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1.
肝癌遗传模式与危险因素病例-对照研究   总被引:3,自引:0,他引:3  
目的探讨肝癌的危险因素及遗传模式,为肝癌的预防提供科学依据。方法采用病例-对照研究,以98例肝癌病例和196名健康对照作为研究对象,询问其暴露史;采用Penrose法、简单分离分析和Falconer法对98例原发性肝癌家系资料进行遗传流行病学研究。结果乙肝病史、亲属肿瘤史、食用盐腌食品史、肝硬化病史、饮用地表水与浅井水、饮酒等因素的比值比分别为5.18,8.40,2.16,9.33,2.56,2.61;单基因显性简单分离分析(分离比1/2)χ2=219.44,P<0.01;单基因隐性简单分离分析(分离比1/4)χ2=67.74,P<0.01;应用Penros法计算同胞肝癌发生率,一般人群肝癌发生率(s/q)接近1/q1/2;先证者一级亲属的遗传度为(58.74±5.43)%。结论乙肝病史、亲属肿瘤史、食用盐腌食品史、肝硬化病史、饮用地表水与浅井水、饮酒等是武威市肝癌发病的危险因素;先证者肝癌遗传不符合单基因显性和隐性遗传而是属于多基因遗传,遗传因素对肝癌的发病具有一定的贡献,约占整个危险因素的3/5。  相似文献   

2.
脑梗死的遗传流行病学研究   总被引:2,自引:1,他引:1       下载免费PDF全文
目的 探讨脑梗死的遗传方式以及遗传因素在脑梗死发病中的作用。方法 采用遗传流行病学配对病例对照研究方法 ,对 112对脑梗死先证者家系和对照家系的脑梗死发病情况进行研究 ,使用Li Mantel Gart法及Falconer法估算脑梗死的分离比和遗传度。结果 病例组一、二级亲属脑梗死患病率明显高于对照组亲属 (P <0 .0 5 ) ;分离比为 0 .14 37(0 .1130~ 0 .174 4 ) ,显著低于0 .2 5 ,不符合单基因遗传性疾病的特征 ;遗传度估算结果 ,患者一、二级亲属遗传度分别为 4 7.84 %±4 .5 5 %和 4 0 .95 %± 13.0 5 % ,其中男性高于女性。结论 脑梗死属多基因遗传方式 ,遗传因素对其发病有一定的作用。  相似文献   

3.
2型糖尿病的遗传流行病学研究   总被引:3,自引:0,他引:3  
目的 探讨遗传因素在2型糖尿病发生中的作用及其一般遗传模式。方法 对21个2型糖尿病先证者进行家系调查,应用Falconer同归法估算遗传度,Penrose’s法、Li-Mantel-Gait法及江三多的阈值模型理论估计2型糖尿病分离比、遗传模式等。结果 2型糖尿病先证者一级亲属患病率为7.6%,高于一般人群患病率;2型糖尿病遗传度为46.8%;Penrose’s法计算同胞患病率(s)/人群患病率(q)为3.312,接近1/q^1/2;简单分离分析结果显示,分离率P为0.131,低于0.25;阈值模型理论推算出2型糖尿病一级亲属的理论发病率为8.0%,实际发病率为7.6%。结论 2型糖尿病有明显遗传倾向,但不符合单基因遗传模式,具有多基因遗传特征。  相似文献   

4.
目的 探讨遗传因素在阿尔茨海默病发生中的作用及其一般遗传模式.方法 对29个阿尔茨海默病先证者进行家系调查,应用Falconer回归法估算遗传度,应用Penrose's法和江三多的阈值模型理论估计阿尔茨海默病的遗传模式等.结果 阿尔茨海默病先证者Ⅰ级亲属的患病率为5.06%,高于一般人群的患病率(0.912%);阿尔茨海默病的遗传度为53.34%;同胞患病率(s)与人群患病率(q)之比为6.348,接近1/q1/2;阈值模型理论推算出阿尔茨海默病Ⅰ级亲属的理论发病率为5.10%.结论 阿尔茨海默病有明显遗传倾向,但不符合单基因遗传模式,具有多基因遗传特征.  相似文献   

5.
[目的]了解遗传因素在淮安地区食管癌发病中的作用及食管癌的遗传模式.[方法]采用以人群为基础的病例对照家系研究,收集97对淮安当地原发性食管癌患者及其对照的家系资料,调查这些家系所有一级亲属的肿瘤发病率;应用多因素非条件Logistic回归估计食管癌家族史的发病风险,Li-Mantel-Gart法计算食管癌的分离比,Penrose法估计遗传模式,Falconer法计算遗传度.[结果]淮安地区食管癌先证者与对照的食管癌家族史差异有统计学意义,先证者家系的一级亲属食管癌患病风险显著高于对照家系,其同胞分离比为0.026(95%CI:0.0003~0.028),Ⅰ级亲属食管癌的遗传度为(24.769±7.038)%.[结论]淮安地区食管癌具有明显的家族聚集性,遗传因素在淮安地区食管癌病因中占一定比重,其遗传模式呈现多基因遗传方式.  相似文献   

6.
血清乙型肝炎表面抗原阳性与食管癌关系的队列研究   总被引:1,自引:0,他引:1  
目的探讨血清乙型肝炎表面抗原(HBsAg)阳性与食管癌发病的关系。方法应用队列研究方法对40岁以上HBsAg阳性队列(550例)和HBsAg阴性队列(881例)的非恶性肿瘤人群随访6年,分别计算观察人年数、食管癌、肝癌和其他恶性肿瘤的人年发病率、相对危险度(RR),并将两队列进行比较。结果6年内随访7740人年,HBsAg阳性队列2943.5人年,发现食管癌19例,人年发病率0.65%,HBsAg阴性队列4796.5人年,发现食管癌7例,人年发病率0.15%,两队列比较,P<0.01。RR4.42,95%可信区间1.62~12.06,归因危险度0.50%,归因危险度百分比77.36%,人群归因危险度百分比51.3%。分层分析显示,性别及年龄均不是混杂因素。肝癌在HBsAg阳性队列中的人年发病率明显高于HBsAg阴性队列(0.44%和0.04%,P<0.01;RR=10.52,95%可信区间为2.21~29.60)。其他恶性肿瘤的人年发病率在两队列间差异无显著性(0.58%和0.52%,P>0.05;RR=1.12,95%可信区间0.51~2.21)。结论血清HBsAg阳性与食管癌发病显著相关,乙型肝炎病毒不仅是原发性肝癌的致癌病毒,还可能是食管癌致癌病毒之一。  相似文献   

7.
目的通过海门市肝癌早诊早治项目的筛查和随访复查,总结经验与成效。方法根据《中国癌症预防与控制规划纲要》和《中国癌症筛查及早诊早治技术方案》,筛查高危地区人群的乙肝表面抗原(HBsAg),建立HBsAg(+)队列人群,每年2次进行甲胎蛋白(AFP)联合B型超声检查,可疑患者再经医院进一步确认是否为肝癌。结果 2010—2012年2 123例乙肝病毒感染者建立HBsAg阳性队列,2010—2018年共随访21 093人次,发现肝癌71人,检出率0.34%。其中早期肝癌41人,早诊率57.75%;治疗68人,治疗率95.77%。肝癌早诊早治项目队列人群的肝癌早诊率(57.75%)明显高于2015年日常系统报告组(4.45%),差异有统计学意义(χ2=114.51,P0.01)。结论对HBsAg(+)队列人群进行定期随访复查,是早期发现肝癌,提高治疗效果的有效措施。  相似文献   

8.
家族性Ⅱ型糖尿病核心家系的遗传方式分析   总被引:3,自引:1,他引:2       下载免费PDF全文
目的 对 1992~ 1998年门诊及住院的家族性Ⅱ型糖尿病 (DM)患者 177个大家系及其中 2 14个核心家系的遗传方式进行研究 ,以探讨该病的遗传学特点。方法 采用家系分析、分离分析、多基因分析和阈值模式分析的方法 ,对家族性Ⅱ型DM大家系及核心家系进行研究。结果  177个大家系的Ⅱ型DM的遗传度为 143.0 6 %± 3 .3% ,提示在这些家系中有一个显性主基因存在。 2 14个核心家系中 ,U×U婚配型的子代分离比为 0 .470 3,U×A婚配型的分离比为 0 .483 8,A×A婚配型的分离比为 0 .6 712。多基因分析和分离分析显示 ,U×A家系不符合多基因遗传和常染色体隐性(AR)遗传 ,符合常染色体显性 (AD)遗传 ,U×U家系既不符合AD遗传 ,又不符合AR遗传。结论 家族性Ⅱ型DM的遗传方式表现遗传异质性 ,在部分家系中存在AD遗传的亚型  相似文献   

9.
儿童单纯肥胖症群体综合干预研究   总被引:1,自引:0,他引:1  
目的探讨儿童单纯肥胖症的群体综合干预方法,降低儿童肥胖发生率。方法从淮北市城区选择8所初级中学作为研究现场,其所有在校学生为研究对象,其中4所学校为干预组(2 346人) ,4所学校为对照组(2 834人)。采用WHO身高标准值为肥胖判断标准。对干预组进行为期3年的群体干预,干预措施包括膳食调整、运动处方、健康教育、行为矫正、耳穴按压等。干预对象为超重儿童及其家长、肥胖儿童及其家长及非肥胖儿童家长。对照组除与干预组同期体检外不施加任何干预措施。结果①经过3年干预,干预组肥胖发生率从9.8%降至7.0 % (P <0 .0 1) ,对照组肥胖发生率从9.8%上升为12 .5 % (P <0 .0 1)。干预后两组肥胖发生率差异有显著意义。②干预后肥胖度干预组从4 5 .9%±11.3%降至34.2 %±11.83% ,差异有显著意义(P <0 .0 5 ) ,对照组从4 6 .2 %±12 .1%上升至4 8.9%±13.7% ,差异无显著意义(P >0 .0 5 )。干预组与对照组儿童身高增长幅度基本一致。③干预后血TCH、TG、APOB及SBP降低,对照组肥胖儿童无明显变化。结论儿童单纯肥胖症群体综合干预可有效降低儿童肥胖发生率和肥胖度。  相似文献   

10.
乙型肝炎病毒感染与肝癌发生的31年随访研究   总被引:4,自引:0,他引:4       下载免费PDF全文
目的 研究乙型肝炎病毒(HBV)与肝癌发生的关系,评价HBsAg长期携带者发生肝癌的结局.方法 利用1976年建立的启东某社区15岁以上自然人群队列[血清筛检确定HBsAg、抗-HBs及丙氨酸转氨酶(ALT),并进行前瞻随访],该数据库与人群癌症登记资料、居民病伤死因资料链接核实,分析1977年1月至2007年12月12351名人群中肝癌等肿瘤的发生情况.结果 队列观察总人年数为355 305.0.HBsAg携带者中发生肝癌173例,发生率为361.55/10万;HBsAg非携带者发生肝癌95例,发生率为30.90/10万,两组比较RR=11.70(95%CI:9.06~15.19);其中男性和女性HBsAg携带者的RR值分别为12.30和10.46.两性各年龄组HBsAg携带者的肝癌发生率均高于非携带者.若以女性非携带者肝癌的发生率为1,则男性非携带者、女性携带者、男性携带者的RR值分别为3.07、10.46和37.76;该四组人群在31年中肝癌发生的累积率分别为0.86%、2.73%、10.22%和34.19%.非条件logistic回归模型分析显示性别(男性)、年龄、HBsAg、ALT为肝癌发生的显著影响因素,抗-HBs为保护因素.HBsAg携带与其他部位癌的发生未见有联系.结论 证实启东自然人群中HBsAg携带与肝癌发生的因果联系;针对HBV感染而采取干预措施是现场肝癌防治的重点.  相似文献   

11.
125个家族高发性2型糖尿病的危险因素研究   总被引:4,自引:1,他引:4       下载免费PDF全文
目的 研究家族高发性2型糖尿病家系人群中可能的遗传和环境危险因素。方法 对1999~2001年门诊及住院的125个家庭高发性2型糖尿病先证者的家庭成员调查家族信息和环境危险因素,比较2型糖尿病患者、糖耐量减低(IGT)患者与非患者在环境危险因素的差异。采用Falconer法估算遗传度,用Penrose法进行多基因分析研究其遗传危险性。结果 三组人群甘油三酯、体重指数、腰臀比值、高血压史及体力活动史的构成比差异有极显著性(P<0.01),而其他血脂项目及冠心病史差异未见显著性。125个大家系的2型糖尿病遗传度为83.42%±5.84%,提示在这些家系中可能有显性主基因存在。多基因分析研究表明在该人群中,2型糖尿病可能符合多基因遗传模式。结论 2型糖尿病为多基因疾病,环境危险因素和遗传因素及其交互作用可能影响其发病。  相似文献   

12.
非胰岛素依赖型糖尿病的遗传流行病学研究   总被引:3,自引:0,他引:3  
目的 探讨非胰岛素依赖型糖尿病一般遗传模式。方法 调查1608名在校儿童非胰岛素依赖型糖尿病上、下3代家族史,收集280个非胰岛素依赖型糖尿病核心家庭,进行非胰岛素依赖型糖尿病家系资料分析。结果 非胰岛素依赖型糖尿型糖尿病患一级亲属患病率2.38%,先证父母、同胞、子女患病率分别为26.00%、2.44%、1.24%,高于一般人群患病率;Penrose法计算同胞患病率/同年龄段患病率为10.1  相似文献   

13.
浙江省815例白癜风患者遗传流行病学研究   总被引:1,自引:0,他引:1  
目的探讨白癜风可能的遗传模式。方法通过调查表得到浙江地区815例白癜风患者及其一、二级亲属的数据。815例白癜风患者中男411例(50.43%),女404例(49.57%),年龄2月龄至71岁。由于缺乏当地白癜风患病率普查数据,因此设立对照组以方便遗传模式及遗传度的计算。468名对照组性别及各年龄段比例与病例组具有可比性。应用Penrose法、Falconer回归法及SAGE—REGTL软件对白癜风患者进行遗传方式分析,遗传度计算及复合分离分析。结果所调查的815例白癜风先证者中,有家族史者128例,无家族史者687例,遗传率15.70%。Penrose法计算出同胞患病率(s)/人群患病率(q)为41.76,不接近1/2q(260.42),也不接近1/4q(130.21),而接近1/√q(22182),提示白癜风符合一种多基因遗传模式。白癜风患者一、二级亲属遗传度分别为59.61%和55.20%,加权遗传度为58.7%。复合分离分析显示孟德尔显性、隐性、加性主基因模型假设均被接受;单纯环境与非传递模型被拒绝;以AIC值判断,显性模型拟合程度最好。结论遗传因素在白癜风发病中占有重要作用,白癜风符合一种多基因或多因子遗传模式,存在主基因效应。  相似文献   

14.
The question of possible heterogeneity among population groups and phenotypic groups on the role of major gene in the etiology of cleft lip with or without cleft palate [CL(P)] was examined using the uniformly collected data in Hawaii. Complex segregation analysis was used to analyze patterns of family resemblance under the mixed model incorporating the effects of major gene and multifactorial inheritance. Analysis of the entire data showed superior fit of the mixed model including the effects of both major gene and multifactorial inheritance over the model of major gene alone or multifactorial inheritance alone. No significant heterogeneity could be detected between the high-incidence group (Oriental or Japanese) and the low-incidence group (non-Oriental) in the underlying general model, although higher heritability was observed in general. When families were classified into "severe" and "mild" phenotypes based on cleft lip vs. cleft lip and palate or unilateral vs. bilateral cleft in the proband, no significant differences could be detected between the two types in the underlying genetic model.  相似文献   

15.
BACKGROUND: Large population-based cohort studies in areas of high hepatitis B virus (HBV) prevalence have provided the evidence establishing hepatitis B surface antigen (HBsAg) carriage as a risk factor for hepatocellular carcinoma (HCC) and liver disease. Fewer studies have examined this in Western countries, where both HBV infection and carriage are less common and transmission patterns differ. This is the only prospective population-based study to examine this relationship in Europe. METHODS: In all, 2681 male and 977 female blood donors in England and Wales, found to be HBsAg positive during routine blood-donation screening, were followed up from recruitment in 1970-1982 to December 1999 and their cause-specific mortality was analysed. This was compared with that of the general population of England and Wales. RESULTS: During a mean of 22 years of follow-up, 17.4% of the 420 deaths were due to HCC or liver disease. There were 20 deaths from HCC in male HBsAg carriers, representing a significantly high standardized mortality ratio (SMR) compared to the male population of England and Wales of 26 (SMR = 26.26; 95% CI: 16.04- 40.54). The HCC incidence rate in males was 33.5 per 100 000 person years and 4.4 per 100 000 person years in females. Men had 8.5 (SMR = 8.50; 95% CI: 6.25- 11.31) and women had 3.9 times the risk of death from liver disease (SMR = 3.89; 95% CI: 1.26-9.09). The risk of circulatory disease deaths was reduced in both males and females. There was a significant increased risk of non-Hodgkins lymphoma that was not apparent in the first decade of follow-up. The increased risk of HCC and liver disease in men fell with follow-up. CONCLUSION: Hepatitis B surface antigen carriage is a significant risk factor in England and Wales for both liver disease and HCC mortality. However, this risk has declined with duration of follow-up. This could be due to natural reversion to HBsAg negativity or as a result of treatment and avoidance of other risk factors. The increased risk of non-Hodgkins lymphoma seen in longer follow-up is likely to be related to HIV infection acquired subsequent to recruitment.  相似文献   

16.
Data on 337 lung cancer families were analyzed to determine if known cohort differences in parental cigarette consumption influence parameters from a segregation analysis. Previous results suggested that, after allowing for an individual's pack-years of tobacco exposure, Mendelian codominant inheritance of an allele that produced an earlier age of onset provided a good fit to the data. In the present study, the data were split into two groups of families: probands age 60 and over (born before WWI) and probands younger than age 60. This partition of the data by age of the proband was done to separate families in which there were parents who were less likely to smoke from those with parents more likely to smoke--predicated on the known increase of smoking prevalence after World War I. For the younger proband families (those with parents more likely to smoke), only Mendelian codominant inheritance adequately fit the data. The hypotheses of no major type, environmental transmission, and Mendelian dominant or recessive inheritance were rejected. In contrast to our earlier findings, the estimate of population susceptibility increased from 28% in the total data to 60% in this subset. In the older proband families (those with parents less likely to smoke), the no major type and environmental hypotheses were rejected; further, none of the Mendelian models could be distinguished. Our results demonstrate that cohort differences, probably in exposure to tobacco, can confound parameters of a segregation analysis, and suggest that the genetic component of lung cancer may be greater than previously estimated. It further suggests that susceptibility to lung cancer occurs as a function of susceptibility to the effects of tobacco smoking.  相似文献   

17.
Copper incorporation studies were performed on individuals from 58 pedigrees, comprising 140 sibships. As previously reported, there is considerable overlap between heterozygotes and normal homozygotes. Segregation analysis supports recessive inheritance of disease, with residual heritability for 64Cu uptake in cultured cells. The population frequency of sporadic cases is compatible with the 1/3 expected for an X-linked lethal with equal mutation rates in egg and sperm, which implies a mutation rate of 6.7 X 10(-6)/gamete/generation. The parameters estimated here are likely to provide the best basis for genetic counseling until more reliable carrier tests are performed on a systematic sample from a large, defined population.  相似文献   

18.
BACKGROUND: The aim of this research was to determine the hepatitis B surface antigen (HBsAg) carrier prevalence among cases of hepatocellular carcinoma (HCC), and the population attributable risk of HBsAg carriage for HCC, by ethnicity in New Zealand. METHODS: The hospital notes of HCC cases registered with the New Zealand Cancer Registry, for the years 1987-1994 inclusive, were viewed to determine the HBsAg status. Results The HBsAg status was determined for 193 cases of HCC. The HBsAg carrier prevalence for non-Europeans with HCC was markedly higher than that for Europeans, being 76.7% for Maori, 80.0% for Pacific Island people, and 88.5% for Asians, compared to 6.0% for Europeans. In addition to the effect of ethnicity, HCC cases aged <60 years were more likely to be HBsAg carriers than those aged > or = 60 years. The estimated population attributable risk of HBsAg for HCC, within each ethnic group, was only marginally less than the HBsAg prevalence due to the high relative risk of HBsAg carriage for HCC. The standardized incidence rate ratios of HCC for Maori, Pacific Island people and Asians compared to Europeans were 9.6, 20.4, and 22.3, respectively. Hepatocellular carcinoma attributable to HBsAg carriage explained 79%, 83%, and 92% of the excess standardized rate of HCC, compared to Europeans, for Maori, Pacific Island people, and Asians, respectively. Conclusions The HBsAg carrier prevalence in non-European cases of HCC in New Zealand is between 75% and 90%. HBsAg carriage explains the majority of the excess rate of HCC in non-Europeans compared to Europeans in New Zealand.  相似文献   

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