心理行为疗法与兴趣激励在儿童弱视治疗中的作用

目的:采用心理行为疗法中正强化疗法与兴趣激励结合治疗儿童弱视,并观察其效果。方法:①选择2000-01/2003-06在开封市儿童医院眼科门诊就诊的弱视患儿172例(287眼)。患者及家长知情同意。随机分为2组:对照组87例(141眼);心理干预组85例(146眼)。②对照组采用眼科常用的综合疗法(戴镜+遮盖+红光闪烁及精细作业训练,1次/d,15min/次);心理干预组在常用综合治疗基础上增加心理行为治疗中的正强化疗法及兴趣激励,及时奖赏孩子不同分级的奖品或出游活动,激发弱视儿童的内在合作动机以提高其顺应性。③观察两组患儿视力变化,每3个月复查、验光1次,进行疗效比较。无效为视力退步、不变或提高0.1;有效为视力增长0.2或0.2以上;显著有效为视力提高达≥0.9。有效率=显著有效+有效例数/该组总例数。④计数资料差异性测定采用χ2检验。结果:弱视患儿172例(287眼)均进入结果分析。干预有效率:两组随干预时间延长而增高。干预3个月时,对照组与心理干预组相近(46.1%,49.3%,P>0.05);但干预6和9及12个月时心理干预组明显高于对照组(71.3%,78.8%,83.5%;55.3%,59.6%,64.5%,χ2=7.83,12.43,13.56,P<0.01)。结论:将适合儿童心理特点的心理行为治疗法中的正强化方法与儿童兴趣激励结合起来,可更有效提高对弱视患儿视力水平的治疗效果。     

转化生长因子β1诱导骨髓间充质干细胞体外构建纤维蛋白胶软骨模块

目的:观察体外构建骨髓间充质干细胞、改良纤维蛋白胶及生长因子的组织工程软骨模块的可行性。方法:实验于2004-07/12在南方医科大学附属珠江医院中心实验室进行。选取新西兰兔10只,密度梯度法分离培养兔骨髓间充质干细胞,在培养系统中加入生长因子(含10μg/L转化生长因子β1,100mol/L地塞米松,50mg/L维生素C,以及1%ITS-A。培养第2,4,6,8天采用四甲基偶氮噻唑法在酶标仪上检测吸光度值表示细胞增殖。于培养7,14d行细胞爬片甲苯胺蓝染色及Ⅱ胶原免疫组化。诱导后骨髓间充质干细胞种植于改良纤维蛋白胶支架上,加入生长因子诱导培养,于培养7,14,21d行形态组织学及透射电镜检查。结果:实验兔10只均进入实验结果分析。①四甲基偶氮噻唑法测定培养第6和8天后,实验组骨髓间充质干细胞增殖的吸收度值高于对照组(实验组:0.4554±0.0206,0.5348±0.0169;对照组:0.4270±0.0255,0.5057±0.0368,P<0.05)。②细胞爬片甲苯胺蓝染色细胞周围有蓝色基质。Ⅱ型胶原免疫组化染色阳性。③诱导后骨髓间充质干细胞在改良纤维蛋白胶支架中培养,Masson染色可见胞浆及细胞周围有胶原的形成;Ⅱ型胶原免疫组化染色阳性。透射电镜可见细胞代谢旺盛。结论:骨髓间充质干细胞、改良纤维蛋白胶及生长因子的组织工程模块体外培养系统中,改良纤维蛋白胶支架相容性好,转化生长因子β等生长因子促进骨髓间充质干细胞在改良纤维蛋白胶支架增殖,诱导分化成软骨细胞表型。     

心理护理对骨肉瘤患者术后生活质量的影响

目的 观察心理护理对骨肉瘤患者手术后生活质量的影响.方法 60例骨肉瘤患者手术后随机分为观察组和对照组,各30例.观察组化疗同时进行心理护理,对照组化疗,无心理护理.2组患者长期随访生存情况、生活质量(参照Karufsky计分评定).结果 观察组生存5年者20例,生存率66.7%,对照组生存5年者14例,生存率46.7%,2组5年生存率有显著性差异(χ2=4.04,P＜0.05).Karuafsky计分:观察组优于对照组,2组有显著性差异(χ2=4.01,P＜0.05).结论 心理护理对骨肉瘤患者生存率及生活质量有较好的改善作用.     

皮-肌反射客观评估穴位按摩法干预痉挛型小儿脑性瘫痪的效果

目的:应用皮-肌反射评估经穴位按摩法对痉挛型小儿脑性瘫痪(简称脑瘫)患儿的治疗效果。方法:选择2000-10/2003-08黑龙江省小儿脑瘫防治疗育中心收治的痉挛型脑瘫患儿50例;男32例,女18例;患儿监护人均同意参加本研究。采用兴奋和抑制性方法对50例痉挛型脑瘫患儿进行穴位按摩,同时采用诱发电位仪进行皮-肌反射的测定,所用主要参数为短潜伏期下降波、长潜伏期上升波和中枢延迟波。在姿势、运动、反射、肌张力四大指标中有一项以上实质进步者为显效。脑瘫症状和体征减轻为有效。临床症状和体征与入院时对比无变化为无效。结果:按意向处理分析,进入结果分析患儿50例。根据疗效将患儿分为显效组20例,有效组26例与无效组4例。有效率92%(46/50)。①显效组:治疗后短潜伏期下降波、长潜伏期上升波波长明显短于治疗前(30.27±2.20),(43.42±3.57),(14.56±2.53)ms;(35.41±1.53),(48.78±3.54),(20.16±3.30)ms,t=3.02,2.94,3.08,P<0.01。②有效组:治疗后短潜伏期下降波、长潜伏期上升波和中枢延迟波波长明显短于治疗前(31.91±3.33),(41.36±2.50),(18.46±1.80)ms;(35.73±3.11),(43.80±3.73),(21.13±2.38)ms,t=2.52,2.64,2.78,P<0.05。结论:经穴位按摩治疗痉挛型脑瘫效果确实,临床效果可经皮-肌反射客观评定证     

ATP binding cassette G8 T400K polymorphism may affect the risk of gallstone disease among Chinese males

BACKGROUND: Supersaturation of bile with cholesterol is a primary step in the formation of cholesterol gallstones. ATP binding cassette (ABC) G5 and G8 play an important role in regulating sterol absorption and secretion. To investigate a possible association between transporter gene polymorphism and gallstone formation, we examined five common polymorphisms in the ABCG5 (Q604E) and ABCG8 (D19H, Y54C, T400K, A632V) genes in patients with gallstone disease (GS). METHODS: Study subjects included 287 patients with GS and 219 gallstone free controls (GSF). Polymorphisms were determined using PCR-RFLP analysis or the Taqman MGB assay. Plasma and biliary lipid levels were measured. RESULTS: 2 SNPs of ABCG8 gene (Y54C and T400K) showed strong linkage disequilibrium (D'=0.824, r2=0.579). Male carriers of the less frequent K allele of ABCG8 T400K had a 2.31-fold elevated risk [95% confidence interval (CI) 1.12 approximately 4.76, P=0.023] for gallstone disease compared to male with the common genotype after the adjustment for age, body mass index. Males with the K allele had lower plasma triglyceride (P=0.044) and biliary phospholipid (P=0.035) levels than TT homozygotes. No such association was found in female or other 4 SNPs. CONCLUSIONS: These findings indicate that the T400K polymorphism in ABCG8 may be associated with the incidence of gallstone disease in males.     

Systematic Prioritization and Integrative Analysis of Copy Number Variations in Schizophrenia Reveal Key Schizophrenia Susceptibility Genes

Schizophrenia is a common mental disorder with high heritability and strong genetic heterogeneity. Common disease-common variants hypothesis predicts that schizophrenia is attributable in part to common genetic variants. However, recent studies have clearly demonstrated that copy number variations (CNVs) also play pivotal roles in schizophrenia susceptibility and explain a proportion of missing heritability. Though numerous CNVs have been identified, many of the regions affected by CNVs show poor overlapping among different studies, and it is not known whether the genes disrupted by CNVs contribute to the risk of schizophrenia. By using cumulative scoring, we systematically prioritized the genes affected by CNVs in schizophrenia. We identified 8 top genes that are frequently disrupted by CNVs, including NRXN1, CHRNA7, BCL9, CYFIP1, GJA8, NDE1, SNAP29, and GJA5. Integration of genes affected by CNVs with known schizophrenia susceptibility genes (from previous genetic linkage and association studies) reveals that many genes disrupted by CNVs are also associated with schizophrenia. Further protein-protein interaction (PPI) analysis indicates that protein products of genes affected by CNVs frequently interact with known schizophrenia-associated proteins. Finally, systematic integration of CNVs prioritization data with genetic association and PPI data identifies key schizophrenia candidate genes. Our results provide a global overview of genes impacted by CNVs in schizophrenia and reveal a densely interconnected molecular network of de novo CNVs in schizophrenia. Though the prioritized top genes represent promising schizophrenia risk genes, further work with different prioritization methods and independent samples is needed to confirm these findings. Nevertheless, the identified key candidate genes may have important roles in the pathogenesis of schizophrenia, and further functional characterization of these genes may provide pivotal targets for future therapeutics and diagnostics.Key words: schizophrenia, copy number variation, prioritization, integrative analysis, NRXN1, CHRNA7     

运动与原发性骨疏松

目的原发性骨质疏松指绝经期后骨质疏松和老年性骨质疏松.绝经期后骨质疏松的发生与妇女雌激素水平迅速下降有关.老年性骨质疏松的发生与整体功能下降、运动减少、营养代谢功能下降等有关.探述运动与原发性骨质疏松的关系. 方法论述了运动减少对骨的影响、骨的力学特性、骨的压电效应、运动与骨质疏松发生的关系. 结果力学刺激的减少,可增加骨质吸收,减少骨形成,造成骨量减少.运动员荷可以使疏松骨骼骨量增加. 结论原发性骨质疏松的发生与该类患者骨运动减少有关,而适当的运动训练可以预防和治疗骨质疏松.