帕利哌酮治疗精神分裂症的临床疗效观察

目的观察帕利哌酮治疗精神分裂症的临床效果。方法 60例精神分裂症患者均给予帕利哌酮治疗,疗程8周,治疗后用阴性症状与阳性症状量表(PANSS)评定临床疗效,用副反应量表(TESS)评定不良反应情况。结果帕利哌酮治疗精神分裂症的总有效率为91.7%。治疗后第2、4、6、8周的PANSS评分均优于治疗前,差异均有统计学意义(P<0.05)。结论帕利哌酮可有效改善精神分裂症患者的阴性症状和阳性症状,促进其认知功能和社会功能的恢复,临床疗效确切,且无严重不良反应,安全性高,值得临床推广应用。     

帕利哌酮缓释片治疗精神分裂症疗效观察

目的探讨帕利哌酮缓释片治疗精神分裂症的临床效果。方法将126例精神病患者按照随机数字表法分为治疗组和对照组,每组63例,治疗组给予帕利哌酮,起始剂量为6 mg/d,并根据病情2周内调整药量;对照组给予奥氮平,起始剂量为5～10 mg/d,并根据病情2周内调整剂量,均为口服治疗,1次/d,给药8周,观察和记录治疗效果,并对结果进行分析。结果治疗组痊愈4例,显效37例,好转14例,无效8例,总有效率为87.3%;对照组组痊愈2例,显效36例,好转15例,无效10例,总有效率为84.1%;两组总疗效比较差异有统计学意义(P>0.05)。结论帕利哌酮缓释片用于治疗精神分裂症患者耐受性好,不良反应轻,可有效的改善患者阳性症状和阴性症状,值得临床推广应用。     

帕利哌酮与利司哌酮治疗精神分裂症近期疗效与安全性比较

目的比较帕利哌酮与利司哌酮治疗精神分裂症的近期疗效及安全性。方法 94例精神分裂症患者分为帕利哌酮组与利司哌酮组,每组47例。帕利哌酮组起始剂量3mg·d~(-1),每隔1～2wk增加剂量1次,增幅为每次3mg,剂量稳定在3～12mg·d~(-1);利司哌酮组起始剂量2m·d~(-1),每隔1～3d增加剂量1次,增幅为每次2mg,2wk内加至4～6mg·d~(-1),观察6wk。于基线及wk 2、4、6末,采用阳性和阴性症状量表(PANSS)评定疗效,采用副反应量表(TESS)评定不良反应。结果最终纳入分析的有91例,其中帕利哌酮组47例,利司哌酮组44例。治疗4、6 wk末2组PANSS总分、阳性症状分、阴性症状分和精神病理症状分均显著降低(P<0.05或P<0.01)。wk 6末帕利哌酮组治疗有效率为70%,利司哌酮组为66%,疗效无显著差异(P>0.05)。wk 2末2组间PANSS总分、阳性症状分和精神病理症状分有非常显著差异(P<0.01),阴性症状分无显著差异(P>0.05);wk 4、wk 6末2组间PANSS总分及各分项分均无显著差异(P>0.05)。帕利哌酮组和利司哌酮组不良发应发生率无显著差异(72%vs.80%,P>0.05),帕利哌酮组锥体外系反应发生显著少于利司哌酮组(P<0.01)。结论帕利哌酮治疗精神分裂症的疗效与利司哌酮相当,且起效较快,锥体外系反应发生较少,安全性较好。     

帕利哌酮缓释片治疗精神分裂症的疗效观察

目的探讨帕利哌酮缓释片治疗精神分裂症的疗效及安全性。方法将40例精神分裂症患者随机分为治疗组和对照组各20例。治疗组给予帕利哌酮缓释片治疗,对照组给予奥氮平治疗,均治疗8周。比较2组临床疗效及不良反应。结果治疗8周后,治疗组总有效率为95．0％高于对照组的65．0％,差异有统计学意义（P〈0．05）;2组不良反应发生率比较差异无统计学意义（P〉0．05）。结论帕利哌酮缓释片是一种安全、有效地治疗精神分裂症的药物,值得临床进一步推广运用。     

帕利哌酮治疗首发精神分裂症患者的疗效研究

目的：研究帕利哌酮治疗首发精神分裂症患者的临床疗效及主要不良反应。方法：收集2012年2月～2014年11月在我院住院的82例首发精神裂症患者,随机分为帕利哌酮组和利培酮组,每组41例,观察8周后应用阳性与阴性症状量表（PANSS）和药物不良反应量表（TESS）评价临床疗效和不良反应。结果：共77例患者完成随访,帕利哌酮组38例,利培酮组39例。治疗4周末帕利哌酮组PANSS各项减分率更明显,两组差异有显著性（P<0.05）;治疗8周末时两组PANSS总分较治疗前均有显著下降（P<0.01）;帕利哌酮组治疗有效率为82.9%,利培酮组治疗有效率为86.5%,疗效差异无显著性（P>0.05）;治疗8周末时两组均未发生严重不良反应,但帕利哌酮组不良反应发生率明显低于利培酮组。结论：帕利哌酮治疗首发精神分裂症疗效与利培酮无明显差异,但起效快,安全性高。     

帕利哌酮缓释片治疗精神分裂症的疗效观察

目的 探讨帕利哌酮缓释片治疗精神分裂症的疗效及安全性.方法 将40例精神分裂症患者随机分为治疗组和对照组各20例.治疗组给予帕利哌酮缓释片治疗,对照组给予奥氮平治疗,均治疗8周.比较2组临床疗效及不良反应.结果 治疗8周后,治疗组总有效率为95.0%高于对照组的65.0%,差异有统计学意义(P<0.05);2组不良反应发生率比较差异无统计学意义(P>0.05).结论 帕利哌酮缓释片是一种安全、有效地治疗精神分裂症的药物,值得临床进一步推广运用.     

帕利哌酮缓释片治疗精神分裂症30例

目的比较帕利哌酮缓释片与奥氮平治疗精神分裂症的疗效与安全性。方法将符合CCMD 3的精神分裂症患者60例随机分为两组各30例, 均先经药物清洗1周。治疗组给予帕利哌酮缓释片,起始剂量3 mg&#8226;d 1,1周后根据病情调整至6 mg&#8226;d 1;对照组给予奥氮平,起始剂量5 mg&#8226;d 1,1周后根据病情调整至10 mg&#8226;d 1。随访观察8周。两组患者均可酌情使用苯二氮类药或抗胆碱能药物。结果治疗组治疗8周后显效率（43.3%）与对照组（50.0%）差异无显著性,两药所致不良反应均较轻,患者耐受性较好。结论帕利哌酮缓释片治疗精神分裂症疗效与奥氮平相当,不良反应少。     

精神分裂症患者HTR2A基因多态性与帕利哌酮和利培酮临床疗效及安全性的关联研究

目的 观察中国汉族精神分裂症患者的5-羟色胺2A受体(HTR2A)基因多态性与帕利哌酮和利培酮治疗精神分裂症患者临床疗效与安全性的关联.方法 入组201名精神分裂症患者,133例门诊或住院患者,随机接受12周帕利哌酮棕榈酸盐(50～150 mg/4周)或利培酮长效注射针剂(25～50 mg/4周)治疗,每2周进行1次疗效和安全性的评定;68例住院患者,接受4周利培酮片(2～6 mg·d-1)治疗,每周进行1次疗效和安全性评定;以试验结束时阳性阴性症状评定量表(PANSS)总减分率为主要疗效评价指标.共选择3个多态性位点,采用限制性酶切片段长度多态性或直接测序,获得基因型.结果 rs7997012各基因型可能与I临床疗效相关联(P＜0.05),位点rs6313和rs6311的各基因型间临床疗效的差别无统计学意义(P＞0.05);位点rs6313和rs6311的各基因型与BARS、SAS评分变化及血AST、ALT升高的水平相关联(P＜0.05).结论 HTR2A 基因与帕利哌酮及利培酮治疗的临床疗效和安全性可能有关联.     

帕利哌酮缓释片治疗精神分裂症的疗效与安全性分析

目的探讨帕利哌酮缓释片治疗精神分裂症的疗效和安全性。方法对100名精神分裂症患者进行为期8周的帕利哌酮缓释片系统治疗,在治疗期间定期进行PANSS、TESS、CGI评定以及血常规、生化系列、心电图检查。结果帕利哌酮缓释片治疗前后PANSS、CGI评分差异有统计学意义(P<0.05)。最常见的不良反应是失眠、头痛和静坐不能。结论帕利哌酮缓释片能有效治疗精神分裂症,无严重不良反应,安全性高,服药方便。     

帕利哌酮缓释片治疗急性精神分裂症疗效及安全性的对照分析

目的探讨帕利哌酮缓释片治疗急性精神分裂症患者的临床疗效及安全性。方法 96例急性精神分裂症患者,使用随机数字表法分为观察组及对照组,各48例。观察组患者给予帕利哌酮缓释片治疗,对照组患者给予利培酮治疗,观察两组患者治疗效果,统计其不良反应发生情况。结果观察组治疗总有效率为93.8%,高于对照组的79.2%,差异有统计学意义(P<0.05)。观察组不良反应发生率为10.4%,低于对照组的27.1%,差异有统计学意义(P<0.05)。结论帕利哌酮缓释片治疗急性精神分裂症患者疗效良好,不良反应发生率低,值得推广。     

PCM1基因多态性与精神分裂症的关联分析

目的 探讨在中国汉族人群中中心粒周围物质1基因( PCM1)多态性与精神分裂症的关联性.方法 采用聚合酶链式反应-限制性片段长度多态( PCR-RFLP)方法,对100例中国汉族精神分裂症患者和100例健康对照者进行PCM1基因1个多态位点rs445422分型.结果 在病例组和对照组中,PCM1位点基因型分布均符合Hardy-Weinberg平衡.在病例组和对照组间的等位基因频率分布差异无统计学意义(P均＞0.05).结论 PCM1基因rs445422多态与中国汉族精神分裂症发病无显著相关.     

Genetic association between the polymorphism of cytosolic PLA2 gene family and schizophrenia

Abnormal phospholipid metabolism in the brain plays an important role in neuropsychiatric diseases. Phospholipase A2 (PLA2) is a crucial element for normal neuro-physiological function. This study aims to investigate the genetic association between the polymorphism of cytosolic phospholipase A2 (cPLA2) family genes and schizophrenia among Han Chinese in the northern part of China. The polymerase chain reaction-based ligase detection reaction (PCR-LDR) was applied to detect the genotype ten single nucleotide polymorphisms (SNPs) of cPLA2 family genes among 201 pedigrees consisting of fathers, mothers and affected offsprings with schizophrenia. The pedigrees were collected from 2000 to 2006. Haplotype relative risk (HRR) test, transmission disequilibrium test (TDT), haplotype transmission analysis and multiple locus analysis were conducted to analyze the genotyping data. The genotypic frequency of cPLA2 gene did not deviate from Hardy-Weinberg equilibrium either in case or control group. HRR and TDT showed that the ten SNPs were not associated with schizophrenia (P > 0.05). Analysis for haplotype transmission showed that no haplotype system was associated with schizophrenia (P > 0.05). The conditioning on allele (COA) and conditioning on gene (COG) tests showed disease associations with the haplotype of rs2162886-rs1668589, rs891014-rs1668589 and rs2307279-rs7542180 (χ² = 6.913, P = 0.032; χ² = 8.393, P = 0.015; χ²= 8.447, P = 0.038). Our data suggest that many loci in the cPLA2 family genes may be associated with schizophrenia.     

DISC1 and schizophrenia]

Molecular mechanisms underlying the pathogenesis of schizophrenia remains elusive. The difficulty in accessing the mechanisms stems from, at least in part, multiple etiologies for schizophrenia. We have studied DISC1, as it was identified as a candidate gene for a schizophrenia-associated mental condition with the single etiology. Thus far, we have obtained evidence that DISC1 may have implications in neurodevelopment. This concept fits with many historical observations found for schizophrenia in association with neurodevelopmental abnormalities. DISC1 may become one of the key molecules in studying the pathogenesis of schizophrenia.     

Possible association between the gamma-aminobutyric acid type B receptor 1 (GABBR1) gene and schizophrenia.

Schizophrenia (SCZ) is a severe neuropsychiatric disorder with a genetic component. The major inhibitory GABA-(gamma-aminobutyric acid) ergic system may be involved. The GABA type B receptor 1 (GABBR1) gene has been localized to 6p21.3, a region linked to SCZ. We therefore investigated five polymorphisms (A-7265G, C10497G, Ser-491-Ser-T1473C, Phe-659-Phe-T1977C, and 3'-UTR A33795G substitutions) in the GABBR1 gene in a sample of 101 DSM-IV SCZ probands and their families, 150 unrelated affected individuals matched with 150 healthy controls, using the transmission disequilibrium test (TDT) and case-control analysis. We did not observe biased transmission of alleles in any of the polymorphisms individually and haplotypes within the gene to SCZ probands. However, a weak significant difference was observed in the A-7265G polymorphism between the allelic frequency (chi2 = 4.310, P = 0.038) and a trend was observed between the genotype frequency (chi2 = 4.970, 2 df, P = 0.083) of SCZ individuals and controls. Further investigations of the role of GABBR1 in SCZ are warranted.     

Evidence for association between the 5' flank of the NOS1 gene and schizophrenia in the Chinese population

Nitric oxide (NO) plays an important role in the dopaminergic and serotonergic system as the second messenger of the NMDA receptor and has possible roles in neurotransmission, neurosecretion, synaptic plasticity, and tissue injury in many neurological disorders, including schizophrenia. There is also genetic evidence to support the human NOS1 (neuronal nitric oxide synthase 1) gene as a promising candidate gene associated with schizophrenia. In this paper we conducted a case-control association study involving 1705 Chinese subjects and 12 genetic markers [11 single nucleotide polymorphisms (SNPs) and 1 microsatellite] mainly in the 5' flank region of the gene by direct sequencing and capillary electrophoresis. We identified SNP rs3782206 and several haplotypes derived from it as being significantly associated with schizophrenia and, specifically, in a paranoid subgroup. Our results strongly support a previous hypothesis that NOS1 contributes to the genetic risk of schizophrenia and suggest that further research on more NOS1 variants and its regular elements are warranted.     

基因多态性与结直肠癌化疗毒性及疗效的关系

摘要： 结直肠癌是发病率和死亡率双高的一种癌症, 化疗是临床中最常用的治疗手段之一, 但不同患者对同样的化疗方案的不良反应和药物敏感性相差很大。越来越多的研究证实这种个体差异与基因多态性密切相关。目前, 基因多态性在结直肠癌靶向治疗中的研究已经普遍被人们接受, 在化疗中的研究也越来越广泛。联合化疗在结直肠癌临床治疗中效果更显著, 明确这些基因多态性位点对于结直肠癌的精准化疗及联合化疗等治疗方法具有重要的指导意义。本文对临床上结直肠癌常用的化疗药物和化疗方案相关的基因多态性及其意义做一综述。     

氨磺必利治疗精神分裂症的疗效及安全性分析

目的:探索分析应用氨磺必利治疗精神分裂症临床效果及其安全性.方法:选择我院收治的精神分裂症患者作为研究对象并进行分组治疗,对照组应用利培酮进行治疗,研究组应用氨磺必利进行治疗.将两组临床疗效进行对比.结果:治疗8周后,两组患者的卡尔加精神分裂症抑郁量表(CDSS)以及阳性阴性症状量表(PANSS)均有减分,研究组减分情况显著多于对照组(P<0.05).两组患者总有效率组间差异无统计学意义(P>0.05).两组患者治疗后EPS增分值、体重增加以及胰岛素抵抗指数增加组间不具有显著差异(P>0.05),研究组治疗后QTc、血糖以及泌乳素增加情况显著幅度显著低于对照组(P<0.05).两组患者不良反应发生率组间差异不具有统计学意义(P>0.05). 结论:应用氨磺必利治疗精神分裂症,可以产生显著的效果,尤其是对抑郁症状以及阴性症状可以产生显著的效果,不良反应发生率低,安全性高,具有推广价值.     

GULP1基因多态性与精神分裂症及其认知功能的相关性研究

目的探讨GULPl基因多态性与精神分裂症及认知功能的关系。方法采用聚合酶链反应限制性片段长度多态性（PCR—RFLP）的方法检测86例精神分裂症患者（观察组）和72名健康人（对照组）的GULPI基因SNPrs2004888多态性;采用韦氏记忆量表（WMS）和威斯康辛卡片分类测验（WCST）评估两组记忆功能和执行功能,并用PANSS量表评定患者的临床症状。观察两组GULPl基因多态性及认知功能的差异。结果两组GULPl基因SNPrs2004888多态性的基因型和等位基因频率差异有统计学意义（x2=35．71、32．21,均P〈0．05）;观察组各基因型组问韦氏记忆量表的理解记忆评分差异有统计学意义（P〈0．05）;G／G与T／T基因型患者比较,错误数、持续错误数和分类个数差异有统计学意义（P〈0．05）。结论GULPl基因SNPrs2004888多态性频度增高与精神分裂症有一定的关联,且与患者的认知功能相关。     

No evidence for an association between G protein beta3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia

OBJECTIVE: Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotic. We evaluated candidate functional polymorphism of the G protein beta3 subunit (GNB3) gene for association with drug-induced TD in the Korean schizophrenic patients. METHODS: We investigated whether the C825T polymorphism of the GNB3 gene is associated with the TD in a Korean sample of schizophrenic patients with (n = 83) and without TD (n = 126), matched for antipsychotic drug exposure and other relevant variables. RESULTS: The distribution of genotypes and allele frequencies of GNB3 were not different between schizophrenic patients with TD and without TD (p > 0.05). CONCLUSION: Within the limitations imposed by the size of the clinical sample, these findings suggest that the GNB3 825 C/T single nucleotide polymorphism (SNP) does not contribute significantly to risk for TD.