Association Between Angiotensin II Receptor Blockers and the Risk of Lung Cancer Among Patients With Hypertension From the Korean National Health Insurance Service-National Health Screening Cohort

Objectives:The objective of this study was to estimate the risk of lung cancer in relation to angiotensin II receptor blocker (ARB) use among patients with hypertension from the Korean National Health Insurance Service-National Health Screening Cohort. Methods:We conducted a retrospective cohort study of patients with hypertension who started to take antihypertensive medications and had a treatment period of at least 6 months. We calculated the weighted hazard ratios (HRs) and their 95% confidence intervals (CIs) of lung cancer associated with ARB use compared with calcium channel blocker (CCB) use using inverse probability treatment weighting. Results:Among a total of 60 469 subjects with a median follow-up time of 7.8 years, 476 cases of lung cancer were identified. ARB use had a protective effect on lung cancer compared with CCB use (HR, 0.75; 95% CI, 0.59 to 0.96). Consistent findings were found in analyses considering patients who changed or discontinued their medication (HR, 0.50; 95% CI, 0.32 to 0.77), as well as for women (HR, 0.56; 95% CI, 0.34 to 0.93), patients without chronic obstructive pulmonary disease (HR, 0.75; 95% CI, 0.56 to 1.00), never-smokers (HR, 0.64; 95% CI, 0.42 to 0.99), and non-drinkers (HR, 0.69; 95% CI, 0.49 to 0.97). In analyses with different comparison antihypertensive medications, the overall protective effects of ARBs on lung cancer risk remained consistent. Conclusions:The results of the present study suggest that ARBs could decrease the risk of lung cancer. More evidence is needed to establish the causal effect of ARBs on the incidence of lung cancer.     

ACE、AT_1R、eNOS基因多态性与重度子痫前期的相关性

目的:探讨血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性、血管紧张素Ⅱ受体Ⅰ(AT1R)基因A1166C多态性和内皮细胞一氧化氮合成酶(eNOS)基因G894T多态性与重度子痫前期发病的关系。方法:应用荧光定量PCR、DNA测序技术检测50例重度子痫前期患者(病例组)与100例正常妊娠妇女(对照组)ACE、AT1R、eNOS基因多态性。结果:病例组ACE基因ID基因型频率(32.0%)显著低于对照组(57.0%,P0.01),DD基因型频率(40.0%)显著高于对照组(20.0%,P0.01);病例组AT1R基因AA基因型频率(78.0%)显著低于对照组(94.0%,P0.01),AC基因型频率(22.0%)显著高于对照组(5.0%,P0.01);相对于AA基因型,携带AC基因型者的OR值为5.303,病例组C等位基因频率(11.0%)显著高于对照组(3.5%,P0.05),相对于A等位基因,携带C等位基因者OR值为3.408;两组eNOS基因各基因型与等位基因频率差异无统计学意义;联合基因型无统计学意义。结论:ACE基因I/D多态性和AT1R基因A1166C多态性与重度子痫前期的发病有关,未发现eNOS基因G894T多态性与重度子痫前期的发病有关,未发现基因间有协同作用。     

多巴胺D_1受体及血管紧张素Ⅱ1型受体基因多态性与妊娠期高血压疾病遗传易感性的研究

目的:探讨多巴胺D1受体(DRD1)和血管紧张素Ⅱ1型受体(AT1R)基因多态性与妊娠期高血压疾病的相关性。方法:应用限制性片段长度多态性聚合酶链反应技术(RFLP-PCR)检测102例患者及108例正常孕妇的DRD1-48A/G和AT1RA1166→C变异多态性,对两组的基因型和等位基因进行分析。结果:DRD1G的分布频率在HDCP组和正常孕妇组分别为27·9%、9·3%,两组间G等位基因频率比较,差异有统计学意义(P<0·01)。HDCP组DRD1基因AG/GG型显著高于正常孕妇组(P<0·01)。AT1RC等位基因在HDCP组和正常孕妇组的分布频率分别为16·2%和5·6%,两组间C等位基因频率比较,差异有统计学意义(P<0·01)。HDCP组AT1R基因AC/CC型较正常孕妇组明显升高(P<0·01)。结论:在中国汉族人群中,多巴胺D1受体基因多态性-48A/G和AT1RA1166位点突变为C多态性与妊娠期高血压疾病发病相关。     

Activation of MEK 1/2 and p42/44 MAPK by angiotensin II in hepatocyte nucleus and their potentiation by ethanol

Hepato-subcellular effect of angiotensin II (Ang II) and ethanol on the p42/44 mitogen-activated protein kinase (MAPK) and MAPK kinase (MEK 1/2) was investigated in the nucleus of rat hepatocytes. Hepatocytes were treated with ethanol (100 mM) for 24 h and stimulated with Ang II (100 nM, 5 min). The levels of p42/44 MAPK and MEK 1/2 were monitored in the nuclear fraction using antibodies. Ang II itself caused significant accumulation of phosphorylated p42/44 MAPK (phospho-p42/44 MAPK) in the nucleus without any significant translocation of p42/44 MAPK protein thereby suggesting activation of p42/44 MAPK in the nucleus. Ang II caused marked accumulation of phosphorylated MEK 1/2 (phospho-MEK 1/2) in the nucleus without any significant accumulation of MEK 1/2 protein. Ratio of phospho-MEK 1/2 to MEK 1/2 protein in the nucleus after Ang II treatment was 2.4 times greater than control suggesting phosphorylation of MEK 1/2 inside the nucleus. Ethanol had no effect on the protein level or the activation of p42/44 MAPK in the nucleus. Ethanol treatment potentiated nuclear activation of p42/44 MAPK by Ang II but not translocation of p42/44 MAPK protein. This was accompanied by potentiation of Ang II-stimulated accumulation of phospho-MEK 1/2 in the nucleus by ethanol. MEK 1/2 inhibitor, U-0126 inhibited Ang II response and its potentiation by ethanol. These results suggest that Ang II-mediated accumulation of phospho-p42/44 MAPK in the hepatocyte nucleus involves MEK 1/2-dependent activation and this effect is potentiated by ethanol.     

Effect of repetitive daily ethanol intoxication on adult rat brain: Significant changes in phospholipase A2 enzyme levels in association with increased PARP-1 indicate neuroinflammatory pathway activation

Collaborating on studies of subchronic daily intoxication in juvenile and adult rats, we examined whether the repetitive ethanol treatments at these two life stages altered levels of key neuroinflammation-associated proteins—aquaporin-4 (AQP4), certain phospholipase A2 (PLA2) enzymes, PARP-1 and caspase-3—in hippocampus (HC) and entorhinal cortex (EC). Significant changes in the proteins could implicate activation of specific neuroinflammatory signaling pathways in these rats as well as in severely binge-intoxicated adult animals that are reported to incur degeneration of vulnerable neurons in HC and EC. Male Wistar rats, ethanol-intoxicated (3 g/kg i.p.) once daily for 6 days over an 8-day interval beginning at 37 days old and repeated at age 68–75 days, were sacrificed 1 h after the day 75 dose (blood ethanol, 200– 230 mg/dl). Analysis of HC with an immunoblot technique showed that AQP4, Ca⁺²-dependent PLA2 (cPLA2 IVA), phosphorylated (activated) p-cPLA2, cleaved (89 kD) PARP (c-PARP), and caspase-3 levels were significantly elevated over controls, whereas Ca⁺²-independent PLA2 (iPLA2 VIA) was reduced ∼70%; however, cleaved caspase-3 was undetectable. In the EC, AQP4 was unchanged, but cPLA2 and p-cPLA2 were significantly increased while iPLA2 levels were diminished (∼40%) similar to HC, although just outside statistical significance (p = 0.06). In addition, EC levels of PARP-1 and c-PARP were significantly increased. The ethanol-induced activation of cPLA2 in association with reduced iPLA2 mirrors PLA2 changes in reports of neurotrauma and also of dietary omega-3 fatty acid depletion. Furthermore, the robust PARP-1 elevations accompanied by negligible caspase-3 activation indicate that repetitive ethanol intoxication may be potentiating non-apoptotic neurodegenerative processes such as parthanatos. Overall, the repetitive ethanol treatments appeared to instigate previously unappreciated neuroinflammatory pathways in vivo. The data provide insights into mechanisms of binge ethanol abuse that might suggest new therapeutic approaches to counter neurodegeneration and dementia.     

缬沙坦对糖尿病肾病合并难治性高血压AT1受体自身抗体阳性患者的临床研究

目的观察缬沙坦对AT1受体自身抗体阳性的糖尿病肾病（DN）合并难治性高血压患者降压作用的临床疗效。方法以合成的AT1受体多肽片段为抗原，应用酶联免疫吸附法检测DN合并二期以上高血压患者161例，其中DN合并难治性高血压91例，AT1受体自身抗体阳性71例（78．0％），DN合并非难治性高血压70例。AT1受体自身抗体阳性11例（15．7％）。将AT1受体自身抗体阳性的DN合并难治性高血压患者71例，随机分为两组：对照组（30例）：给予卡托普利25mg每日3次，尼群地平20mg每6h1次，氢氯噻嗪12．5mg每日1次，肠溶阿司匹林100mg每日1次；治疗组（41例）：给予缬沙坦160mg每日1次，尼群地平20mg每6h1次，氢氯噻嗪12．5mg每日1次，肠溶阿司匹林100mg每日1次。结果临床降压效果评定，治疗组总有救率为85．4％。明显高于对照组的3313％，两组比较差异有统计学意义（P〈0．01）。结论对AT1受体自身抗体阳性的DN合并难治性高血压患者，有针对性地选择AT1受体拮抗剂，可取得满意的临床降压疗效。     

IL-1RN内含子2和外显子2基因多态性的分布特点及其与血脂的相关关系

目的 探讨武汉地区汉族健康人群白细胞介素-1受体拮抗剂基因(IL-1RN)第2号内含子中可变数串联重复序列(VNTR)多态性和第2号外显子 8006位点单核苷酸多态性(SNP)的分布特点及其与血脂的相关关系。方法 采用聚合酶链反应(PCR)和PCR-限制性片段长度多态性(RFLP)的分析方法,检测了251名武汉地区汉族健康者IL-1RN(VNTR)和IL-1RN( 8006)多态性,同时检测其血脂、IL-1和IL-1Ra水平。结果 IL-1RN(VNTR)的等位基因以Ⅰ型最为常见,其次为Ⅱ型,Ⅳ型较为罕见;IL-1RN( 8006)的等位基因以T型最为常见,其次为C型;IL-1RN(VNTR)的等位基因Ⅱ总是伴随着IL-1RN( 8006)的等位基因C而出现;这两种多态性的分布在男女间差异不显著,且与血脂、IL-1和IL-1Ra水平间不存在相关关系(P>0.05)。结论 武汉地区汉族健康人群IL-1RN内含子2和外显子2中均存在基因多态性,其等位基因间存在连锁不平衡;这两种多态性与血脂、IL-1和IL-1Ra水平间不存在相关关系。     

缬沙坦对糖尿病肾病合并难治性高血压AT1受体自身抗体阳性患者的临床研究

目的观察缬沙坦对AT1受体自身抗体阳性的糖尿病肾病(DN)合并难治性高血压患者降压作用的临床疗效。方法以合成的AT1受体多肽片段为抗原,应用酶联免疫吸附法检测DN合并二期以上高血压患者161例,其中DN合并难治性高血压91例,AT1受体自身抗体阳性71例(78.0%),DN合并非难治性高血压70例,AT1受体自身抗体阳性11例(15.7%)。将AT1受体自身抗体阳性的DN合并难治性高血压患者71例,随机分为两组:对照组(30例):给予卡托普利25mg每日3次,尼群地平20mg每6h1次,氢氯噻嗪12.5mg每日1次,肠溶阿司匹林100mg每日1次;治疗组(41例):给予缬沙坦160mg每日1次,尼群地平20mg每6h1次,氢氯噻嗪12.5mg每日1次,肠溶阿司匹林100mg每日1次。结果临床降压效果评定,治疗组总有效率为85.4%,明显高于对照组的33.3%,两组比较差异有统计学意义(P<0.01)。结论对AT1受体自身抗体阳性的DN合并难治性高血压患者,有针对性地选择AT1受体拮抗剂,可取得满意的临床降压疗效。     

Increased consumption of ethanol and sugar water in mice lacking the dopamine D2 long receptor

Individual differences in dopamine D2 receptor (D2R) expression in the brain are thought to influence motivation and reinforcement for ethanol and other rewards. D2R exists in two isoforms, D2 long (D2LR) and D2 short (D2SR), produced by alternative splicing of the same gene. The relative contributions of D2LR versus D2SR to ethanol and sugar water drinking are not known. Genetic engineering was used to produce a line of knockout (KO) mice that lack D2LR and consequently have increased expression of D2SR. KO and wild-type (WT) mice of both sexes were tested for intake of 20% ethanol, 10% sugar water and plain tap water using established drinking-in-the-dark procedures. Mice were also tested for effects of the D2 antagonist eticlopride on intake of ethanol to determine whether KO responses were caused by lack of D2LR or overrepresentation of D2SR. Locomotor activity on running wheels and in cages without wheels was also measured for comparison. D2L KO mice drank significantly more ethanol than WT in both sexes. KO mice drank more sugar water than WT in females but not in males. Eticlopride dose dependently decreased ethanol intake in all groups except male KO. KO mice were less physically active than WT in cages with or without running wheels. Results suggest that overrepresentation of D2SR contributes to increased intake of ethanol in the KO mice. Decreasing wheel running and general levels of physical activity in the KO mice rules out the possibility that higher intake results from higher motor activity. Results extend the literature implicating altered expression of D2R in risk for addiction by delineating the contribution of individual D2R isoforms. These findings suggest that D2LR and D2SR play differential roles in consumption of alcohol and sugar rewards.     

Lifestyle intervention might easily improve blood pressure in hypertensive men with the C genotype of angiotensin II type 2 receptor gene

BACKGROUND/OBJECTIVESRecent studies have reported an association of the angiotensin II type 2 receptor (AT2R) 3123Cytosine/Adenine (3123C/A) polymorphism with essential hypertension and cardiovascular diseases. The purpose of the study was to investigate whether the AT2R 3123C/A polymorphism affects blood pressure for free-living hypertensive men during a 5-month intervention period.SUBJECTS/METHODSThe subjects were free-living hypertensive Japanese men aged 40 to 75 years who agreed to intervention in the period from 2004 to 2011. Detection of the AT2R 3123C/A polymorphism was determined by polymerase chain reaction. The dietary intervention was designed to decrease salt level and to increase potassium level through cooking instructions and self-monitoring of the diet. The exercise session consisted of activities such as stretching, resistance training, and walking. Blood pressure, urinary sodium and potassium excretion, dietary and lifestyle data, and non-fasting venous blood sample were collected at baseline and after the intervention period.RESULTSThirty nine subjects were eligible for participation and the follow-up rate was 97.4%. The C allele proportion was 57.9%. AT2R 3123C/A polymorphism was X-chromosome-linked, therefore we analyzed the C and A genotypes. At baseline, no significant differences were observed between the genotype groups. After the intervention, there were no significant differences in lifestyle habit between the groups. Nevertheless, the estimated salt excretion (g/day) was significantly decreased only in the C genotype (13.0-10.3, P = 0.031). No significant change was observed in systolic blood pressure (SBP) (mmHg) in the A genotype, but a significant decrease was observed in the C genotype (150.0-141.5, P = 0.024).CONCLUSTIONSIn the C genotype, it might be easy to improve SBP through lifestyle intervention in free-living hypertensive Japanese men, however generalization could not be achieved by the small sample size.     

胰高血糖素样肽1受体激动剂与二肽基肽酶4抑制剂治疗2型糖尿病的效果比较

目的比较胰高血糖素样肽1(GLP-1)受体激动剂与二肽基肽酶4(DPP-4)抑制剂治疗2型糖尿病的效果。方法以2018年2月—2019年2月某医院收治的120例2型糖尿病患者为研究对象进行回顾性研究。60例作为GLP-1受体激动剂组,60例列入DPP-4抑制剂组。GLP-1受体激动剂组给予二甲双胍导入治疗+利拉鲁肽治疗,DPP-4抑制剂组给予二甲双胍导入治疗+西格列汀治疗,比较两组治疗效果。结果GLP-1受体激动剂组患者治疗后空腹血糖(FBG)、餐后2 h血糖(2hPBG)、糖化血红蛋白(HbAlc)、BMI水平分别为:[(5.95±0.86)、(9.33±1.71)、(6.13±0.88)、(24.42±2.13)]mmol/L,低于DPP-4抑制剂组(P<0.05);GLP-1受体激动剂组患者治疗后胰岛素分泌指数(HOMA-B)水平为(60.52±7.12)pmol/L,高于DPP-4抑制剂组(P<0.05);GLP-1受体激动剂组患者治疗后总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)水平低于DPP-4抑制剂组(P<0.05);GLP-1受体激动剂组患者治疗后低密度脂蛋白胆固醇水平高于DPP-4抑制剂组(P<0.05);两组患者用药期间不良反应发生率差异无统计学意义(P>0.05)。结论GLP-1受体激动剂治疗2型糖尿病效果更佳,而DPP-4抑制剂用药更为方便,临床可根据实际情况选择。     

Decreased somatostatin is related to the hypersensitivity of intestinal epithelia to LPS via upregulated TLR4-TBK1 pathway in rats chronically exposed to ethanol

Chronic alcoholics are predisposed to the development of a systemic inflammatory response syndrome, which is usually triggered in the gut. This study aimed to investigate in rats the role of intestinal epithelial inflammatory responsiveness in the susceptibility of alcoholics to excessive inflammation. Thirty Wistar rats were randomly divided into three groups: 10 rats killed immediately after acclimation (baseline control), 10 rats treated with 25% (vol/vol) ethanol for 6 months (ethanol group), and 10 rats given double-distilled water until killed simultaneously with the ethanol group (9-month control). The intestinal microflora, the epithelial histology and ultrastructure, the level of Toll-like receptor 4 (TLR4), TANK-binding kinase-1 (TBK1), and activated nuclear factor-κB (NF-κB) in the intestinal mucosa, and somatostatin (SST) levels in plasma and small intestine were evaluated in each group. Isolated intestinal epithelia from each rat were used to examine lipopolysaccharide (LPS) responsiveness with or without SST pretreatment by quantification of TLR4, TBK1, activated NF-κB, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). Compared with both the control groups, the amount of mucosal Escherichia coli in the ethanol group was not changed, whereas the number of intestinal lactobacilli in the ethanol group was significantly reduced (P < .05). Mild inflammatory injury and upregulation of TLR4 and TBK1 were observed in the intestinal mucosa of the ethanol group. The LPS-enhanced in vitro expression of TLR4, TBK1, and production of IFN-γ and TNF-α in isolated intestinal epithelia of the ethanol group were significantly higher than those in either control group (P < .05) and were dramatically inhibited by SST (P < .05), whereas NF-κB was activated by LPS only in the control groups. The plasma and intestinal levels of SST in the ethanol group were significantly lower than those in either control group (P < .05). These findings suggest that impairment of intestinal SST production by chronic ethanol administration leading to upregulation of the TLR4-TBK1 pathway may be one of the mechanisms underlying the LPS hypersensitivity of intestinal epithelia.     

VEGF及其受体在上皮性卵巢癌组织中的表达及预后

目的 研究血管内皮生长因子（VEGF）及其受体血管内皮生长因子受体1（VEGFR1）、血管内皮生长因子受体2（VEGFR2）在上皮性卵巢癌中表达及临床预后意义。方法 采用SP免疫组化法检测139例不同卵巢组织VEGF及其受体VEGFR1、VEGFR2的表达及在上皮性卵巢癌组织中的共表达情况,并结合临床资料进行统计分析。结果 VEGF及其受体VEGFR1、VEGFR2在上皮性卵巢癌组织中的染色强度明显高于良性卵巢肿瘤及正常卵巢组织;并且VEGF及其受体在上皮性卵巢癌组织中的表达与临床分期、腹水量的差异均具有统计学意义（χ^2=4．207,P＝0．034;χ^2=7．432,P＝0．007）;在相关分析中高表达的VEGF与VEGFR2（r＝0．316,P＜0．05）、VEGFR1与VEGFR2（r＝0．415,P＜0．05）均存在相关性;VEGF及其受体三者共高表达较非共高表达患者的5年生存率差异具有统计学意义（χ^2＝4．043,P＝0．044）。结论 高表达和共表达VEGF及其受体VEGFR1和VEGFR2的患者可能存在较差预后,并且三者共表达及高表达可作为一项指导临床应用抗肿瘤血管生成药物（ Bev）靶向治疗的疗效预测分子。     

碱性成纤维细胞生长因子对卵巢癌的影响

目的观察Ras-Raf-ERK 1/2途径介导的碱性成纤维细胞生长因子(bFGF)对卵巢癌细胞系CAOV3细胞增殖和凋亡影响,探讨bFGF及其信号转导途径与卵巢癌发生发展关系。方法以bFGF和促细胞分裂剂激活性蛋白激酶1(MEK1)抑制剂PD98059处理CAOV3细胞,用四甲基偶氮噻唑蓝(MTT)法检测细胞增殖情况,流式细胞术检测细胞凋亡情况,蛋白印迹(Western blot)检测细胞外信号调节蛋白激酶1/2(ERK1/2)的活性。结果bFGF处理后细胞增殖比明显增加,且与bFGF水平呈剂量依赖关系,bFGF浓度为75 ng/ml时细胞增殖比最高为140%;bFGF使无血清诱导的凋亡细胞比例下降[(33.20±5.32)%~(2.38±3.36)%];bFGF诱导ERK1/2活性增高。PD98059可抑制bFGF的这些作用。结论bFGF通过Ras-Raf-ERK 1/2途径介导,促进卵巢癌CAOV3细胞增殖,抵抗无血清诱导凋亡。在卵巢癌发生发展过程中,bFGF信号传递发挥了重要作用。     

白假丝酵母菌刺激体外培养人阴道上皮细胞表达TLR2的效果

目的:探讨体外培养人阴道上皮细胞表达的Toll样受体2(TLR2)是否受白假丝酵母菌孢子的调节.方法:采用实时定量逆转录聚合酶链反应(qRT-PCR)检测热灭活白假丝酵母菌孢子处理12h和24 h的体外培养的人阴道上皮细胞TLR2 mRNA的表达水平.结果:阴道上皮细胞表达的TLR2 mRNA水平在热灭活白假丝酵母菌孢子作用12 h和24 h时均明显高于无刺激的对照组(P＜0.05).结论:体外培养人阴道上皮细胞表达的TLR2 mRNA在白假丝酵母菌孢子作用12h和24h增加,人阴道上皮细胞在识别和启动防御白假丝酵母菌感染中TLR2可能起重要作用.     

PPP1R3基因Asp905Tyr多态性与安徽省汉族人群2型糖尿病相关性研究

目的 研究1型蛋白磷酸酶的骨骼肌特异糖原靶向调节亚单位基因(PPP1R3)Asp905Tyr多态性与安徽省汉族人群2型糖尿病相关性。方法 选取安徽省合肥地区汉族2型糖尿病患者262例,健康成人104名,运用聚合酶链反应限制性片段长度多态性技术(PCR-RFLP)进行基因型测定。以体重指数(BMI)25kl/m~2为分割点,将病例组和对照组进行分层分析。结果 PPP1R3基因Asp905Tyr多态性与安徽省汉族人群2型糖尿病没有明显的相关性;以BMI<25kg/m~2基因型Tyr/Tyr组为参照组,BMI≥25kg/m~2携有Asp 905等位基因个体的糖尿病发病风险明显增加(OR=3.69,95％CI:1.38～8.89,P=0.006)。结论 PPP1R3基因Asp 905Tyr多态性可能不是安徽省汉族人群2型糖尿病主要的致病因素。肥胖与Asp905等位基因间的交互作用可增加糖尿病的发病风险。     

人类免疫缺陷病毒1感染相关的基因多态性在中国汉族人群中的分布

目的　调查中国汉族人群中人类免疫缺陷病毒 1(HIV 1)感染相关的CCR5△ 32、CCR2 6 4I和SDF1 3’A等位基因突变频率和多态性的特点。方法　以 12 5 1例汉族人群为研究对象 ,应用PCR、PCR/RFLP(聚合酶链反应 /限制性片段长度多态性分析 )和DNA直接测序等方法进行检测 ,并用统计学方法进行分析。结果　发现中国汉族人群中存在CCR5△ 32等位基因突变 (均为杂合子基因型 ) ,突变频率为 0 .0 0 119,和西欧及美国白人相比 ,中国人群中CCR5△ 32基因突变频率极低 ,而CCR2 6 4I和SDF1 3’A基因突变频率相对较高 ,分别为 0 .2 0 0 2 3和 0 .2 872 3。结论　中国汉族人群的CCR5△ 32、CCR2 6 4I和SDF1 3’A等位基因的突变和多态性特点 ,具有一定的代表性。由于CCR5△ 32突变率低 ,中国汉族人群对性接触传播的HIV 1病毒 (R5 )株可能有较大的遗传易感性     

人类免疫缺陷病毒1感染相关的基因多态性在中国汉族人群中的分布

目的：调查中国汉族人群中人类免疫缺陷病毒１（ＨＩＶ－１）感染相关的ＣＣＲ５Δ３２、ＣＣＲ２－６４１和ＳＤＦ１－３‘Ａ等位基因突变频率和多态性的特点。方法：以１２５１例汉族人群为研究对象,应用ＰＣＲ、ＰＣＲ／ＲＦＬＰ（聚合酶链反应／限制性片段长度多态性分析）和ＤＮＡ直接测序等方法进行检测,并用统计学方法进行分析。结果：发现中国汉族人群中存在ＣＣＲ５Δ３２等位基因突变（均为杂合子基因型）,突变频率为１