构建中国男性青少年人体静态平衡能力的软件评价平台

以目前平衡能力测试技术、计算机软件编程为平台,构建适合中国男性少年平衡能力的评价体系及配套软件的平台。分别运用因子分析、探索性分析、离差评分等数理统计方法对测试数据进行统计学分析,建立14~18岁男性少年平衡能力评级体系。运用VC++6.0和VC++2005等计算机技术,解决从信息提取、指标细化、分析处理、模块构建、多目标参数融合等一系列关键问题。少年期静态平衡能力评价系统,让人体平衡能力的评价更加方便、更加快捷。     

Association study of EP1 gene polymorphisms with suicide completers in the Japanese population

Background

Both environmental and genetic factors have been reported to be involved in suicidal behaviors. Considerable evidence indicates that impulsive aggression is one of the important risk factors that contribute to suicide. A recent study has shown that prostaglandin E2 type 1 receptor (EP1) signaling regulates impulsive-aggressive behaviors in mice under both social and environmental stresses. To test the possible involvement of the EP1 gene in suicide, we carried out an association study of EP1 gene polymorphisms with suicide completers in the Japanese population.

Methods

We studied 5 SNPs including one SNP in exon 2 (rs3745459) and four SNPs in the potential promoter region of the EP1 gene (rs3810255, rs3810254, rs3810253 and rs10416814) in 374 healthy control and 287 completed suicide victims using standard Taqman probe genotyping assays.

Results

No significant differences of the genotypic distribution, allelic frequency or haplotype distribution between controls and suicide completers were found. Gender based analysis revealed that genotypic, allelic and haplotypic distributions of rs3810255, rs3810254, rs3810253 and rs10416814 SNPs were significantly different between the female control and female suicide groups, although the differences did not withstand correction for multiple comparisons.

Conclusion

We could not find an association of EP1 gene with suicide in the Japanese population. Because several SNPs in the promoter region of the EP1 gene were nominally significantly associated with suicide in the female, further studies with a larger sample size and different population are needed to confirm this result.     

Cerebrovascular hemodynamics in patients with cerebral arteriosclerosis

The present study observed hemodynamic changes in 26 patients with cerebral arteriosclerosis using a cerebral circulation dynamics detector and transcranial Doppler. In patients with cerebral arteriosclerosis the blood supply and flow rate in the bilateral carotid arteries and the blood flow rate in the anterior cerebral and middle cerebral arteries were similar to normal controls, but the cerebral vascular resistance, critical pressure and pulsatility index were increased, and cerebral arterial elasticity and cerebral blood flow autoregulation were decreased. Compared with the le-sioned hemisphere of patients with cerebral infarction, the total blood supply and blood flow rate of patients with cerebral arteriosclerosis were higher. Compared with normal subjects, patients with cerebral arteriosclerosis exhibited cognitive disturbances, mainly in short-term memory, attention, abstract capability, and spatial and executive dysfunction. Results showed that cerebral arteriosclerosis does not directly affect the blood supply of a cerebral hemisphere, but affects cognitive function. The increased cerebral vascular resistance and reduced autoregulation of cerebral blood vessels may be important hemodynamic mechanisms of arteriosclerosis-induced cerebral infarction.     

5-羟色胺2A受体T102C基因多态性与卒中后抑郁的关联研究

目的 探讨5-羟色胺(5-HT)2A受体T102C基因多态性与卒中后抑郁(PSD)的关系,研究PSD的遗传发病机制.方法 选择珠江医院神经内科自2010年1月至2010年12月收治的汉族住院患者为研究对象,根据有无并发抑郁症将其分为PSD组(97例)及单纯卒中组(72例).采用PCR和限制性片断长度多态性(RFLP)技术测定2组患者5-HT2A受体T102C等位基因频率及基因型.结果 PSD组中突变型C等位基因频率(43.3％)低于单纯脑卒中组(59.0％),突变纯合子C/C基因型频率(20.6％)也低于单纯卒中组(34.7％),差异均有统计学意义(x2=0.179,P=0.004;x2=7.855,P=0.020).结论 5-HT2A受体T102C基因可能是PSD的易感基因,C等位基因是罹患PSD的保护因子.     

巴曲酶可影响人外周血内皮祖细胞定向分化及增殖能力

背景：近年来内皮祖细胞促进机体血管新生方面的重要作用已形成共识,但内皮祖细胞的定向分化和扩增的问题是影响其疗效和广泛开展的主要原因。 目的：观察人外周血内皮祖细胞体外分离、纯化、扩增和诱导分化为内皮细胞的可行性。 方法：用密度梯度离心法从外周血获取单个核细胞,接种于包被有人纤维连接蛋白的细胞培养板中,培养6 d后,收集贴壁细胞。以血管内皮细胞生长因子和碱性成纤维细胞生长因子对贴壁细胞进行诱导培养。另外,分别以0.05,0.1,0.2 BU/mL巴曲酶培养贴壁细胞,观察内皮祖细胞的增殖能力。 结果与结论：经血管内皮细胞生长因子和碱性成纤维细胞生长因子诱导后的细胞形态上表现内皮细胞特征,经流式细胞仪测定表达血管内皮细胞特有表面标志CD31和vWF,说明诱导后的细胞为内皮细胞。巴曲酶在体外培养条件下可增加血内皮祖细胞的数量,以0.1 BU/mL浓度作用显著,且作用时间与血内皮祖细胞增殖能力的改善呈正相关。     

穿孔素基因及蛋白功能研究进展

背景：穿孔素颗粒酶是细胞毒性细胞杀伤靶细胞重要途径之一,近年来发现很多淋巴系统增殖性疾病与穿孔素基因突变有关。目的：综述了穿孔素基因的研究进展,阐述其基因突变与蛋白表达的关系,进而探讨其与淋巴细胞增殖病发病的关系。方法：应用计算机检索CNKI和PubMed数据库中1998-01/2008-12关于细菌生物膜耐药机制的文章,在标题和摘要中以“穿孔素;基因;突变;白血病;淋巴瘤”或“perforin; gene; mutation;lymphoproliferative disease”为检索词进行检索。选择文章内容与穿孔素基因突变相关,同一领域文献则选择近期发表或发表在权威杂志文章。初检得到285篇文献,根据纳入标准选择65篇文章进行综述。 结果与结论：穿孔素基因突变,相应的引起穿孔素蛋白表达的缺失、减低或活性下降,结果机体对肿瘤细胞和病毒感染细胞的杀伤清除能力减弱,可能导致淋巴系统异常增生甚至发生肿瘤,对于穿孔素基因突变与蛋白表达的深入研究,有助于阐明其与淋巴细胞增殖病的关系。     

多巴反应性肌张力障碍患者的GCH1基因突变检测

目的分析多巴反应性肌张力障碍(dopa responsive dystonia,DRD)患者的GCH1基因突变。方法我们抽取21例来自医院门诊及住院的散发型多巴反应性肌张力障碍患者的肘静脉血,并提取外周血全基因组DNA。Primer3设计GCH1基因6个外显子的引物,PCR扩增GCH1基因的外显子及周边部分内含子序列,并对PCR产物进行测序。测序结果与正常序列进行比对,发现碱基变异后进行序列分析以确定是否多态。结果成功扩增21位DRD患者GCH1基因的6个外显子。经过分析,GCH1基因外显子序列未发现基因突变。仅在4个患者的1号外显子发现1个单核苷酸多态(SNP)c.68CT,该SNP没有产生氨基酸的改变。结论本地区多巴反应性肌张力障碍患者未发现GCH1基因突变,DRD患者可能存在其他致病基因。GCH1基因突变检测目前仍不能作为早期诊断的依据。     

Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury

In the present study, human umbilical cord blood mesenchymal stem cells were injected into a rat model of traumatic brain injury via the tail vein. Results showed that 5-bromodeoxyuridine-labeled cells aggregated around the injury site, surviving up to 4 weeks post-transplantation. In addition, transplantation-related death did not occur, and neurological functions significantly improved. Histological detection revealed attenuated pathological injury in rat brain tissues following human umbilical cord blood mesenchymal stem cell transplantation. In addition, the number of apoptotic cells decreased. Immunohistochemistry and in situ hybridization showed increased expression of brain-derived neurotrophic factor, nerve growth factor, basic fibroblast growth factor, and vascular endothelial growth factor, along with increased microvessel density in surrounding areas of brain injury. Results demonstrated migration of transplanted human umbilical cord blood mesenchymal stem cells into the lesioned boundary zone of rats, as well as increased angiogenesis and expression of related neurotrophic factors in the lesioned boundary zone.     

Involvement of p38/NF-κB signaling pathway in the nucleus accumbens in the rewarding effects of morphine in rats

The nucleus accumbens (NAc) is one of the important brain regions for the acquisition of morphine-induced conditioned place preference (CPP), which is a valuable paradigm for detecting the rewarding effects of drugs. However, the underlying molecular mechanisms remain largely unknown. In the present study, we investigated the role of p38 and nuclear factor kappa B (NF-κB) in the NAc in the acquisition of morphine-induced CPP. The results showed that repeated morphine treatment induced the acquisition of CPP and increased the phosphorylation of p38, IκB-α and NF-κB p65 in the NAc. Microinjection of p38 inhibitor SB203580 into the NAc prior to the application of morphine prevented the acquisition of CPP and inhibited the activation of p38, IκB-α and NF-κB p65. Furthermore, pre-infusion of pyrrolidine dithiocarbamate (PDTC), a selective NF-κB inhibitor, into the NAc blocked the CPP but also the phosphorylation of NF-κB p65 induced by morphine. It is concluded that the activation of p38/NF-κB p65 signaling pathway in the NAc plays a critical role in the morphine CPP.