3种霍乱弧菌检测方法在外环境标本中的应用研究

目的：通过改进霍乱弧菌检测的技术手段，提高外环境标本中霍乱弧菌的检出率。方法：将常规分离鉴定法、PCR检测法和胶体金免疫层析试验法同时用于检测霍乱流行期间的外环境标本，并对其现场应用结果进行比较分析。结果：3种方法检测80份外环境标本霍乱弧菌的结果显示：它们均未出现假阳性，3种方法各有优势，且结果相互符合性好，但也存在各自弱点。结论：只用单一种方法来检测外环境标本霍乱弧菌存在明显不足。建议在外环境霍乱监测中选用胶体金法进行初筛，再用常规法和PCR法检测。最大限度减少漏检的可能性。     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

A Clinical Study of Reversing Left Ventricular Hypertrophy in Hypertensive Patients by Adalat

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常用消毒剂及自来水对弓形虫速殖子活力的影响

目的了解常用消毒剂及自来水对弓形虫速殖子活力的影响。方法将各种消毒剂分别加入等体积含弓形虫速殖子的小鼠腹水中，在不同时间内观察虫体胎盘蓝（trypanblue）着色率及活动率，并将经消毒剂处理不同时间的速殖予接种昆明鼠，观察速殖子能否在接种鼠体内复苏繁殖，导致小鼠死亡。用类似方法观察自来水时速殖子的影响。结果除甲醛个速殖子在常用浓度的不同消毒剂中，lmin月台盘蓝着色率均为100％，活动率为0。经消毒剂处理1min的速殖子接种小鼠后，各组接种鼠（包括甲醛处理组）无一死亡。经自来水处理4h的速殖子接种小鼠后仍能在小鼠体内复苏繁殖，小鼠于接种1wk内全部死亡。结论弓形虫速殖子对常用消毒剂均很敏感；而在自来水中途殖子可保持感染力4h以上。     

鄂托克前旗马场井村改水降氟15年病情防治效果分析

目的：了解改水降氟后地氟病的防治效果。方法：水氟，尿氟测定均为电极法，氟斑牙诊断为Dean‘s法。结果：该村自1985年改饮低氟水，水氟含量由改水前的6.05mg/L降至改水后的0.48mg/L。改水后未出现新的氟骨症患者，8-12岁儿童氟斑牙患病率呈逐年下降趋势，改水后7-15年间氟斑牙病率均已稳定，表明病情得到有效控制，且达到稳定控制状态，结论：坚持长年饮用低氟水，地方性氟中毒就能得到有效控制。     

Long-term neurotoxicity of chlorpyrifos: spatial learning impairment on repeated acquisition in a water maze.

Organophosphate compounds are cholinesterase inhibitors widely used in agriculture, industry, household products, and even as chemical weapons. Their major mechanism of acute toxic action is the inhibition of acetylcholinesterase, which is responsible for the degradation of the neurotransmitter acetylcholine. An organophosphorus ester-induced chronic neurotoxicity (OPICN) syndrome has been proposed. The OPICN syndrome could result from both long-term exposure to subclinical doses of OPs and after acute poisoning. Development of animal models for the cognitive decline are required and could later help to elucidate the mechanisms involved in this long-term effect on the central nervous system. Previously, we have found performance decrements in a four-trial repeated acquisition spatial task in a water maze. The present study includes two experiments to extend the long-term behavioral effects observed. Rats were injected either once or twice with chlorpyrifos (CPF) and then tested months after in a two-trial repeated acquisition task in a water maze. Our results confirm and extend the long-term behavioral effects of subcutaneous administration of CPF. The two treatments used produced performance decrements that suggest functional central nervous system alterations.     

饮用水电化学法杀菌副产物三氯甲烷生成因素的研究

目的　了解电化学杀菌过程中副产物三氯甲烷的生成因素。方法　取滤后水 (三层滤料快滤池后、投放液氯前 )分别以石墨、Ti(基 ) - Ti为电极 ,配制不同 SO42 - 和 Cl- 浓度的实验水样 ,调节不同槽电流密度 ,电解不同时间后 ,取样分析 ,考察在不同条件下 CHCl3 的产生情况。结果　采用 Ti(基 ) - Ti电极的间歇电解过程中产生的 CHCl3 比采用石墨电极时多 ,且电流密度越大 ,产生的 CHCl3 越多。加入微量电解质 Na2 SO4对 CHCl3 的产生量无显著影响 ;加入微量电解质 Na Cl,〔CHCl3 〕随〔Cl- 〕的增大而增大。结论　在饮用水电解杀菌时应采用石墨电极 ,电解时间不宜超过 10分钟 ,电流密度宜 1m A/ cm2 ,以使 CHCl3 的生成量最小     

Ineffectiveness of organic calcium channel blockers in antagonizing long-term potentiation

Evidence has accumulated suggesting that the presence of calcium is critical for development of hippocampal long-term potentiation (LTP). However, there is a paucity of information about whether calcium's role in LTP is pre- or postsynaptic. In the present study, we examined the effectiveness of nitrendipine, verapamil, flunarizine and the benzodiazepine diazepam in: blocking voltage-dependent calcium channels; blocking synaptic transmission; and preventing development of LTP. Using the in vitro slice preparation, we obtained intracellular and extracellular recordings from guinea pig hippocampal CA1 pyramidal cells. At the cellular level, all 4 drugs were ineffective in blocking voltage-dependent calcium spikes (TTX resistant) and the calcium-dependent afterhyperpolarization. Verapamil and diazepam appeared to antagonize synaptic transmission, as reflected in smaller population spike amplitudes. Development of long-term potentiation was not affected by the presence of verapamil, flunarizine and diazepam. Nitrendipine appeared to reduce the percentage of slices exhibiting LTP; however, ethanol, the vehicle used to dissolve nitrendipine, was shown in separate experiments to reduce the percentage of slices exhibiting LTP. These results suggest that neither the organic calcium channel blockers--nitrendipine, verapamil, and flunarizine--nor micromolar concentrations of diazepam are potent blockers of extrasynaptic voltage-sensitive calcium channels in hippocampus. They thus cannot be used to demonstrate a specific pre- or postsynaptic calcium role in LTP.     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.     

ProTx-I and ProTx-II: gating modifiers of voltage-gated sodium channels.

The tarantula venom peptides ProTx-I and ProTx-II inhibit voltage-gated sodium channels by shifting their voltage dependence of activation to a more positive potential, thus acting by a mechanism similar to that of potassium channel gating modifiers such as hanatoxin and VSTX1. ProTx-I and ProTx-II inhibit all sodium channel (Nav1) subtypes tested with similar potency and represent the first potent peptidyl inhibitors of TTX-resistant sodium channels. Like gating modifiers of potassium channels, ProTx-I and ProTx-II conform to the inhibitory cystine knot motif, and ProTx-II was demonstrated to bind to sodium channels in the closed state. Both toxins have been synthesized chemically, and ProTx-II, produced by recombinant means, has been used to map the interaction surface of the peptide with the Nav1.5 channel. In comparison, beta-scorpion toxins activate sodium channels by shifting the voltage dependence of activation to more negative potentials, and together these peptides represent valuable tools for exploring the gating mechanism of sodium channels.