氯米帕明和艾司西酞普兰治疗强迫症临床疗效的对比观察

目的对比观察氯米帕明和艾司西酞普兰治疗强迫症的临床疗效及不良反应。方法选取牡丹江神经精神病医院自2008年3月至2009年11月的强迫症患者84例,采用随机数字方法,分成两组,氯米帕明组42例,应用氯米帕明50～200mg/d治疗,艾司西酞普兰组42例,应用10～20mg/d治疗,两组均以8周作为1个疗程,观察1疗程治疗后两组GI和TESS。结果氯米帕明组和艾司西酞普兰组两组在治愈率方面无统计学意义(P>0.05);不良反应发生率方面氯米帕明组要高于艾司西酞普兰组,二者之间存在统计学差异(P<0.05)。结论氯米帕明和艾司西酞普兰治疗强迫症均有较好的疗效,在治愈率方面类似,但氯米帕明可能会出现不良反应的概率明显高于艾司西酞普兰。     

文拉法辛缓释剂与氯米帕明治疗躯体化障碍的疗效比较

［摘要］目的比较文拉法辛缓释剂与氯米帕明治疗躯体化障碍的疗效和不良反应。方法躯体化障碍患者130例,随机分为两组。治疗组64例,对照组66例,分别用文拉法辛缓释剂与氯米帕明治疗8周。用90项症状清单（SCL 90）中的躯体化、抑郁和焦虑3个因子总分以及临床疗效总评量表 病情严重程度（CGI SI）评定症状变化,用不同减分率评定疗效。用不良反应量表（TESS）评定药物不良反应。结果治疗组痊愈率61.8%,总有效率89.1%;对照组痊愈率44.4%,总有效率75.9%,两组疗效比较差异有显著性（P＜0.05）。各时点TESS测评组间比较,差异均有显著性（P＜0.05）。结论 文拉法辛缓释剂治疗躯体化障碍疗效确切,不良反应较小。     

西酞普兰治疗以头痛为主诉的抑郁性情感障碍31例

［摘要］目的比较西酞普兰与阿米替林治疗以头痛为主诉的抑郁性情感障碍的疗效和安全性。方法将符合入选标准的患者91例随机分为治疗组31例、对照1组30例和对照2组30例，分别口服西酞普兰20 mg·d 1、阿米替林100～150 mg·d 1和镇痛对症药物治疗6周；分别于治疗前和治疗后1,2,4,6 周末采用汉密尔顿（HAMD）量表评分，用TESS量表评定不良反应。结果治疗6周后，治疗组和对照1组临床好转率分别达87.1%和 86.7%，多数患者头痛缓解、睡眠改善、生活和工作能力恢复，对照2组临床好转率仅26.7%。治疗后1,2周，治疗组HAMD评分较治疗前明显下降（P＜0.05），而对照1组评分较治疗前下降不明显(P＞0.05)；治疗组和对照1组治疗后4～6周HAMD评分均较治疗前明显下降(P＜0.01)，但两组差异无显著性(P＞0.05)；治疗组不良反应较对照1组少而轻，与对照2组相当。结论 西酞普兰治疗以头痛为主诉的抑郁性情感障碍疗效与阿米替林相当，但起效较快，安全性高，不良反应轻微。     

艾司西酞普兰治疗抑郁症116例

摘要 目的 观察艾司西酞普兰治疗抑郁症的疗效和安全性。方法抑郁症患者297例,分为艾司西酞普兰（20 mg·d－1）组116例,度洛西汀（60 mg·d－1）组105例,帕罗西汀（20 mg·d－1）组76例,疗程6周。于治疗前及治疗1,2,4,6周末采用汉密尔顿抑郁量表（HAMD）17项作为主要指标评价疗效,用不良反应量表（TESS）评定不良反应。结果艾司西酞普兰组、度洛西汀组与帕罗西汀组的有效率分别为81.7%,77.8%及79.4%,三者差异无统计学意义（P＞0.05）;艾司西酞普兰组的患者中出现恶心不良反应发生率虽然高于其他两组,但差异亦无统计学意义。结论艾司西酞普兰起效迅速,不良反应适中,是一种新型安全的抑郁症治疗物。     

西酞普兰治疗躯体化障碍的临床疗效

［摘要］目的观察西酞普兰治疗以胃肠道症状为主的躯体化障碍的临床效果。方法躯体化障碍患者112例,根据症状特点分为A组（以胃肠道症状为主）61例,B组（非胃肠道症状为主）51例,均给予西酞普兰片20 mg, po,qd。治疗6个月。于治疗前及治疗后1,2,4,6个月末测评汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）、不良反应量表（TESS）。结果两组HAMD 和HAMA总分之和组间比较从治疗1个月末开始差异有显著性（P＜0.05）,A、B组有效率分别为70.5%,80.4%（P＜0.05）,各时期TESS评分比较差异无显著性（P＞0.05）,且B组的胃肠道反应少于A组（P＜0.05）。结论西酞普兰治疗以胃肠道症状为主的躯体化障碍的疗效不及非胃肠道症状为主的患者,且前者的胃肠道不良反应更多。     

西酞普兰联合利培酮治疗难治性躯体化障碍的对照研究

目的探讨西酞普兰联合利培酮治疗难治性躯体化障碍的疗效和安全性。方法将83例难治性躯体化障碍患者随机分为两组,研究组（n=42）采用西酞普兰联合利培酮治疗,对照组（n=41）仅用西酞普兰,治疗6周。于入组前及入组后第二、四、六周末分别用汉密尔顿抑郁量表（HAMD）,汉密尔顿焦虑量表（HAMA）及不良反应量表（TESS）进行评定。结果两组在治疗后第二周末开始HAMD、HAMA总分组间比较差异有统计学意义（P〈0.05）,两组间疗效差异也有统计学意义（P〈0.05）。药物不良反应两组间差异无统计学意义（P〉0.05）。结论西酞普兰联合利培酮治疗难治性躯体化障碍的疗效和安全性较好。     

西酞普兰和阿米替林治疗抑郁症的比较

目的 :比较西酞普兰和阿米替林治疗抑郁症的疗效和不良反应 ,方法 :抑郁症病人 88例 ,采用西酞普兰 2 2mg±s 6mg( 2 0～ 4 0mg·d 1) ,po ,疗程为 6wk。另用阿米替林治疗同类病人 87例 ,剂量为 10 0mg± 10mg( 50～ 150mg·d 1) po ,疗程为6wk。在治疗前及治疗后 1,2 ,4 ,6wk末予MAMD ,CGI ,TESS量表评定临床疗效。结果 :西酞普兰显效率 79% ,阿米替林组显效率 75% (P >0 .0 5) ,西酞普兰组不良反应较阿米替林组少。结论 :西酞普兰与阿米替林治疗抑郁症疗效相当 ,前者较后者起效快 ,不良反应少。     

文拉法辛与氯米帕明治疗强迫症的药物经济学评价

目的评价文拉法辛和氯米帕明治疗强迫症的药物经济学效果。方法将40例符合CCMD-2-R强迫症诊断标准的患者随机分成两组各20例，分别给予文拉法辛和氯米帕明治疗，剂量均为50～250 mg·d^-1，po，疗程均为8周。观察疗效，并进行药物经济学评价。结果两组治疗后Ycale Brown及HAMD量表评分均显著改善（P＜0.05）；两组疗效比较差异无显著性（P＞0.05），不良反应发生率文拉法辛（55.6%）明显低于氯米帕明（86.7%）（P＜0.05）；药物经济学评价显示氯米帕明治疗强迫症优于文拉法辛。结论氯米帕明治疗强迫症成本 效果优于文拉法辛，但鉴于其不良反应较高，依从性差，复发率较高，其药物经济学价值尚待进一步评价。     

加巴喷丁联合西酞普兰滴定治疗慢性偏头痛伴广泛性焦虑障碍临床疗效分析

目的：探讨加巴喷丁联合西酞普兰对慢性偏头痛（CM）伴广泛性焦虑障碍患者的临床疗效、安全性及两药的有效剂量。方法：按照随机数字表法将210例慢性偏头痛患者纳入加巴喷丁联合西酞普兰组（治疗组）105例和托吡酯联合西酞普兰组（对照组）105例,均治疗6个月。分别记录2组患者治疗前及治疗3,6个月后每月发作天数、偏头痛严重程度视觉模拟评分（VAS）、偏头痛特异性生活质量问卷（MSQ V2.1）、头痛影响测定-6（HIT-6）、匹兹堡睡眠质量指数（PSQI）、汉密尔顿焦虑量表（HAMA）评分和药物不良反应。结果：持续治疗6个月,2组患者头痛发作天数、VAS、HIT-6、PSQI、MSQ V2.1评分均下降,治疗组患者头痛天数下降更显著,对照组患者MSQ V2.1总评分下降更显著（均P<0.05）。2组患者有效率差异无显著性（P>0.05）。加巴喷丁（1.2 g·d^-1）或者托吡酯（100 mg·d^-1）联合西酞普兰（10 mg·d^-1）是理想的治疗CM伴广泛性焦虑障碍的药物剂量。2组药物不良反应发生率均较低（P>0.05）。结论：加巴喷丁（1.2 g·d^-1）联合西酞普兰（10 mg·d^-1）能显著减少CM伴广泛性焦虑障碍患者偏头痛发作天数,降低偏头痛患者疼痛程度,改善睡眠,提高生活质量,不良反应小,疗效不劣于托吡酯联合西酞普兰治疗方案。     

西酞普兰合并利培酮治疗躯体形式障碍的对照研究

目的研究西酞普兰联合利培酮治疗躯体形式障碍（SD）的疗效及其安全性。方法101例躯体形式障碍患者随机分为2组,研究组予以西酞普兰合并利培酮治疗,对照组单用西酞普兰治疗,疗程均为8周。治疗前与治疗后第2、4、6、8周采用症状自评量表（SCL-90）、汉密尔顿抑郁量表（HAMD）评定临床疗效,不良反应症状量表（TESS）评定不良反应。结果治疗后2组SCL-90、HAMD评分较治疗前减少,差异有统计学意义（P〈0.01）,8周末研究组有效率82%,对照组54%,2组差异有统计学意义（P〈0.05）,并且在治疗2周末研究组较对照组显效快,差异有统计学意义（P〈0.05）。2组不良反应均表现较轻,大多出现在治疗的早期,经对症治疗逐渐缓解。结论西酞普兰联合利培酮治疗躯体形式障碍较单用西酞普兰疗效好,起效快,且不增加不良反应。     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Steroidal sapogenin contents in some domestic plants

In order to find out the values of the steroid resources for the future use. the compositions and contents of steroidal sapogenins from 13 domestic plants have been investigated. As a result,Dioscorea nipponica, D. quinqueloba andSmilax china were found to have large amount of diosgenin. And pennogenin inTrillium kamtschaticum andParis verticillata, yuccagenin inAllium fistulosum, hecogenin inAgave americana and neochlorogenin inSolanum nigum were appeared to be major steroidal sapogenins.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.