丙戊酸镁与碳酸锂治疗躁狂发作对照研究国内文献Meta分析

目的探讨丙戊酸镁治疗躁狂发作的疗效和不良反应。方法用Meta分析方法对14项丙戊酸镁与碳酸锂治疗躁狂发作对照研究文献再分析。结果丙戊酸镁治疗躁狂发作其治疗前后组内比较,加权平均效应d=17.50,95%CI为14.54～20.46,效应极强（Z=11.59,P〈0.01）。丙戊酸镁与碳酸锂治疗躁狂发作比较,加权平均效应d=0.50,95%CI为-0.57～1.58,差异无统计学意义（Z=0.92,P〉0.05）。结论丙戊酸镁与碳酸锂治疗躁狂发作的疗效及不良反应相当。     

丙戊酸镁与碳酸锂对躁狂症预防治疗的对照研究

目的　评价丙戊酸镁预防治疗躁狂症的疗效和副反应。方法　１１５ 例躁狂症患者出院时按原服用丙戊酸镁或碳酸锂自然分为丙戊酸镁组（４６ 例） 和碳酸锂组（６９ 例） ,进行预防治疗研究。使用 Ｂ Ｒ Ｍ Ｓ、 Ｔ Ｅ Ｓ Ｓ 帮助评定疗效和副反应。结果　平均随访３６ 个月,丙戊酸镁组有效率８６９５ ％ ,副反应发生率４５６５ ％ ;碳酸锂组有效率８４０６ ％ ,副反应发生率４４９２ ％ ,经 Ｒｉｄｉｔ 分析２ 组比较无显著性差异。丙戊酸镁对碳酸锂预防治疗无效的病例依然有效。结论　丙戊酸镁可作为预防治疗躁狂症的选用药物。     

丙戊酸镁联用氯硝西泮治疗躁狂症对照研究

目的：探讨丙戊酸镁联用氯硝西泮治疗躁狂症的疗效与安全性。方法：对符合中国精神疾病分类方案与诊断标准第2版修订本62例躁狂症患者，其中40例用丙戊酸镁联用氯硝西泮，22例用碳酸锂治疗。疗程6周。以躁狂量表(BRMS)评定疗效，副反应量表(TESS)评定不良反应。结果：两组疗效差异无显著性。联用组不良反应明显低于对照组。结论：丙戊酸镁联用氯硝西泮治疗躁狂症．疗效确切，起效时间与安全性优于碳酸锂。     

双相情感性精神障碍预防性治疗的对照研究

目的：评价丙戊酸镁预防性治疗双相情感障碍的儿及副作用。：９６例频发双相情感精神障碍的病人随机分为两组,分别使用丙戊酸镁（４７例）和碳酸锂（４９例）进行预防性随访时间为３９个月,使用躁狂量表（ＢＲＭＳ）、汉密尔顿抑郁量表（ＨＡＭＩ）,和副反应（ＴＥＳＳ）评定疗效和副作用。结果：丙戊酸镁缄及碳酸锂组预防性治疗有效率分别为８５．０％和８２．１％,副作用发生率分别为８１。．０％和５７．１％,经Ｒｉｄｉｔ分     

静脉滴注免疫球蛋白与激素对比治疗格林-巴利综合征的meta分析

目的比较静脉注射大剂量免疫球蛋白（IVIG）与激素治疗格林-巴利综合征（GBS）患者疗效及安全性。方法对国内有关包括IVIG与激素治疗GBS随机对照试验进行meta分析,评价纳入文献的方法学质量后,采用RevMan4．2．10软件对提取的数据进行分析。结果共纳入10个随机对照试验（RCTs）研究,IVIG组共计384例,激素组441例：（1）IVIG与激素治疗GBS的有效率合并检验分析,结果为Z=5．41,P〈0．00001,0R=4．48,95％可信区间（CI）为（2．60,7．72）;（2）IVIG与激素治疗GBS的治愈率合并检验分析结果Z=8．40,P〈0．00001,OR=4．56,95％CI（3．20,6．50）;（3）IVIG与激素治疗GBS的起效时间比较,评价研究发现存在异质性,采用随机效应模型进行综合检验,结果为：Z=17．47,P〈0．00001,WMD=-4．0,95％CI（-4．45,-3．55）。结论IVIG治疗GBS总有效率、治愈率明显优于激素,起效快,在条件允许的情况下,应尽早应用IVIG进行治疗。但IVIG价格昂贵,面对那些不能负担昂贵治疗费用或不能耐受IVIG的患者,激素仍是一个有价值的治疗选择;目前国内IVIG与激素治疗GBS这一领域仍缺乏设计严谨、方法科学的临床研究。     

丙戊酸镁缓释片合并喹硫平治疗反复躁狂发作的长期疗效及安全性

目的探讨丙戊酸镁合并喹硫平治疗反复躁狂发作的长期疗效及安全性．方法将66例各类情感障碍躁狂发作患者分为丙戊酸镁组和丙戊酸镁合并喹硫平组（下称合并治疗组）,每组各33例。急性期治疗6周后随访5年。基线及疗效采用倍克-拉范森躁狂量表（BRMS）评定。随访内容包括复发次数,药物剂量,长期疗效及安全性。结果急性期治疗后BRMS减分率丙戊酸镁组为（42±27）％,合并治疗组为（57±24）％,两组间的差异有统计学意义（P〈0．05）。5年内躁狂复发次数丙戊酸镁组为（3．3±2．0）次,合并治疗组为（1．9±1．6）次,两组间的差异有统计学意义（P〈0．01）;抑郁复发次数丙戊酸镁组为（1．8±2．0）次,合并治疗组为（1．9±1．8）次,两组间的差异无统计学意义（P〉0．05）。合并治疗组的丙戊酸镁剂量明显低于单用丙戊酸镁组（P〈0．01）。两组总体不良反应的差异无统计学意义。结论丙戊酸镁合并喹硫平维持治疗情感障碍可减少躁狂复发率,且安全性较高。     

丙戊酸镁与碳酸锂及安慰剂治疗躁狂症双盲对照研究

本研究用国产丙戊酸镁与碳酸锂及安慰剂治疗躁狂症,通过随机双盲对照,结果显示,丙戊酸镁组显效率92.3%。碳酸锂组显效率80%,安慰剂组显效率16.67%。丙戊酸镁组除2例有头晕及轻度共济失调外,无其它严重副作用,可以认为丙戊酸镁是一种安全有效的抗躁狂药物。     

碳酸锂联合丙戊酸钠和利培酮治疗急性躁狂发作的对照研究

目的探讨碳酸锂分别联合丙戊酸钠和利培酮治疗急性躁狂发作的疗效和安全性。方法将94例急性躁狂发作患者随机分为两组,碳酸锂联合丙戊酸钠47例,碳酸锂联合利培酮47例,疗程均为8周。分别于治疗前及治疗后的第2、4、8周,采用躁狂量表（BRMS）评定临床疗效,治疗时出现的症状量表（TESS）评定安全性。结果碳酸锂分别联合戊酸钠和利培酮治疗急性躁狂发作的疗效相当（P〉0.05）,但前者起效快、不良反应少（P〈0.05）。结论碳酸锂联合丙戊酸钠治疗急性躁狂发作起效快、疗效显著、不良反应少,安全性高。     

丙戊酸镁与碳酸锂治疗躁狂症的对照性研究

３０例躁狂症病人随机分为丙戊酸镁与碳酸锂两个组，进行为期４周的治疗，使用Ｂｅｃｈ－Ｒａｆａｅｌｓｏｎ躁狂量表和１９８１年中华医学会神经精神科分会制定的５级疗效标准进行疗效评定，两组ＢＲＭＳ评分在治疗前后均有显著差异，丙戊酸镁的显效率为６４．２９％，碳酸锂为６８．７５％。两组间疗效无显著性差异。     

丙戊酸镁缓释片与碳酸锂治疗躁狂发作的临床对照研究

目的评价丙戊酸镁缓释片与碳酸锂治疗躁狂发作的临床疗效和不良反应。方法随机对60例躁狂发作患者分别给予丙戊酸镁释片与碳酸锂治疗,疗程6周。结果丙戊酸镁缓释片与碳酸锂治疗躁狂发作疗效相近,前者起效快,且不良反应显著低于后者,患者耐受性好。结论丙戊酸镁缓释片治疗躁狂发作疗效肯定,起效快,不良反应小,治疗安全性高,可作为治疗躁狂发作的首选药物。     

The neuroendocrinology of stress and the pathophysiology and therapy of depression and anxiety

Clinical and preclinical studies have gathered substantial evidence that stress response alterations play a major role in the development of major depression, panic disorder, and post-traumatic stress disorder. The stress response, the hypothalamic pituitary adrenocortical (HPA) system and its modulation by corticotropin-releasing hormones (CRH),corticosteroids,and their receptors, and the roles of natriuretic peptides and neuroactive steroids are described. We review the role of the HPA system in major depression, panic disorder, and post-traumatic stress disorder and its possible relevance for treatment. Impaired glucocorticoid receptor function in major depression is associated with an excessive release of neurohormones such as CRH, to which a number of signs and symptoms characteristic of depression can be ascribed. In panic disorder, a role of central CRH in panic attacks has been suggested. Atrial natriuretic peptide (ANP) is causally involved in sodium lactate-induced panic attacks. Furthermore, preclinical and clinical data on its anxiolytic activity suggest that nonpeptidergic ANP receptor ligands may be potentially useful in the treatment of anxiety disorders. Post-traumatic stress disorder is characterized by a peripheral hyporesponsive HPA system and elevated CRH concentrations in the CSF. This dissociation is probably related to an increased risk of this disorder. We further review recent data that describe an important role of GABA(A)-receptor modulatory,3 alpha-reduced neuroactive steroids in major depression, anxiety, and its treatment. Antidepressants are effective in both depression and anxiety disorders and have major effects on the HPA system,especially on glucocorticoid and mineralocorticoid receptors. Normalization of HPA system abnormalities is a strong predictor of the clinical course, at least in major depression and panic disorder. Currently,CRH-R1 or glucocorticoid receptor antagonists and ANP receptor agonists are being studied and may provide future treatment options more closely related to the pathophysiology of these disorders.     

Polymorphisms of DRD4 and DRD3 and risk of avoidant and obsessive personality traits and disorders

We investigated whether polymorphisms of the dopamine D4 receptor (DRD4) and polymorphisms of the dopamine D3 receptor (DRD3) were associated with personality disorder symptomatology rather than with personality traits such as novelty seeking. DNA was obtained from 145 depressed patients in a clinical trial. These patients were assessed for the presence of personality disorder symptoms and disorders. The 2-repeat allele of the DRD4 exon III polymorphism was associated with increased rates of avoidant and obsessive personality disorder symptomatology. The T,T genotype of the DRD4 -521 C>T polymorphism was also associated with increased rates of avoidant and obsessive personality disorder symptomatology. The Gly9,Gly9 genotype of the DRD3 Ser9Gly polymorphism was associated with increased rates of obsessive personality disorder symptomatology. None of these three polymorphisms were associated with novelty seeking or other temperament traits on the Temperament and Character Inventory. Our results suggest that genetic polymorphisms of DRD4 and DRD3 may well be associated with personality traits, and that conflicting findings to date may arise from the problem of phenotype definition.     

癫痫共病抑郁的机制及临床诊疗

本文目的是探讨癫痫共病抑郁的可能机制及临床诊疗。癫痫是一种常见的、慢性的、致残性的神经疾病,癫痫患者生活质量下降,存在明显的负性情绪,常伴发各种精神疾病。癫痫与抑郁具有共同的神经生物学基础,可能存在共同的发病机制。本文从癫痫共病抑郁的发病机制、临床诊断及治疗方面予以总结归纳。     

沙盘游戏疗法在地中海贫血患儿心理干预中的应用

本文目的是对沙盘游戏疗法在地中海贫血患儿心理干预中的应用进行综述,以期为地中海贫血患儿的心理康复提供参考。地中海贫血是以珠蛋白生成障碍为主要特征的遗传性疾病,由于长期输血治疗,患儿存在较多的心理和行为问题。沙盘游戏疗法作为一种有效、实用的儿童心理治疗方法,对提高地中海贫血患儿的康复效果、改善生存质量有重要的临床意义。     

Cultural Identity and Experiences of Prejudice and Discrimination of Afghan and Iranian Immigrant Youth

In culturally diverse and immigrant receiving societies, immigrant youth can be subject to prejudice and discrimination. Such experiences can impact on immigrant youth’s cultural identity and influence their psychosocial outcomes. This paper presents findings of a study that examined cultural identity and experiences of prejudice and discrimination among Afghan (N = 9) and Iranian (N = 17) immigrant youth in Canada. The study had a prospective, comparative, longitudinal qualitative design. Data was gathered through focus groups, interviews, journals and field logs. Four main themes emerged on participants’ experiences of prejudice and discrimination: (a) societal factors influencing prejudice; (b) personal experiences of discrimination; (c) fear of disclosure and silenced cultural identity; and (d) resiliency and strength of cultural identity. Drawing from Rosenberg’s (Conceiving the self, Basic Books, New York, 1979) self-concept framework and Romero and Roberts (J. Adolesc., 21:641–656, 1998) distinction between prejudice and discrimination, results indicated that youth’s extant and presenting cultural identity were affected. Inclusive policies and practices are needed to promote youth integration in multicultural and immigrant receiving settings.

Modulators and inhibitors of gamma- and beta-secretases

Most gene mutations associated with Alzheimer's disease point to the metabolism of amyloid precursor protein as a potential cause. The beta- and gamma-secretases are two executioners of amyloid precursor protein processing resulting in amyloid-beta. Significant progress has been made in the selective inhibition of both proteases, regardless of structural information for gamma-secretase. Several peptidic and nonpeptidic leads were identified for both targets.