白细胞介素-10启动子基因多态性与缺血性卒中相关性的Meta分析

目的 系统评价IL-10启动子基因（IL-10-1082A/G、IL-10-819T/C ）多态性与缺血性卒中（i s chemi c stroke,IS）发病风险的相关性。 方法 计算机检索Pubmed、Embase、Web of Science、万方数据库及中国知网数据库发表的有关IL-10启 动子基因多态性与IS发病风险相关性的研究,检索时限为从建库至2019年2月,由2名评价者按照纳入 与排除标准选择研究、提取资料。采用RevMan 5.3软件进行荟萃分析。 结果 共纳入13篇病例对照研究,其中12篇文献研究了IL-10-1082A/G 基因多态性与I S的易感性,6 篇文献研究了IL-10-819T/C 基因多态性与I S的易感性。结果显示,在总体人群中,IL-10-1082A/G基因多 态性与I S发病风险之间存在相关性（G vs A：OR 0.71,95%CI 0.59～0.86,P＜0.001;GG vs AA：OR 0.61, 95%CI 0.49～0.76,P＜0.001;AG vs AA：OR 0.72,95%CI 0.55～0.94,P =0.020;GG+AG vs AA：OR 0.68, 95%CI 0.53～0.87,P =0.002;GG vs AG+AA：OR 0.68,95%CI 0.52～0.89,P =0.005）;而IL-10-819T/C 基因多态性与IS发病风险无明显相关性（P＞0.05）。对中国人群进行亚组分析后,Meta分析结果与总 体人群一致。 结论 IL-10-1082A/G基因的多态性与IS风险显著相关,该基因是卒中易感基因;而IL-10-819T/C基因 多态性与IS的发病风险无明显关联。     

CTLA-4+49A/G多态性与多发性硬化相关性的meta分析

目的探讨CTLA-4+49A/G多态性与多发性硬化(MS)的相关性。方法通过检索PubMed数据库收集有关CTLA-4+49A/G多态性与MS相关的病例-对照研究,文献检索时间从建库至2013-09期间。采用RevMan 4.2统计软件对其结果进行分析。结果共纳入25个以高加索和亚洲人群为研究对象的MS病例对照研究,包括高加索MS患者4663例和高加索健康对照4249例,亚洲MS患者563例和亚洲健康对照667例。各研究的等位基因和基因型频数结果未见明显发表偏倚。25个研究合并后,G/A、GG+GA/AA、GG/GA+AA合并的OR值分别为1.00(95%CI为0.96~1.06,P=0.91)、1.01(95%CI为0.93~1.10,P=0.73)、0.99(95%CI为0.88~1.10,P=0.81)。高加索人群的研究合并后,G/A、GG+GA/AA、GG/GA+AA合并的OR值分别为1.00(95%CI为0.94~1.06,P=0.99)、0.99(95%CI为0.91~1.08,P=0.85)、1.01(95%CI为0.90~1.14,P=0.83)。亚洲人群的研究合并后,G/A、GG+GA/AA、GG/GA+AA合并的OR值分别为1.03(95%CI为0.87~1.22,P=0.73)、1.22(95%CI为0.95~1.57,P=0.12)、0.83(95%CI为0.61~1.12,P=0.22)。结论 CTLA-4+49A/G多态性与MS无相关性。     

中国汉族人群PARK16基因多态性与帕金森病易患性的关联

目的 探讨PARK16基因单核苷酸多态性(SNP)与帕金森病(PD)易患性的关系,分析其SNP的基因型和等位基因频率及不同基因型的优势比(OR)和其临床特征.方法 采用病例-对照研究选择PD患者226例和362名健康对照,利用TaqMan荧光定量PCR方法检测中国汉族人群中PARKl6基因Rs947211和Rs823128基因多态性,并对不同基因型临床资料进行分析.结果 PARKl6基因的多态性位点Rs947211在PD组基因型频率为∶GG 34.1%(77/226)、AG 46.0%(104/226)、AA 19.9%(45/226),对照组分别为23.8%(86/362)、53.0%(192/362)、23.2%(84/362),2组基因型频率差异具有统计学意义(以野生型GG为参考,AG∶OR=0.57,95%CI 0.38～0.85,P=0.006;AA∶OR=0.55.95%CI,0.34～0.85,P=0.015).以PD组野生型GG为参照,暴露于A等位基因型(AA+AG)的OR=0.56,95%CI0.38～0.82,P=0.003.晚发型PD(LOPD)Rs947211的基因型频率与对照组比较差异亦有统计学意义(AG∶OR=0.46,95%C/0.27～0.78,P=0.004∶AA∶OR=0.35,95%C/0.18～0.68,P=0.002).PD组3种基因型在临床表现上差异没有统计学意义.Rs823128在PD组基因型频率分布与对照组差异无统计学意义(以野生型AA为参照,AG∶OR=1.12,95%CI0.75～1.68,P=0.568;GG∶OR=0.99,95%CI0.35～2.76,P=0.994).结论 中国汉族人群中PARK16基因与PD易患性相关.

Abstract：

Objective To investigate the association between PARK16 gene polymorphism and Parkinson's disease(PD)susceptibility in Chinese Han population.and to analyze its single-nucleotide polymorphism(SNP)genotypes,frequencies and odds ratios(OR)of different genotypes.Methods The association between two SNP loci in PARK16 gene(Rs947211,Rs823128)and PD susceptibility was investigated by TaqMan quantitative polymerase chain reaction(PCR)in 226 PD patients and 362 healthy controls.Allele and genotype frequencies were calculated by the Chi-square test,and the clinical data were also analyzed.Results Three genotypes of Rs947211(GG,AG and AA)account for 34.1%(77/226),46.0%(104/226),19.9%(45/226)in the PD group,and 23.8%(86/362),53.0%(192/362),23.2%(84/362)in the control group,respectively.There was significant difference between two groups (P<0.05).Setting the GG genotype as the reference,OR values of AG and AA genotype were 0.57(95%CI0.38-0.85,P=0.006)and 0.55(95%CI 0.34-0.85,P=0.015),while the OR value for exposure to the A allele(AA+AG)was 0.56(95%CI0.38-0.82,P=0.003).Genotypes of Iate-onset PD were also significantly different from the controls(OR valne of AG=0.46,95%CI 0.27-0.78,P=0.004:OR value of AA=0.35.95%CI 0.18-0.68,P=0.002).And there was no diffefence in clinical features among the 3 genotypes. The frequency of Rs823128, another locus, in PD group was not significantly different from the control group( AA genotype as the reference, OR value of AG was 1. 12, 95% CI 0. 75-1.68, P = 0.568; OR value of GG was 0.99, 95% CI 0.35-2.76, P = 0.994). Conclusion Polymorphism of PARK 16 locus Rs947211 is associated with PD patients in Chinese Han population.     

PON3Ala99Ala基因多态性与散发性肌萎缩侧索硬化易感性关联研究

目的 探讨散发性肌萎缩侧索硬化(sALS)发病是否与对氧磷酶3 (PON3) Ala99Ala基因多态性相关。方法 应用聚合酶链式反应-限制性酶切片段长度多态性(PCR-RFLP)对117例健康对照和108例sALS患者进行PON3Ala99Ala基因多态性分析。结果 本研究中病例组与健康对照组人群PON3Ala99Ala基因多态性符合Hardy-Weinberg遗传平衡定律,具有代表性。sALS组与对照组之间PON3Ala99Ala基因的三种基因型分布比较无差异(P=0.157)。PON3Ala99Ala基因A和G等位基因分布在对照组、sALS组中进行组间比较,差异无统计学意义(P=0.257)。与AA基因型比较,AG基因型、GG基因型和AG+GG基因型均不增加患sALS的风险(分别为OR=1.68,95%CI=0.95～2.98;OR=0.63,95%CI=0.11～3.54;OR=1.55,95%CI=0.89～2.71)。结论 PON3Ala99Ala基因多态性不增加sALS发病易感性。     

三磷酸腺苷结合盒转运子A1基因多态性与散发性阿尔茨海默病的关系

目的 探讨三磷酸腺苷结合盒转运子A1（ATP—binding cassette transporter 1，ABCA1）基因第6外显子D→A（R219K）多态性位点与散发性阿尔茨海默病（sporadic Alzheimer disease，SAD）易患性的关系。方法 采用病例．对照研究方法，利用聚合酶链反应．限制性片段长度多态性（PCR—RFLP）技术对168例SAD患者和215名健康对照的ABCA1基因多态性进行检测，比较不同基因型与阿尔茨海默病（AD）发病风险之间的关系。结果 SAD组ABCA1基因第6外显子G—A多态位点A等位基因频率明显低于对照组（37．8％ vs 48．1％，）（X^2=8．204，P=0．004）；SAD组AA基因型频率也明显低于对照组（14．3％ vs 22．8％，）（X^2=8．230，P=0．016）。Logistic回归分析表明，校正年龄、性别和ApoEe4等位基因的影响后，携带A等位基因者（G／A＋A／A基因型）比携带GG基因型者AD发病风险降低43．0％（OR 0．57，95％CI 0．36—0．91，P=0．019），而AA纯合子比携带GG基因型者AD发病风险降低60．0％（OR 0．40，95％ CI 0．21—0．77，P：0．006）。结论 ABCA1基因第6外显子D—A多态性与SAD相关，携带A等位基因或者AA基因型对SAD发病可能有一定的保护作用。     

内皮源性一氧化氮合酶基因多态性与缺血性脑卒中相关性研究

目的通过病例对照研究,探讨内皮源性一氧化氮合酶(eNOS)基因多态性与缺血性脑卒中的关系。方法采用聚合酶链反应(PCR)和限制性片断长度多态性(RFLP)技术,对452例缺血性脑卒中患者和153例健康对照人群的eNOS基因rs3918181位点进行基因多态性检测。结果大动脉粥样硬化型脑梗死组的基因型与等位基因频率与正常对照组比较P>0.05,无统计学意义。腔隙性脑梗死组eNOS基因AA AG基因型频率明显高于对照组,相对于GG基因型,暴露于AA AG基因型人群的OR值为1.644(95%CI 1.124～2.405)。腔隙性脑梗死A等位基因频率也显著高于对照组,相对于G等位基因,A等位基因OR值为1.419(95%CI 1.061～1.898)。结论内皮源性一氧化氮合酶(e-NOS)基因rs3918181位点多态性与腔隙性脑梗死相关;A等位基因可能增加中国汉族人罹患腔隙性脑梗死的风险。     

脂联素基因单核苷酸多态rs266729、 rs2241766、rs822396与老年缺血性 脑血管病亚型相关性研究

目的 探讨中国北方青岛地区汉族人群脂联素（adiponectin,ADIPOQ）基因多态性与老年缺血性脑血
管病发病的相关性。
方法 入组年龄大于60岁的老年缺血性脑血管病患者,按急性卒中治疗低分子肝素试验（Trial
of Org 10172 in Acute Stroke Treatment,TOAST）分型,选取大动脉粥样硬化性（large artery
atherosclerosis,LAA）和小动脉闭塞性（small artery occlusion,SAO）两种亚型患者,其中LAA 144例,
SAO 221例;402例同期查体者进行病例对照研究。对比两组的ADIPOQ基因多态性。
结果 rs266729（-11377C/G）的基因型分布在LAA组、SAO组与对照组3组中有显著差异（P =0.036）。
3组中两两比较显示,SAO组中rs266729（-11377C/G）GG基因型分布显著高于对照组（P =0.009）;在
隐性［P =0.004,比值比（odds ratio,OR）=2.478,95%可信区间（confidence interval,CI）=1.31～4.70］、
累加模式（P =0.003,OR 2.680,95%CI 1.39～5.15）下,rs266729（-11377C/G）基因型分布在SAO组与
对照组中也有显著差异,G 等位基因能增加SAO型缺血性脑血管病的风险,但在显性模式下差异无显
著性。rs822396（-3964A/G）、rs2241766（-45T/G）的基因型分布在LAA组、SAO组与对照组3组中均
无显著差异。
结论 rs266729（-11377C/G）G 等位基因与老年缺血性脑血管病发病相关,其G 等位基因变异可增
加老年患者SAO型缺血性脑血管病的风险。     

Pin基因启动子-842G/C位点多态性与散发性阿尔茨海默病的关联分析

目的:探讨Pin1基因-842G/C位点多态性与散发性阿尔茨海默病(SAD)遗传易感性的关系。方法:应用聚合酶链反应限制性片段长度多态性(PCR-RELP)方法检测46例SAD患者和52名健康老年人的Pin1基因启动子多态性分布特征,并通过比值比(OR)分析基因与SAD之间的关系。结果:Pin1基因启动子多态性(842G/C)与SAD的发病风险不相关,C等位基因与G等位基因的OR=0.90(95%CI=0.37～2.19),而GG基因型与非GG型基因频率在SAD组与健康对照组比较差异无统计学意义(P>0.05)。结论:Pin1基因启动子-842G/C位点多态性可能并不是SAD发病的独立遗传危险因素,与SAD的发病无关。     

基质金属蛋白酶-7血清水平及其基因-181A/G多态性对颈动脉斑块稳定性的影响

目的 探讨基质金属蛋白酶-7(matrix metalloproteinase-7,MMP-7)血清水平及其基因启动子区-181 A/G多态性对颈动脉斑块稳定性的影响.方法 503例患有颈动脉粥样硬化性疾病的患者根据B型超声检查结果分为颈动脉易损斑块组(118例)和稳定斑块组(385例).采用ELISA法检测两组患者血清MMP-7水平,同时运用聚合酶链反应-限制性片段长度多态性方法(PCR-RFLP)分析两组患者MMP-7基因启动子-181A/G多态性.结果 易损斑块组血清MMP-7水平为(19.31 ± 8.10)μg/L,而稳定斑块组为(14.98±4.97)μg/L,两者相比差异有统计学意义(t=5.49,P=0.00).MMP-7基因启动子-181位点AG+GG基因型及G等位基因总体分布在易损斑块组和稳定斑块组间比较差异有统计学意义(OR=1.81,P=0.025和OR=1.71,P=0.029).易损斑块组内AG+GG基因型患者血清MMP-7水平较从基因型者高(t=2.62,P=0.01),而稳定斑块组内AG+GG基因型和AA基因型间MMP-7血清水平相比差异无统计学意义(t=6.51,P=0.52).结论 血清MMP-7水平可能成为颈动脉易损斑块检测的一个生物学指标.MMP-7基因启动子区-181A/G多态性可能影响MMP-7蛋白的表达,从而与颈动脉易损斑块的遗传易患性密切相关.

Abstract：

Objective To explore the influence of plasma matrix metalloproteinase-7 ( MMP-7 ) levels and genetic polymorphism of MMP-7 - 181 A/G on the stability of carotid plaque.Method According to carotid ultrasound examination, 503 patients with carotid atherosclerotic lesions were consecutively recruited and divided into vulnerable plaque group (n = 118) and stable plaque group (n = 385).Plasma MMP-7 levels were measured by enzyme-linked immunosorbent assay (ELISA), and MMP-7 -181 A/G genotypes were determined by polymerase chain reaction-restiction fragment length polymorphism (PCR-RFLP).Results Plasma MMP-7 levels in carotid vulnerable plaque group were significantly enhanced as compared to stable plaque group (t =5.49, P =0.00).The frequency of MMP-7 -181G allele in vulnerable plaque group was significantly higher than that in stable plaque group (11.4% vs 7.0% ,χ2 = 4.78, P= 0.029).Compared to AA genotype, the genotypes with - 181G allele (AG + GG) significantly increased susceptibility to carotid vulnerable plaque ( χ2 = 5.01, OR = 1.81, P = 0.025 ) .When further analyzing the relationship between genotype and plasma MMP-7 levels, no significant differences of plasma MMP-7 levels were observed between AA genotype and AG + GG genotype in stable plaque group.However, in vulnerable plaque group, plasma MMP-7 levels of AG + GG genotype were significantly higher than that of AA genotype( t = 2.62, P = 0.01).Conclusion The present findings suggest that plasma MMP-7 level may be a biomarker for carotid vulnerable plaque.Genetic polymorphism of - 181 A/G in MMP-7 promoter may affect the expression of MMP-7, and seems to be implicated in susceptibility to carotid vulnerable plaque.     

弗雷明汉卒中高风险增加新型冠状病毒病患者的炎症反应及不良预后

目的 探讨弗雷明汉卒中危险因素负荷对2019冠状病毒病（coronavirus disease 2019，COVID-19）患者
循环炎症反应及预后的影响。
方法 本研究为单中心回顾性研究，分析了158例就诊于武汉大学中南医院隔离病区的COVID-19患
者。根据弗雷明汉10年卒中风险评分，将所有受试者分为卒中低危组（风险＜10%）、中危组（风险
10%～20%）和高危组（风险＞20%）。收集患者住院后每周的血清炎症指标检查结果，包括CRP、IL-6
和降钙素原（procalcitonin，PCT），连续4周。预后指标定义为病程4周内死亡、病程4周时仍需住院治疗
和痊愈。比较3组间预后和不同时间点的炎症指标差异，采用多元Logistic回归分析弗雷明汉卒中风险
与COVID-19患者4周预后的关系。
结果 发病第1周内的炎症指标在3组之间无显著的差异，第2周、第3周和第4周血清I L-6和PCT
水平在3组间有显著差异，第2周和3周的血清CRP水平也有显著的差异。低危组患者的血清CRP
和IL-6自第2周开始逐渐降低，PCT水平相对平稳，而高危组患者的IL-6和PCT水平在第4周明显上
升。多元Logi sti c回归分析结果显示，与弗雷明汉卒中高危组相比，低危组的死亡风险降低（OR
0.062，95%CI 0.004～0.772，P =0.031），低危组（OR 0.117，95%CI 0.031～0.396，P =0.001）与中危组
（OR 0.108，95%CI 0.025～0.501，P =0.004）患者病程第4周仍需要住院治疗的风险也均降低。中介效
应模型分析显示当纳入第2周IL-6水平为协变量时，弗雷明汉卒中低危组与死亡和第4周仍需住院治
疗之间的回归系数显著下降（死亡：β下降13.7%，OR 0.071，95%CI 0.005～0.815；仍需治疗：β下降
19.1%，OR 0.128，95%CI 0.034～0.452）。
结论 与弗雷明汉卒中高风险相比，卒中低、中风险COVID-19患者的炎症反应水平较低，不良预后
的风险较低。     

Role of Interleukin-10 (-1082A/G) gene polymorphism with the risk of ischemic stroke: a meta-analysis

The role of anti-inflammatory Interleukin-10 (IL-10) cytokine gene polymorphism with the risk of ischemic stroke (IS) remains controversial. The aim of present meta-analysis was to investigate the association of IL-10 (-1082 A/G) gene polymorphism with the risk of IS. A literature search for candidate gene association studies published before 29 February 2016 was conducted in the PubMed, EMBASE, Google Scholar, and TRIP database. The following search terms were used: ‘Interleukin-10’ or ‘IL-10’ and ‘Ischemic stroke’ or ‘IS’ and ‘Cerebral Infarction’ or ‘CI’ and ‘genetic polymorphism’ or ‘single nucleotide polymorphisms’ or ‘SNP’. Fixed or random effects models were used to estimate the pooled odds ratios (ORs) and 95% confidence intervals (CIs). Begg’s funnel plot was used to assess the potential for publication bias. In our meta-analysis, five case-control studies involving 1209 IS cases and 1139 controls were included. Overall, there was no significant association between IL-10 (-1082 A/G) [rs1800896] and risk of IS under dominant [AA + AG vs. GG], recessive [AA vs. AG + GG], and allelic [G vs.A] models. However, based on Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, we observed significant association of IL-10 (-1082 A/G) gene polymorphism with the risk of IS for Large Vessel Disease (LVD), Small Vessel Disease (SVD), and other (others due to determined and undetermined etiology) subtypes of IS. This is the first meta-analysis to conclude that IL-10-1082A/G gene polymorphism is associated with the risk of LVD, SVD, and other subtypes of IS. Further well-designed large sample size studies based on TOAST classification are needed to validate these findings.     

Association between interleukin-10 polymorphisms and Alzheimer's disease: a systematic review and meta-analysis

It has been hypothesized that polymorphisms of interleukin (IL)-10 genes affect the risk of developing late onset Alzheimer's disease (AD). However, results of different studies are often inconsistent. Our aim was to investigate by meta-analysis the association of the common polymorphisms comprehensively defining the genetic variability of the IL-10 gene with AD risk. Fifteen studies investigating the association between IL-10 polymorphisms (-1082, -819, -592) and AD were found and analyzed. The model-free approach was applied to meta-analyze these case-control genetic association studies. Available data suggested an association between -1082 polymorphism and AD risk with a marginal statistical significance (GG versus AG/AA: pooled odds ratio [OR]: 0.82, 95% confidence interval CI: 0.65-1.02) and evidence of a moderate degree of between-study heterogeneity (χ2 = 27.13, d.f. = 13, p = 0.01, I2 = 52%). For the -819 and -592 polymorphisms, we did not find an association with AD, but significant between-study heterogeneity made genotype data pooling unacceptable. Analysis by IL-10 haplotype showed that the -1082G/-819C/-592C haplotype is associated with a lower risk of AD, although with a marginal statistical significance, probably due to the low number of studies included (GCC versus other genotypes: OR: 0.61, 95% CI: 0.32-1.15; I2: 85%). Current findings suggest a possible association between -1082 A > G polymorphism and the risk of developing AD; this effect is more evident in the oldest patients. The high degree of between-study heterogeneity, due to several underpowered studies and to other methodological problems of individual studies underlies the need for further methodologically adequate studies.     

具有脑梗死病史的新型冠状病毒肺炎患者临床特征

目的 分析具有脑梗死病史的2019冠状病毒病（coronavirus disease 2019,COVID-19）（即新型冠状病 毒肺炎）患者临床特点,以提高临床救治率。 方法 回顾性分析武汉火神山医院既往有脑梗死病史的COVID-19患者的临床资料,根据《新型冠 状病毒肺炎诊疗方案（试行第五版修正版）》临床分型标准,分为普通型和重型两组,比较两组患者 的一般病史资料、临床表现、合并症及实验室检查的特点。 结果 共纳入60例符合入组条件的患者,其中普通型31例,重型29例。临床结局出院54例,转院3 例,死亡3例。重型患者较普通型患者更易出现呼吸衰竭（20.7% vs 3.2%,P =0.049）、急性心肌损伤 （17.2% vs 0,P =0.022）等并发症。实验室检查方面,重型患者中性粒细胞计数、D-二聚体、乳酸脱氢 酶、CRP水平高于普通型患者,差异有统计学意义。中性粒细胞计数（OR 1.799,95%CI 1.208～2.678, P =0.004）、淋巴细胞计数（OR 0.038,95%CI 0.004～0.359,P =0.004）为重型患者的独立影响因素。 结论 既往有脑梗死病史的COVID-19患者合并基础疾病较多,中性粒细胞计数升高和淋巴细胞计 数降低是重型患者的独立影响因素。     

高同型半胱氨酸对合并非瓣膜性心房颤动的急性脑梗死患者近期预后的影响

目的 探讨同型半胱氨酸（homocysteine，Hcy）对合并非瓣膜性心房颤动的急性脑梗死患者近期预
后的影响。
方法 前瞻性连续纳入合并非瓣膜性心房颤动的急性脑梗死的住院患者，所有患者均在发病48 h
内住院。收集患者的基线临床资料及相关实验室检查结果。随访患者发病90 d时临床预后，良好预后
定义为mRS评分≤2分。采用多因素Logistic回归分析，探讨合并非瓣膜性心房颤动的急性脑梗死患者
90 d预后的独立影响因素。
结果 共纳入患者112例，男性46例（41.1%），年龄45～92岁，平均76.23±9.02岁。其中良好预
后患者53例（47.3%）。多因素回归分析显示，入院时NIHSS评分高（OR 1.632，95%CI 1.185～2.250，
P =0.03）、高血糖（OR 1.360，95%CI 1.052～1.758，P =0.019）、高Hcy水平（OR 1.702，95%CI
1.133～2.557，P =0.010）是影响患者90 d预后的独立危险因素。
结论 高Hcy是合并非瓣膜性心房颤动的急性脑梗死患者短期不良预后的独立影响因素。     

Correlating interleukin-10 promoter gene polymorphisms with human cerebral infarction onset

Evidence suggests that interleukin-10 (IL-10) deficiency exacerbates inflammation and worsens the outcome of brain ischemia. In view of the critical role of the single nucleotide polymorphic sites -1082 (A/G) and -819 (C/T) in the promoter region of the IL-10 gene, we hypothesized that they are associated with cerebral infarction morbidity in the Chinese Han population. We genotyped these allelic gene polymorphisms by amplification refractory mutation system-polymerase chain reaction methods in 181 patients with cerebral infarction (cerebral infarction group) and 115 healthy subjects (control group). We identified significant differences in genotype distribution and allele frequency of the IL-10-1082 A/G allele between cerebral infarction and control groups (χ² = 6.643, P = 0.010). The IL-10-1082 A allele frequency was significantly higher in the cerebral infarction group (92.3%) than in the control group (86.1%) (P = 0.015). Moreover, cerebral infarction risk of the AA genotype was 2-fold higher than with the AG genotype (OR = 2.031, 95%CI: 1.134–3.637). In addition, AA genotype together with hypertension was the independent risk factor of cerebral infarction (OR = 2.073, 95%CI: 1.278–3.364). No statistical difference in genotype distribution or allele frequency of IL-10-819 C/T was found between cerebral infarction and control groups (P > 0.05). These findings suggest that the IL-10-1082 A/G gene polymorphism is involved in cerebral infarction, and increased A allele frequency is closely associated with occurrence of cerebral infarction.     

大脑中动脉分布区缺血性卒中患者的临床和影像学特征及复发危险因素

目的 分析大脑中动脉（middle cerebral artery,MCA）分布区非心源性缺血性卒中患者的临床和影像 学特征及复发的危险因素。 方法 连续入选发病7 d以内的MCA分布区非心源性缺血性卒中患者。收集患者的人口学信息、血管 病的危险因素和发病时的主要症状及体征,评价患者的头颅磁共振影像包括急性梗死灶的部位、 数量、分布特征、责任动脉有无狭窄、缺血性卒中的病因分型。随访患者1年内有无缺血性卒中或短暂 性脑缺血发作（transient ischemic attack,TIA）复发,通过多元Logistic回归分析患者复发的危险因素。 结果 研究共入组926例患者,责任MCA狭窄≥70%的患者（447例）常见多发梗死灶（338例,75.6%） 和分水岭梗死（317例,70.9%）,而责任MCA无狭窄或狭窄程度<70%患者（479例）常见MCA穿支分 布区单发梗死灶（247例,55.3%）。冠状动脉粥样硬化性心脏病[比值比（odds ratio,OR）7.55,95%可 信区间（confidence interval,CI）2.85～20.0,P <0.001]、缺血性卒中病史（OR 3.49,95%CI 1.52～8.01, P =0.003）、缺血性卒中发病前3个月内反复TI A史（OR 22.7,95%CI 8.35～61.6,P <0.001）、新发梗死 灶为多发（OR 5.26,95%CI 1.33～20.8,P =0.018）是患者1年内缺血性卒中或TIA复发的危险因素。 结论 对于非心源性缺血性卒中患者,MCA分布区梗死灶的分布特征与MCA狭窄程度有关。新发梗 死灶为多发、既往有缺血性心脑血管病病史的患者1年缺血性卒中或TIA复发风险高。     

PDE4D基因SNP83多态性与缺血性卒中预后的相关性研究

目的探索磷酸二酯酶4D(phosphodiesterase 4D,PDE4D)基因的基因多态性(single nucleotide polymorphism,SNP)83(rs966221)与缺血性卒中预后的相关性。方法连续入组2009年10月~2011年7月北京天坛医院神经内科住院的缺血性卒中患者736例,采用Sequenom Massyarray技术检测SNP83位点基因分布情况。采用Logistic回归模型分析不同遗传模型下该位点基因多态性与卒中后3个月联合终点事件(包括卒中复发、死亡和其他血管事件等)和预后不良[改良Rankin量表(modified Rankin Scale,m RS)评分1]的相关性,并对卒中亚型进行分层分析。结果本研究共纳入736例患者,其中677例患者完成3个月的随访,失访率为8.02%。与未发生联合终点事件组的患者相比,发生联合终点事件组的患者年龄较大[(67.02±0.70)vs(59.98±3.35),P0.001],既往心房颤动病史比例较高(9.3%vs 3.7%,P=0.048),入院时美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分较高[11(5~16)vs 5(2~9),P0.001],且差异具有显著性,而两组的其他基线信息(如性别、民族、婚姻状况、居住方式、既往吸烟、饮酒、高血压、糖尿病、高脂血症和冠状动脉粥样硬化性心脏病等)差异无显著性(P0.05)。进行基因多态性分析发现,与未发生联合终点事件患者相比,发生联合终点事件患者中SNP83AG+GG基因型的比例较高(50.0%vs 36.7%,P=0.007),调整年龄、入院时NIHSS评分和既往心房颤动病史,Logistic回归分析显示该位点在显性模型(AG+GG vs AA)下与缺血性卒中后联合终点事件发生相关[调整后的比值比(odds ratio,OR)1.84,95%可信区间(confidence interval,CI)1.04~3.26],但并未发现该位点与卒中预后不良相关。结论 PDE4D基因SNP83 AG/GG基因型与缺血性卒中后联合终点事件发生相关。     

轻度血管性认知障碍影响因素分析

目的 探讨轻度血管性认知障碍（mild vascular cognitive impairment,mVCI）的影响因素。 方法 选取2015年8月-2018年10月收治于邯郸市第一医院神经内科的发病14 d内急性缺血性卒中 的患者为研究对象,行简易精神状态检查表、蒙特利尔认知评估量表测评,对其认知功能进行评估, 并根据其得分情况分为mVCI组及认知正常组。对比两组患者的临床资料的差异,采用单因素分析和 多因素Logistic回归分析探讨mVCI的影响因素。 结果 最终共纳入205例患者,mVCI组97例,认知正常组108例。①单因素分析显示,mVCI组患者低 文化程度（P =0.006）、高血压（P =0.032）、糖尿病（P =0.041）及吸烟（P =0.026）的比例显著高于 认知功能正常组,差异有统计学意义。mVCI组患者的血浆同型半胱氨酸水平（P =0.016）、TG水平 （P =0.040）、TC水平（P =0.026）以及匹兹堡睡眠质量指数（P＜0.001）显著高于认知正常组,差异有 统计学意义。②多因素Logistic回归分析显示,同型半胱氨酸水平升高（OR 1.139,95%CI 1.012～1.283, P =0.031）和主观睡眠质量差（OR 1.301,95%CI 1.107～1.530,P =0.001）是mVCI发生的独立危险因素, 而文化程度高（OR 0.652,95%CI 0.434～0.978,P =0.039）是mVCI 的保护性因素。 结论 高同型半胱氨酸血症及睡眠质量差是mVCI的独立危险因素,而文化程度高是mVCI的保护性 因素。