亡率为491.72/10万,标化死亡率为297.75/10万。男性标化死亡率(300.71/10万)高于女性(280.89/10万)(χ2=9.558,P=0.002);0~14岁、15~64岁和65岁及以上年龄组年均死亡率分别为27.07/10万,176.98/10万、4161.45/10万。前五位的主要死因为循环系统疾病、肿瘤、呼吸系统疾病、损伤和中毒以及内养代免(内分泌,营养和代谢疾病及免疫疾患)。15年年均期望寿命为76.61岁,其中男性75.42岁,女性77.97岁。对居民寿命影响最大的死因为循环系统疾病,去除该死因后,期望寿命可提高15.71岁,增长了20.37%。[结论]慢性病尤其是心脑血管疾病仍是今后预防控制的重点,男性的健康问题以及老年问题应引起社会的广泛关注和重视。     

Synergistic neurotoxic effects of arsenic and dopamine in human dopaminergic neuroblastoma SH-SY5Y cells.

Parkinson's disease is an environmentally influenced, neurodegenerative disease of unknown origin that is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the brain. Arsenic is an environmental contaminant found naturally in ground water, industrial waste, and fertilizers. The initial goal of the present study was to determine if a mixture of arsenite (As(+3)) and dopamine (DA) could cause enhanced degeneration of dopaminergic neuronal cells. Additional goals were to determine the mechanism (apoptosis or necrosis) of As- and DA-induced cell death and if death could be attenuated by antioxidants. The cell culture model employed was the SH-SY5Y neuroblastoma cell line that has been shown to possess differentiated characteristics of dopaminergic neurons. The results demonstrated that a mixture of As(+3) and DA was synergistic in producing the death of the SH-SY5Y cells when compared with exposure to either agent alone. A mixture of 10muM As(+3) and 100muM DA produced almost a complete loss of cell viability over a 24-h period of exposure, whereas, each agent alone had minimal toxicity. It was shown that necrosis, and not apoptosis, was the mechanism of cell death produced by exposure of the SH-SY5Y cells to the mixture of As(+3) and DA. It was also demonstrated that the antioxidants, N-acetylcysteine, and Sulforaphane, attenuated the toxicity of the mixture of As(+3) and DA to the SH-SY5Y cells. This study provides initial evidence that As(+3) and DA synergistically can cause enhanced toxicity in cultured neuronal cells possessing dopaminergic differentiation.