阿戈美拉汀的药理机制及临床疗效

抑郁症是一种高患病率和高致残性疾病,现有的治疗药物主要是以单胺递质系统作为靶点。阿戈美拉汀是一种新型抗抑郁药,同时具有褪黑激素能激动和5-HT2C受体拮抗作用,动物实验和临床研究均显示出明确的抗抑郁效果,并且表现出起效时间早、药物耐受性好等特点,成为抗抑郁治疗的新选择。本综述总结了阿戈美拉汀的药理作用和临床疗效,希望有助于临床实践者更清楚认知该药,合理使用。     

支气管哮喘与急性呼吸道感染患儿血浆β防御素3水平的对照研究

目的β防御素3(HBD3)除了具有天然免疫功能,还发挥调节后天适应性免疫的作用。本研究拟通过支气管哮喘患儿、急性上呼吸道感染患儿及正常儿血浆HBD3浓度的比较,探讨HBD3在哮喘发病中的作用。方法研究对象选择2009年4月到12月在哈尔滨医科大学附属第一医院儿科就诊病例共81例,其中哮喘组21例,为急性发作期支气管哮喘患儿,感染组29例,为急性上呼吸道感染患儿,正常对照组31例,为健康体检儿。采用酶联免疫吸附试验(ELISA)法进行血浆HBD3水平测定。同时测定血嗜酸性粒细胞总数和白细胞数,9例哮喘儿测定了血清IgE浓度。结果血浆HBD3浓度正常儿为(8.028±1.078)μg/ml,哮喘患儿(12.212±1.124)μg/ml感染患儿(8.976±1.110)μg/ml,哮喘患儿与急性呼吸道感染及正常儿3组总体比较,血浆HBD3浓度明显升高,差异有显著性(F=4.448,P<0.05);哮喘组与正常组比较,差异显著,P<0.01;哮喘组与感染组比较,差异有显著性P<0.05;感染组与正常组比较,差异无显著性P>0.05;同时发现血浆HBD3水平与血清总IgE,血嗜酸性粒细胞及白细胞水平无显著相关性。结论支气管哮喘发作时HBD3表达升高,HBD3可能是超越感染之外,参与哮喘发病的独立因素。HBD3是否始动因素尚待进一步探索。     

2371例孕妇产前诊断的指证及其结果分析

目的分析产前诊断指证与胎儿染色体检测结果的关系。方法 2371例有产前诊断指证的孕妇,进行羊膜腔穿刺或脐静脉穿刺术,取羊水细胞或脐血细胞培养,作胎儿染色体核型分析。结果 2371例孕妇共检出胎儿染色体异常60例,染色体异常率为2.53%,显著高于一般人群的异常率（P〈0.01）。其中孕母血清唐氏筛查阳性组和高龄孕妇组的异常率分别为1.63%（13/794）、2.32%（15/646）,产前胎儿超声异常标记组胎儿染色体异常率16.12%（15/93）,夫妇一方为染色体平衡易位携带者组的胎儿染色体异常率达71.4%（5/7）,21-三体儿检出25例,占异常率的41.67%（25/60）,其中一例连续两次诊断出21-三体儿。结论出现胎儿染色体异常率最高的指证,依次为平衡易位携带、产前超声发现胎儿异常标记、高龄孕妇、孕母血清唐氏筛查阳性。掌握好产前诊断指证,可更有价值地控制和减少出生缺陷的发生。     

职业中专生自我同一性与自我概念的相关研究

目的:探讨职业中专生自我同一性和自我概念之间的关系,并与普高生进行比较。方法:采用自我同一性状态问卷、田纳西自我概念量表对300名职专生和100名普高生进行调查。结果:①职专生自我同一性的意识早闭、总体早闭的得分显著高于普高生;②职专生的家庭自我得分显著低于普高生;③职专生的自我同一性和自我概念的总分间存在显著正相关。意识扩散、人际扩散与自我批评显著正相关;意识获得与道德自我显著正相关;人际获得与自我满意、自我概念总分间显著正相关;总体获得与道德自我、家庭自我和自我满意显著正相关;同一性总分与道德自我、家庭自我、社会自我和自我满意显著正相关。结论:职专生的自我同一性和自我概念关系密切,同一性获得有利于建构积极的自我概念,自我概念越积极亦越有利于同一性获得。     

微生物药物研究进展与发展趋势

微生物药物作为广泛使用的临床药物具有重要的地位,尤其是在抗感染、抗肿瘤、降血脂和抗器官移植排异方面具有不可替代的作用。     

趋化因子及其受体CXCL16/CXCR6在人肺癌转移中的作用

目的 探讨CXCL16/CXCR6在肺癌的表达模式及其对肺癌细胞系生物学行为的影响.方法 免疫组织化学技术分析CXCL16/CXCR6蛋白在人肺癌组织的表达;免疫细胞化学分析CXCL16/CXCR6在3种肺癌细胞系A549、95D和H292的表达;MTT试验及迁移、侵袭试验分别分析CXCL16时A549、95D和H292细胞体外增殖活力和侵袭能力的调节作用.结果 人肺癌组织高表达CXCR6和CXCL16蛋白;A549、95D和H292细胞均表达CXCL16和CXCR6蛋白;外源性CXCL16可明显促进A549、95D和H292细胞的体外增殖活力和侵袭能力,且CXCL16中和抗体可以有效阻断CXCL16蛋白对3种肺癌细胞系的刺激作用.结论 CXCL16/CXCR6可能是参与肺癌侵袭转移的分子.     

肠道病毒71型山东临沂分离株全基因组序列分析

目的 自1例死亡患儿的标本中分离EV71,并分析其全基因组序列特点,研究其基因序列的改变是否与其神经毒力有关.方法 咽拭子标本采自山东临沂市人民医院1例死亡患儿,在人横纹肌瘤细胞(RD)上分离EV71,分段扩增获得EV71的全序列,用BLAST、Bioedit和MEGA 4进行序列分析.结果 获得1株EV71分离株SDLY107,基因组全长7405 bp,全基因组核苷酸序列与2008年的阜阳株Fuyang.Anhui.P.R.C/17.08/2同源性最高,为98.6%,与原型株BrCr/70的同源性为80.0%,与神经毒型株MS/87的同源性为86.5%.系统进化分析表明,SDLY107与中国大陆的北京株、河南株、广西株、深圳株、兰州株、阜阳株、重庆株、浙江株的亲缘关系较近,按照传统的VP1基因分型方法,可归为C4亚型,是近年来我国大陆流行的主要基因亚型.氨基酸序列分析发现,SDLY107与其他毒株相比,有2个特有的突变(E947D,K1873R).结论 SDLY107分离株属于C4亚型,氨基酸突变E947D和K1873R可能与EV71的致病性有关.

Abstract：

Objective To isolate enterovirus 71 from a death children,and analyze whether the neurovirulence was related to the variation of nucleotide and amino acid. Methods Enterovirus 71 was isolated from throat swabs which were colleted from Shandong Linyi People's Hospital. The full length genome was sequenced by amplification with RT-PCR and sequencing of 9 overlapped gene fragments covering full length of the genomes. The nucleotide and amino acid sequenced was aligned by BLAST, Bioedit and MEGA 4. Results A strain of enterovirus 71 was isolated and named as SDLY107. The full length was 7405 bp. The results of homology analysis of overall nucleotide sequence showed that strain Fuyang. Anhui. P. R. C/17.08/2 had highest homology (98.6%)with strain SDLY107, and the homology was 80.0% between strain SDLY107 with prototype strain BrCr/70,and 86. 5% between strain SDLY107 with nerve strain MS/87. Phylogenetic analysis showed that the phylogeny was close between SDLY107 with some isolated strains from Chinese Mainland, such as Beijing, Henan, Guangxi, Sbenzhen, Lanzhou, Fuyang, Chongqing and Zhejiang strains, which was clustered for C4 subtype. The results of amino acid sequence analysis showed that there were 2 mutations, E947D and K1873R, for strain SDLY107. Conclusion SDLY107 belonged to C4 subtype, amino acid mutations E947D and K1873R of which may be relevant to the pathogenicity of EV71.     

Dyna CT与Embolization Guidance技术在前列腺动脉栓塞中的应用

目的探讨Dyna CT与Embolization Guidance技术在前列腺动脉栓塞中的应用。方法收集我科使用SIEMENS Artis Zeego数字减影血管造影机检查和图像采集进行前列腺动脉栓塞的38例患者,用Dyna CT技术明确前列腺癌供血动脉与其他侧支的情况,Embolization Guidance技术指导进行安全性的前列腺癌供血动脉栓塞。结果 38例患者经两名高年资主任医师指导分别进行前列腺癌动脉栓塞术。Dyna CT联合DSA确认前列腺动脉65侧,比例达85.5%(65/76),其中24例患者显示双侧前列腺动脉,10例确认单侧前列腺动脉;前列腺动脉开口起源于髂内动脉38条,起源于闭孔动脉11条,起源于膀胱下动脉9条,起源于阴部内动脉5条,起源于直肠下动脉2条。利用Embolization Guidance技术完成前列腺动脉栓塞89.2%(58/65),其中24例患者完成双侧栓塞,10例完成单侧栓塞,4例因血管迂曲不能进行超选择栓塞。结论 Dyna CT联合Embolization Guidance技术能够准确地显示前列腺优势供血动脉,在前列腺动脉栓塞治疗中具有重要的应用价值。     

Breakpoint characterization of a novel ～59?kb genomic deletion on 19q13.42 in autosomal-dominant retinitis pigmentosa with incomplete penetrance

The aim of this study was to identify and characterize the underlying molecular mechanisms in autosomal-dominant retinitis pigmentosa (adRP) with incomplete penetrance in two Swedish families. An extended genealogical study and haplotype analysis indicated a common origin. Mutation identification was carried out by multiplex ligation-dependent probe amplification (MLPA) and sequencing. Clinical examinations of adRP families including electroretinography revealed obligate gene carriers without abnormalities, which indicated incomplete penetrance. Linkage analysis resulted in mapping of the disease locus to 19q13.42 (RP11). Sequence analyses did not reveal any mutations segregating with the disease in eight genes including PRPF31. Subsequent MLPA detected a large genomic deletion of 11 exons in the PRPF31 gene and, additionally, three genes upstream of the PRPF31. Breakpoints occurred in intron 11 of PRPF31 and in LOC441864, ‘similar to osteoclast-associated receptor isoform 5.'' An almost 59 kb deletion segregated with the disease in all affected individuals and was present in several asymptomatic family members but not in 20 simplex RP cases or 94 healthy controls tested by allele-specific PCR. A large genomic deletion resulting in almost entire loss of PRPF31 and three additional genes identified as the cause of adRP in two Swedish families provide an additional evidence that mechanism of the disease evolvement is haploinsufficiency. Identification of the deletion breakpoints allowed development of a simple tool for molecular testing of this genetic subtype of adRP.