内皮型一氧化氮合酶基因G894T多态性与颈动脉粥样硬化的相关性

目的探讨天津市汉族老年人群内皮型一氧化氮合酶(eNOS)基因G894T多态性与颈动脉粥样硬化(CAS)的关联性。方法选择接受颈动脉超声检查患者427例,根据超声检查结果分为CAS组1 30例和对照组297例。采用PCR-RFLP方法分析G894T多态性基因型,同时对所有对象检验血脂等危险因素。结果 CAS组基因型GT、GT+TT和T等位基因频率明显高于对照组(P<0.05,P<0.01)。调整了年龄和性别后,基因型GT+TT与CAS的关联差异有统计学意义(OR=1.89,95%CI:1.20～2.98,P=0.007)。对其他危险因素调整后,logistic回归分析,基因型GT+TT不是CAS的独立危险因素(OR=1.43,95%CI:0.85～2.40,P=0.1 78)。在CAS组中,不同斑块类型的分布、斑块总面积和Crouse积分在T等位基因携带者与非携带者差异无统计学意义(P>0.05)。结论 eNOS基因G894T多态性的基因型GT+TT与CAS的发生相关,但不是CAS的独立危险因素,与CAS的严重程度亦无关联。     

内皮型一氧化氮合酶和N5，N10-亚甲基四氢叶酸还原酶基因多态性与苏皖地区汉族人群早发冠心病易感性的相关关系

目的 探讨内皮型一氧化氮合酶(eNOS)基因第7外显子G894T突变和N5,N10-亚甲基四氢叶酸还原酶(MTHFR)基因C677T突变与苏皖地区汉族人群早发冠心病(PCAD)发病的关系.方法 采用病例对照研究的方法,应用聚合酶链反应-限制性片长多态性(PCR-RFLP)技术,分别检测131例PCAD患者(PCAD组)和131例年龄、性别相匹配的无冠心病者(对照组)的eNOS和MTHFR基因的单核苷酸多态性,判定其基因型并统计各基因型及等位基因的频率.结果 eNOS基因G894T多态性在PCAD组和对照组中的基因型分布(x2=2.072,P=0.355)和T等位基因频率(x2=0.727,P=0.394)差异均无统计学意义.MTHFR基因C677T基因型在PCAD组CT和TT型分布均高于对照组(x2 =14.290,P=0.001),T等位基因频率亦高于对照组(x2=16.339,P =0.000),差异有显著性(P＜0.05).Logistic回归分析显示,携带MTHFR基因C677TTT基因型是PCAD发病的独立危险因素.结论 eNOS基因G894T多态性可能与苏皖地区汉族人群PCAD发病无关;MTHFR基因677C/T多态性的TT基因型可能增加苏皖地区汉族人群PCAD的患病风险,T等位基因可能是PCAD的遗传易感基因.     

新疆汉族和哈萨克族人群内皮型一氧化氮合酶基因T786C和G894T多态性与原发性高血压的相关分析

目的探讨新疆汉族和哈萨克族内皮型一氧化氮合酶基因G894T、T786C多态性与原发性高血压的相关性。方法选取新疆塔城地区哈萨克族高血压患者363人和正常血压者370人,选取汉族高血压患者346人,正常血压者385人,运用多重单碱基延伸分型技术进行内皮型一氧化氮合酶基因G894T、T786C多态性分析,阐明两民族基因型、等位基因频率分布、连锁不平衡模式及构建的单体型与原发性高血压的相关性。结果超重、肥胖、甘油三酯异常及年龄51岁以上是两民族患高血压的共同相关危险因素。总人群、原发性高血压组及正常血压组中两民族内皮型一氧化氮合酶基因G894T、T786C位点等位基因频率分布差异均有统计学意义(P<0.05),两位点间不存在强连锁不平衡。汉族和哈萨克族人群内皮型一氧化氮合酶基因两位点共构成4种单体型:GT(75.3%和79.6%)、GC(10.8%和10.5%)、TT(5.7%和9.8%)及TC(8.2%和0.1%)。两民族单体型频率分布最高为GT,汉族和哈萨克族人群单体型频率分布最低分别是TC、TT,且两民族间单体型GT、TT、TC频率分布差异有统计学意义(P<0.05)。结论新疆汉族和哈萨克族人群内皮型一氧化氮合酶基因G894T、T786C位点多态可能与原发性高血压不相关。     

染色体7q35区基因多态性与糖尿病肾病的易感性

目的　探讨染色体 7q35区的醛糖还原酶(AR)和内皮细胞型一氧化氮合酶 (eNOS)基因多态性与中国北方汉族人 2型糖尿病肾病(DN)之间的关系。方法　采用PCR RFLP技术,检测AR基因启动子区C( -106)T点突变和eNOS基因第 7外显子G894T点突变;采用琼脂糖凝胶直接电泳PCR产物,检测eNOS基因第 4内含子 27bp的插入 /缺失(4a/4b)多态,分析 134例 2型糖尿病组(包括 70例DN+组和64例DN-组)和 85名正常对照(NC)组的AR、eNOS基因多态性与DN易感性的关系。结果　AR基因的C等位基因、C/C基因型和eNOS基因的T、4a等位基因及T/G、4a/4b基因型频率在DN-组和NC组间差异无统计学意义,而在DN+组则显著高于DN-组(均P<0. 05)。随着携带以上基因型数目的增加,发生DN的相对危险度(OR)也明显增加 (χ2 =8. 43,P<0. 05 )。结论　eNOS基因的T/G、4a/4b基因型和AR基因的C/C基因型可能均为DN的易感基因型;发生DN的相对危险度与携带易感基因型数量有关,三者同时存在时,发生DN的OR值最高。     

内皮型一氧化氮合酶基因多态性在血管性认知障碍发病中的作用

目的探讨内皮型一氧化氮合酶(eNOS)基因多态性在血管性认知障碍(VCI)发病中的作用。方法选取146例VCI患者(VCI组),160例健康体检者(对照组)进行病例对照研究。应用PCR-RFLP技术测定eNOS基因894G/T位点及4b/4a位点单核苷酸多态性的分布,并进一步经高血压分层,分析各基因型与VCI之间的关系。结果两组间eNOS基因894G/T位点各基因型和等位基因频率比较,差异均有统计学意义(P<0.05),经过高血压分层后,在高血压(+)的亚组中,这种差异同样存在统计学意义(P<0.05)。两组间eNOS基因4b/4a位点各基因型和等位基因频率比较,差异均无统计学意义(P>0.05)。结论 eNOS基因894G/T位点多态性与VCI和高血压存在相关性,T等位基因可能是其易感基因。eNOS基因894G/T位点多态性可能是通过影响高血压而间接影响认知功能。     

内皮型一氧化氮合酶基因启动子-786位点多态性与原发性高血压发病相关性的研究

目的 研究内皮型一氧化氮合酶（eNOS）基因启动子-786位点多态性与原发性高血压发病的相关性,同时研究此位点多态性与原发性高血压的程度及血压节律是否相关.方法 采用病例对照研究的方法,以232例原发性高血压患者与130名健康中老年人的血白细胞为样本,应用聚合酶链反应-限制性片段长度多态性技术检测两组的eNOS基因启动子-786位点T/C多态性,比较两组的基因型和等位基因的分布频率.高血压组内按高血压的危险分层分为低危、中危、高危组分别为89、78、65例,按血压节律性分为杓型与非杓型组分别为109、123例,比较各组eNOS基因启动子-786位点的基因型和等位基因的分布频率.结果 eNOS基因启动子-786位点T/T、T/C和C/C基因型在高血压组中分别为22.84％、50.87％、26.29％,在正常中老年人组中分别为36.15％、53.08％、10.77％,此位点高血压组与正常中老年人组的基因分布频率差异有统计学意义.eNOS基因启动子-786位点T/T、T/C和C/C基因型在高血压低危、中危、高危各组中分布频率无显著差异,在依据血压节律的分组中差异也无统计学意义.结论 ①eNOS基因启动子-786位点与原发性高血压发病有一定程度的相关性;②eNOS基因启动子-786位点T/T是原发性高血压的保护性基因;③eNOS基因启动子-786位点的基因型与原发性高血压的程度及血压节律改变无明显相关性.     

原发性高血压4个相关候选基因多态性与天津汉族人群原发性高血压的关系

目的 探讨原发性高血压(EH)4个相关候选基因多态性与天津汉族人群EH的关系.方法 选择天津汉族EH患者177例(EH组)及健康对照者212例(对照组),采用单碱基延伸—微阵列芯片法和PHASEv2.1单体型分析软件,检测和分析SELE rs5361 A/C、eNOS rs1799983 G/T、GNB3 rs5443 C/T和AGT rs699 C/T的基因多态性和单体型.结果 4个候选基因的基因型频率和等位基因频率,两组比较均无统计学意义(P均＞0.05).两组共检出15种单体型,其中EH组11种.单体型在两组分布比较差异无统计学意义(P＞0.05).结论 SELE rs5361A/C、eNOS rs1799983 G/T、GNB3 rs5443 C/T和AGT rs699 C/T的多态性与天津汉族人群EH发病无关.     

内皮型一氧化氮合酶基因多态性与冠心病的关系

内皮型一氧化氮合酶(eNOS)基因被列为冠心病(CHD)的一个候选易感基因。本文对与冠心病关系较为密切的三种eNOS基因多态性:4b/a、T786C和G894T的研究进展作一综述,对进一步认识冠心病的发病机制具有重要意义。     

内皮型一氧化氮合酶基因T786C多态性与缬沙坦降压疗效的关系

目的　探讨内皮型一氧化氮合酶 (eNOS)基因T786C多态性对缬沙坦降压疗效的影响。方法　采用多聚酶链式反应结合限制性内切酶片段长度多态分析方法检测 16 7例健康人和 2 6 7例高血压患者的eNOS基因T786C多态性。其中 10 9例病人口服缬沙坦治疗 4周。结果　 (1)EH组CT CC基因型和C等位基因频率显著高于对照组 (P <0 0 5 ) ;高血压患者中CT CC基因型携带者的舒张压 (99.6 6± 6 5 9)mmHg均高于TT基因型携带者 (97 32± 7 4 4 )mmHg ,且有显著性差异。(2 )缬沙坦对CT CC基因型患者降低收缩压和舒张压的作用强于TT基因型 ,(P <0 0 5 )。结论　eNOST786C基因多态性可作为高血压病人选用血管紧张素Ⅱ受体拮抗剂的参考指标之一。     

内皮型一氧化氮合酶基因T786C多态性与缬沙坦降压疗效的关系

目的探讨内皮型一氧化氮合酶(eNOS)基因T786C多态性对缬沙坦降压疗效的影响.方法采用多聚酶链式反应结合限制性内切酶片段长度多态分析方法检测167例健康人和267例高血压患者的eNOS基因T786C多态性.其中109例病人口服缬沙坦治疗4周.结果(1)EH组CT+CC基因型和C等位基因频率显著高于对照组(P＜0.05);高血压患者中CT+CC基因型携带者的舒张压(99.66±6.59)mmHg均高于TT基因型携带者(97.32±7.44)mmHg,且有显著性差异.(2)缬沙坦对CT+CC基因型患者降低收缩压和舒张压的作用强于TT基因型,(P＜0.05).结论eNOS T786C基因多态性可作为高血压病人选用血管紧张素Ⅱ受体拮抗剂的参考指标之一.     

Endothelial NO synthase genotype and risk of preeclampsia: a multicenter case-control study

Polymorphisms in the endothelial NO synthase (eNOS) gene have been evaluated as risk factors for preeclampsia. However, data from small studies are conflicting. We assessed whether eNOS genotypes alter the risk of preeclampsia in a population in which the incidence of this disorder is high. A total of 844 young pregnant women (322 preeclamptic and 522 controls) were recruited from 5 cities. Genotyping for the Glu298Asp, intron-4 and -786T-->C polymorphisms in the eNOS gene was conducted. Multivariate odds ratios (ORs) were obtained to estimate the association of individual polymorphisms and haplotypes with preeclampsia risk. No increase in the risk of preeclampsia for the intron-4 or -786T-->C polymorphisms was observed under any model of inheritance. In contrast, in women homozygous for the Asp298 allele, the adjusted OR for preeclampsia was 4.60 (95% confidence interval [CI], 1.73 to 12.22) compared with carriers of the Glu298 allele. After a multivariate analysis, carriage of the "Asp298-786C-4b" haplotype was also associated with increased risk of preeclampsia (OR, 2.11 [95% CI, 1.33 to 3.34]) compared with carriers of the "Glu298-786T-4b" haplotype. The eNOS Glu298Asp polymorphism and the Asp298-786C-4b haplotype are risk factors for preeclampsia.     

Endothelial nitric oxide synthase gene haplotype association with systemic lupus erythematosus

Endothelial nitric oxide synthase (eNOS) catalyses the production of nitric oxide, which has been shown to participate in the pathogenesis of systemic lupus erythematosus (SLE). eNOS gene polymorphism may have an effect on eNOS gene expression, eNOS protein synthesis and enzymatic activity. We investigated the influence of eNOS gene polymorphisms on susceptibility to SLE. eNOS T-786C, G894T and intron 4 27-base pair tandem repeat (VNTR4) polymorphisms were investigated in 152 SLE patients and 184 controls using RFLP-PCR, direct sequencing and fragment analysis. Allele, genotype and haplotype frequency comparisons, Hardy-Weinberg equilibrium and linkage disequilibrium (LD) analysis were performed. No significant association was detected between SLE and single-nucleotide polymorphisms (SNPs) T-786C and G894T. VNTR4 allele 4b was associated with susceptibility to SLE (OR 1.89, p?=?0.023), as was the genotype 4bb (OR 2.41, p?=?0.007). However, allele 4a was protective (OR 0.53, p?=?0.023), as was genotype 4ab (OR 0.41, p?=?0.007). T-786C and VNTR4 were in high LD (r (2?)=?0.34). Haplotypes T4bC and C4aG of the three tested polymorphisms had a susceptibility effect on SLE (OR 1.89 and 4.23 at p?=?0.005 and 0.001, respectively), while haplotypes T4aG and C4bG had a protective effect (OR 0.06 and 0.11 at p?=?0.000001 and 0.0005, respectively). The novel finding in our study is that individual eNOS polymorphisms probably do not exert a major influence on susceptibility to SLE, but they have significant effects when combined within a specific haplotype.     

Endothelial nitric oxide synthase Glu298Asp, 4b/a, and T-786C polymorphisms in type 2 diabetic retinopathy

Objective The possible association between the endothelial nitric oxide (eNOS) gene T‐786C (promoter region), 27‐bp repeat 4b/4a (intron 4), and Glu298Asp (exon 7) polymorphisms with diabetic retinopathy (DR) was investigated. Design A retrospective case‐control study. Patients A total of 872 type 2 diabetes (T2DM) patients were studied, of whom 383 presented with preproliferative/proliferative retinopathy (DR group), and 489 with absent/mild retinopathy (DWR group). Measurements Glu298Asp and T‐786C genotyping was carried out by PCR‐RFLP analysis, while 4b/4a was assessed by PCR. Genotype distribution was compared using the χ²‐test, and the contributions of the polymorphisms to DR were analysed by haplotype analysis and multivariate regression analysis. Results Lower prevalence of mutant 4a (P = 0·011), and heterozygous 4b/4a (P = 0·042) were seen in the DR compared to the DWR groups; the allele and genotype distribution of the Glu298Asp and T‐786C polymorphisms were comparable between DR and DWR groups. Three‐loci haplotype analysis demonstrated significant association between eNOS variants and DR, with protective [haplotype 122 (Glu298/4a/‐786C)], and susceptible haplotypes [haplotypes 112 (Glu298/4b/‐786C) and 222 (Asp298/4a/‐786C)] identified. Multivariate regression analysis confirmed the association between haplotypes 122 (P = 0·015); 112 (P = 0·027), and 222 (P = 0·048) and DR, after controlling for potential covariates (including age, sex, age of disease onset; HbA1c; hypertension, total cholesterol). Conclusions This study identifies genetic variation at the eNOS locus as genetic risk factor for diabetic retinopathy, which may serve as a useful marker of increased susceptibility to the risk of retinopathy.     

Association of the genetic variants of endothelial nitric oxide synthase gene with angiographically defined coronary artery disease and myocardial infarction in South Indian patients with type 2 diabetes mellitus

IntroductionThe polymorphic variants of endothelial nitric oxide synthase (eNOS) gene have been implicated in endothelial dysfunction and are highly relevant to macroangiopathies. We investigated the relationship between eNOS gene T-786C, G894T, intron 4a/b polymorphisms and coronary artery disease (CAD) in South Indian type 2 diabetic (T2DM) individuals.MethodsWe screened 283 T2DM patients, inclusive of 160 with angiographically defined CAD, 73 with myocardial infarction (MI), 89 without MI and 121 T2DM individuals with no evidence of CAD for eNOS gene polymorphisms.ResultsThere appeared to be a significant difference in the genotype and allele distribution of eNOS T-786C polymorphism between T2DM groups with and without CAD (p = 0.004), albeit no significant association with MI was observed. The frequencies of TC and CC genotypes and ? 786C allele were considerably higher in patients with triple vessel disease (TVD) as compared to those without CAD (p = 0.003), thereby associating this polymorphism with severity of CAD. Genotype and allele distributions of G894T and intron 4a/b polymorphisms were not significantly different between T2DM subjects with and without CAD/MI. Significant linkage disequilibrium was observed between intron 4a/b and T-786C polymorphisms. Multiple logistic regression analysis revealed a significant and independent association of eNOS T-786C polymorphism and other putative risk factors with CAD/TVD in T2DM individuals.ConclusionsThese findings reveal a significant association between eNOS T-786C polymorphism, CAD/TVD and coincident putative risk factors in T2DM individuals in South Indian population.     

Genetic susceptibility to atrial fibrillation in patients with congestive heart failure

BACKGROUND: Previous reports demonstrate an association between atrial fibrillation (AF) and certain polymorphisms in genes controlling the production of angiotensin-converting enzyme (ACE) and endothelial nitric oxide synthase (eNOS). OBJECTIVES: The purpose of this study was to examine the association between polymorphisms of ACE and eNOS gene complexes and AF in an unselected series of patients with congestive heart failure (CHF). METHODS: In each of the 340 unselected, unrelated patients with CHF, common polymorphisms in ACE (I/D) and eNOS (T786C, G894T, and intron 4b/a) gene complexes were evaluated. Associations between individual genotypes and the presence of AF were assayed. RESULTS: AF was present in 51 patients (15%) and was significantly associated with the ACE D/D (odds ratio 1.5) and eNOS 894 T/T genotypes (odds ratio 3.2). There were no significant associations between AF and eNOS 786 or eNOS intron 4 genotypes. CONCLUSION: In patients with CHF, the presence of AF was significantly associated with certain ACE and eNOS genotypes.     

An additive effect of endothelial nitric oxide synthase gene polymorphisms contributes to the severity of atherosclerosis in patients on dialysis

BACKGROUND: Reduced synthesis of nitric oxide (NO) is considered a major proatherogenic mechanism in patients with end-stage renal disease (ESRD), but genetic factors impinging on this mechanism have been little studied in this population. METHODS: We tested the relationship between carotid intima-media thickness (IMT) and three endothelial NO synthase (eNOS) polymorphisms (G894T, T-786C, and 27-bp repeat in intron 4) in an ethnically and geographically homogeneous group of 147 patients with ESRD. RESULTS: The IMT was significantly thicker (P = .01) in patients with the TT genotype (G894T polymorphism) than in patients with TG or GG genotypes, and a similar association was observed for the T-786C polymorphism (P = .02). These relationships remained statistically significant (P = .02 and .01), also in multivariate models including traditional and emerging risk factors for atherosclerosis. Moreover, there was a direct association between the number of risk alleles and IMT (no risk allele: 0.97 +/- 0.22 mm, 1 risk allele: 1.03 +/- 0.20 mm, 2 risk alleles: 1.07 +/- 0.22 mm, > or =3 risk alleles: 1.23 +/- 0.36 mm, P < .001) that remained statistically significant in a multiple regression model. CONCLUSIONS: In patients on dialysis the risk alleles of G894T and T-786C polymorphisms of the eNOS gene are associated with carotid atherosclerosis. The additive effect of the two polymorphisms may contribute to the severity of atherosclerosis independently of other risk factors and of endogenous substances that influence the NO synthesis in this population.     

Susceptible and protective eNOS haplotypes in hypertensive black and white subjects

Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene have been inconsistently associated with hypertension. This inconsistency may derive from population stratification secondary to ethnic diversity, and consideration limited to only one rather than combinations of polymorphisms. We studied three genetic variations in the eNOS gene: a single nucleotide polymorphism in the promoter region (T-786C), in exon 7 (Glu298Asp), and a variable number of tandem repeats in intron 4 (b/a) of the eNOS gene in hypertensives (112 whites and 91 blacks) and normotensives (113 whites and 87 blacks). In addition, we also examined the association of eNOS gene haplotypes with hypertension in white and black subjects. No differences were observed in the frequencies of genotypes and alleles of the three polymorphisms when white hypertensives and white normotensives were compared, or when black hypertensives and black normotensives were compared (all P>0.05). Conversely, the haplotypes "T Asp b" and "C Glu b" were more common among white (16 and 24%, respectively) and black (17 and 16%, respectively) normotensives than in white (7 and 8%, respectively) and black (4 and 6%, respectively) hypertensives, respectively (all P<0.0039). In addition, the haplotype "C Asp b" was more commonly found in white hypertensives than in white normotensives (P=0.0007). These results suggest a contribution of eNOS haplotypes to the development of hypertension that is obscured when specific eNOS genotypes alone are considered. In addition, our results suggest two eNOS haplotypes associated with a protective effect against hypertension in both ethnic groups, and one eNOS haplotype conferring susceptibility to hypertension in white subjects.     

Lack of evidence for association between endothelial nitric oxide synthase gene polymorphisms and coronary artery disease in the Australian Caucasian population

BACKGROUND: Genetic polymorphism in the gene for endothelial nitric oxide synthase (eNOS) has been identified as a potential risk factor for the development of premature coronary artery disease (CAD). We determined whether the eNOS 4ab, G894T, and T-786C polymorphisms are associated with premature coronary artery disease. DESIGN: A case-control study. METHODS: PCR-based assays were used to compare the frequency of eNOS gene polymorphisms in 573 Caucasian subjects aged under 50 years presenting with symptomatic CAD and documented by coronary angiography, with or without myocardial infarction, to that of 624 similarly aged community controls without a history of symptomatic CAD. RESULTS: We found no difference in the frequency of 4ab genotypes between cases and controls: in the CAD subjects, the 4aa, 4ab, and 4bb genotype frequencies were 1.9%, 24.3% and 73.8% respectively, compared to 2.2%, 25.5% and 72.3% respectively for the controls. There was also no significant difference between cases and controls in the frequency of any allele (4a/4b, 894G/894T, -786C/-786T), or genotype for any of the polymorphisms. Similarly, logistic regression analysis showed no evidence for an association of the polymorphisms with premature CAD or myocardial infarction or any indication of an interaction between the polymorphisms and other CAD risk factors, including smoking. CONCLUSIONS: In a large case-control study, and in contrast to some earlier positive findings by others, we have found no evidence for an association between several eNOS gene polymorphisms and premature CAD in an Australian Caucasian population.     

Variants of endothelial nitric oxide synthase gene are associated with components of metabolic syndrome in an Arab population

Genetics plays a crucial role in the development of metabolic syndrome (MetS). Here we examined the association between endothelial nitric oxide synthase (eNOS) gene polymorphisms and MetS in a Saudi Arabian cohort to extend the understanding of the genetic basis of MetS in diverse ethnic populations. Anthropometric, clinical and biochemical parameters as well as genotyping for 894G>T, -786T>C variants of eNOS gene by PCR-RFLP and 4a/b by direct PCR were performed in 886 Saudi Arabians (477 MetS and 409 Non-MetS). The genotype distribution (TT, p=0.001; TC, p=0.001; TC+CC, p=0.001) and allele (T, p=0.007; C, p=0.007) frequency of the -786T>C SNP were significantly different between Non-MetS and MetS subjects which remained significant after Bonferroni correction. Moreover: 1) the GT and GT+TT genotypes of the 894G>T SNP were associated with elevated blood pressure (p=0.017, and p=0.022, respectively); 2) the ab variant of 4a/b polymorphism was associated with decreased HDL levels (p= 0.044); and 3) the TC+CC genotype and C allele of the -786T>C SNP were associated with increased fasting glucose levels (p=0.039, and p=0.028, respectively). Also, G-a-C was identified as the risk haplotype for MetS susceptibility (p=0.034). The results suggest a significant association of 894G>T, 4a/b and -786T>C polymorphisms with MetS and its components is present in an Arab population. A genetic predisposition to develop abnormal metabolic phenotypes, consistent with an increased prevalence of metabolic phenotypes can be detected in this ethnic group.