缺血性心脏病与β-纤维蛋白原基因bcl-I多态性和血浆纤维蛋白原水平的关系

目的:探讨β纤维蛋白原基因bcl-I多态性与血浆纤维蛋白原水平及缺血性心脏病发病机制的关系。方法:应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法对57例心肌梗塞组和50例健康对照组进行β-纤维蛋白原基因bcl-I多态性分析;采用组织凝血活酶法测定血浆纤维蛋白原水平。结果:酶切后可见在2 500 bp和1 100 bp+1 400 bp碱基对位置分别发现2个等位基因B1和B2。携带B1等位基因心肌梗塞患者血浆纤维蛋白原水平(3.28±0.94)g.L-1明显高于健康对照组(2.74±0.54)g.L-1(P<0.05),携带B2等位基因心肌梗塞患者血浆纤维蛋白原水平(3.97±1.02)g.L-1明显高于健康对照组(3.25±0.61)g.L-1(P<0.05);B2等位基因频率明显增高(P<0.05);B2基因携带者血浆纤维蛋白原水平明显高于同组内B1基因携带者血浆纤维蛋白原水平(P<0.05)。结论:血浆纤维蛋白原水平升高与心肌梗塞有关联;β-纤维蛋白原基因bcl-I多态性与血浆纤维蛋白原水平及心肌梗塞有关联,β-纤维蛋白原基因bcl-I多态性可能是缺血性心脏病危险因素及遗传易感标志之一。     

β-纤维蛋白原基因-455G/A多态性与脑梗死的关系

①目的　研究 β 纤维蛋白原基因启动子区域 - 4 5 5G/A基因变异与血浆纤维蛋白原水平及脑梗死的相关性。②方法　随机抽取住院高血压脑梗死病人 86例 (脑梗死组 ) ,高血压非脑梗死病人 85例 (高血压组 ) ,门诊健康查体者 90例 (对照组 ) ,用多聚酶链反应加HaeⅢ内切酶检测 β 纤维蛋白原基因启动子区域 - 4 5 5G/A的多态性。③结果　脑梗死组A-455等位基因的分布频率明显高于高血压组及对照组 (χ2 =7.0 1、4 .4 0 ,P <0 .0 1、0 .0 5 )。④结论　血浆中纤维蛋白原水平受 β 纤维蛋白原基因 - 4 5 5G/A多态性的影响 ,A-455等位基因是脑梗死的一个相对独立的危险因素。     

冠心病患者血浆纤维蛋白原β-148C/T 基因多态性的研究

为研究β纤维蛋白原基因启动子区 Hind β多态性和血浆纤维蛋白原浓度与冠心病之间的关系。对确诊的冠心病患者 5 6例 ,健康对照组 4 4例 ,采用酚 /氯仿抽提方法从白细胞中提取人基因组 DNA ,经多聚酶链式反应(PCR)加 Hind 内切酶技术检测目的基因片段 ,采用自动化检测系统求出血浆纤维蛋白原 (Fg)浓度。结果发现 :冠心病患者βHind 多态性与血浆纤维蛋白原浓度间存在显著正相关 (r=0 .7,P<0 .0 0 1) ,以非βHind 酶切位点缺失的CT、 CC基因型血浆纤维蛋白原浓度明显增高 (P<0 .0 1)。提示 :β Hind 多态性可能是冠心病患者动脉血栓形成的主要原因之一     

缺血性心脏病与β-纤维蛋白原基因bcl-Ⅰ多态性和血浆纤维蛋白原水平的关系

目的:探讨β纤维蛋白原基因bcl-Ⅰ多态性与血浆纤维蛋白原水平及缺血性心脏病发病机制的关系.方法:应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法对57例心肌梗塞组和50例健康对照组进行β-纤维蛋白原基因bcl-Ⅰ多态性分析;采用组织凝血活酶法测定血浆纤维蛋白原水平.结果:酶切后可见在2 500 bp和1 100 bp 1 400 bp碱基对位置分别发现2个等位基因B1和B2.携带B1等位基因心肌梗塞患者血浆纤维蛋白原水平(3.28±0.94)g·L-1明显高于健康对照组(2.74±0.54)g·L-1(P＜0.05),携带B2等位基因心肌梗塞患者血浆纤维蛋白原水平(3.97±1.02)g·L-1明显高于健康对照组(3.25±0.61)g·L-1(P＜0.05);B2等位基因频率明显增高(P＜0.05);B2基因携带者血浆纤维蛋白原水平明显高于同组内B1基因携带者血浆纤维蛋白原水平(P＜0.05).结论:血浆纤维蛋白原水平升高与心肌梗塞有关联;β-纤维蛋白原基因bcl-Ⅰ多态性与血浆纤维蛋白原水平及心肌梗塞有关联,β-纤维蛋白原基因bcl-Ⅰ多态性可能是缺血性心脏病危险因素及遗传易感标志之一.     

FcεRⅠβ基因多态性与湖北地区儿童变应性哮喘的关系

目的　探讨IgE高亲和力受体 β链基因 (FcεRⅠβ)启动子 - 10 9位和编码区Glu2 37Gly基因多态性与湖北儿童变应性哮喘及血浆总IgE的关系。方法　采用聚合酶链反应 限制性片段长度多态性技术检测 110例儿童变应性哮喘患者和 92例相匹配对照者FcεRⅠ β基因启动子区 - 10 9位和编码区Glu2 37Gly两位点多态性。结果　①儿童变应性哮喘患者FcεRⅠ β基因启动子区 - 10 9位T/T、T/C和C/C基因型频率是 0 391、 0 4 91和 0 118;与对照相比差异无显著性意义 (χ2 =0 0 2 34,P >0 0 5 ) ,但儿童变应性哮喘组T/T基因型患者血浆总IgE对数值为 2 4 78± 0 94 4 ,与T/C基因型的 2 2 87± 1 114和C/C基因型的 2 315± 0 86 6相比差异具有显著性意义 (F =4 336 ,P <0 0 1)。②FcεRⅠ βGlu2 37Gly位点Glu/Glu、Glu/Gly和Gly/Gly型频率为 0 5 91、 0 36 4和 0 0 4 5 ,与正常对照相比差异具有显著性意义 (χ2=6 5 86 ,P <0 0 5 ) ,Gly/Gly型血浆总IgE对数值为 2 6 2 3± 0 96 2 ,与Glu/Glu的 2 30 6± 0 915和Glu/Gly的 2 4 18±0 894相比差异具有显著性意义 (F =6 6 5 4 ,P <0 0 1)。结论　IgE高亲和力受体 β链启动区 - 10 9位T/T型与血浆总IgE相关 ,编码区 2 37位Gly/Gly型与儿童变应性     

瘦素基因启动子区-2548G/A功能多态性与抗精神病药源性肥胖的相关分析

目的　探讨瘦素基因启动子区 - 2 5 4 8G/A功能多态性是否与首次治疗精神分裂症患者的抗精神病药物 (APS)急性期治疗导致的体重增加相关。方法　采用聚合酶链反应 限制片段长度多态性 (PCR RFLP)技术分析 12 8例患者 (男 6 1例 ,女 6 7例 ) - 2 5 4 8G/A等位基因和基因型分布频率 ,APS(利培酮或氯丙嗪 )单药治疗 10周 ,治疗前后每周测体重和体重指数 (BMI) ,采用MRI测治疗前后腹部脂肪分布 (30例 ) ,分析等位基因和基因型与基础体重指标和其变化值的相关性 ;同时分析 38名性别、年龄和BMI相匹配的健康对照者 ,其中 2 2例进行MRI扫描。结果　治疗后患者体重增加是基础体重的 (6 .2± 5 .7) % ,腹部脂肪增加是基础腹部皮下脂肪 (SUB)的 (38.5± 4 2 ) %、腹内脂肪的 (4 0 .0± 4 1.2 ) % ;- 2 5 4 8G/A等位基因和基因型在患者组和对照组分布频率差异无显著意义 ;在体重增加≤ 7%和 >7%患者组等位基因和基因型分布频率差异有非常显著意义 (χ2 =7 5 2 9,df =1,P =0 .0 0 6 ;OR =1.94 1;95 %CI:1.175～ 3.2 0 7) ;基因型对患者组或对照组的基础体重指标无显著影响 ;与携带G等位基因患者相比 ,AA基因型携带者治疗后BMI(P =0 .0 0 3)和SUB(P =0 .0 0 9)明显增加。结论　瘦素基因启动子区 - 2 5 4 8G/A功能多态     

白细胞介素-6基因启动子-572C/G多态性与脑梗死关系的研究

目的　探讨白细胞介素 6(IL 6)基因启动子 5 72C/G多态性各等位基因及基因型在脑梗死患者中的分布频率 ,并分析其基因型及血清水平与脑梗死的关系。方法　采用聚合酶链反应 限制性片段长度多态性 (PCR RFLP)技术检测 160例脑梗死患者及 175例健康者 (对照组 )IL 6基因启动子 5 72C/G多态性 ,同时采用酶联免疫吸附试验 (ELISA)检测两组IL 6水平。结果　脑梗死组IL 6血清水平显著高于对照组 (P <0 .0 1) ,IL 6基因启动子 5 72C/G基因型频率和等位基因频率在脑梗死组和对照组间比较差异有显著性 (P <0 .0 5 ) ,经等位基因频率的相对风险分析发现 ,G等位基因携带者发生脑梗死的风险是C等位基因的 1.60 6倍 (OR =1.60 6,95 %CI:1.10 5～ 2 .3 3 4) ,携带G等位基因的脑梗死患者IL 6血清水平显著高于不携带者 (P <0 .0 5 )。结论　IL 6基因启动子 5 72C/G多态性与脑梗死的发病具有相关性 ,G等位基因可能是脑梗死发病的遗传易感基因 ,携带G等位基因的个体可能通过促进IL 6的高度表达进而增加脑梗死的发病风险     

血纤维蛋白原浓度对心绞痛分型的临床意义

目的 :探讨血纤维蛋白原浓度测定对心绞痛分型的临床意义。方法 :根据加拿大心脏病学会心绞痛分型标准 ,将2 5 8例入选的心绞痛患者 ,分成不稳定性心绞痛组 (UAP组 ,n=16 2 )及稳定性心绞痛组 (SAP组 ,n=96 ) ,同时测定两组血浆纤维蛋白原浓度。结果 :不稳定性心绞痛组血纤维蛋白原浓度明显高于稳定性心绞痛组 (4 5 8.5 6± 186 .32 ) mg/dl比 (4 0 1.15± 14 8.6 2 ) mg/ dl,P<0 .0 1。结论 :血纤维蛋白原浓度有助于心绞痛的分型 ,纤维蛋白原升高提示 ,不稳定性心绞痛患者有较强的血栓形成病理基础     

E-选择素S128R多态性与冠心病的关系

目的　探讨 E-选择素 S12 8R多态性与冠心病的关系。　方法　用聚合酶链反应 -限制性片段长度多态性 (PCR- RFL P)方法探查 E-选择素 S12 8R多态性在对照组和冠心病组中的基因频率分布。　结果　冠心病组 R等位基因频率高于对照组 (11.96 % vs 4 .71% ,P<0 .0 5 ) ,SR+RR基因型者空腹血浆 E-选择素水平高于 SS基因型者 (33.2 3± 7.2 0 vs 2 2 .5 8± 8.2 8ng/ m l,P<0 .0 5 )。　结论　 E-选择素 S12 8R多态性与冠心病的发生有关 ,R等位基因可能是冠心病的危险因素     

PAI-1基因启动子区4G/5G多态性与肺心病的相关性

①目的　探讨血浆纤溶酶原激活物抑制因子 1 (PAI 1 )基因启动子区单核苷酸插入 /缺失 (4G/ 5G)多态性与肺心病的相关性。②方法　以外周血白细胞基因组为模板 ,应用多聚酶链反应 (PCR)检测 4 0例健康查体者和 6 0例肺心病病人 (其中并发肺栓塞 1 9例 )PAI 1基因启动子区 4G/ 5G多态性的基因型。③结果　对照组与肺心病组比较PAI 1基因启动子区 4G/ 5G多态性基因型差异无显著性。肺心病组女性 4G等位基因频率高于男性 ,差异有显著性 (χ2 =4 .30 ,P <0 .0 5 )。肺栓塞组 4G/ 4G基因型与 4G等位基因频率和对照组相比差异无显著性。④结论　PAI 1基因多态性与肺心病无明显相关性 ,4G等位基因在女性中有可能与其他因素协同促进肺心病的发生。     

急性脑梗死患者β纤维蛋白原—455G／A基因多态性和血浆纤维蛋？…

目的 探讨β－纤维蛋白原基因启动子区－４５５Ａ／Ｇ多态性和血浆纤维蛋白原水平的关系以及在缺血性及脑血管病中的作用。方法 应用ＰＣＲ－ＲＦＬＰ（ＨａｅⅢ）方法对９１例脑梗死患者、７４例选择性无血栓患者和９８例年轻健康献血员进行β－纤维蛋白质基因启动子区－４５５Ａ／Ｇ多态性分析;血浆纤维蛋白原水平测定使用凝血酶原时间法。计算资料间比较使用ｔ检验,但由于纤维蛋白原浓度呈患者明显较无血栓对照组高（２２．７     

β-FIBRINOGEN PROMOTER-455 G／A （HaeⅢ） POLYMORPHISM PREDICTION OF PLASMA FIBRINOGEN BUT NOT OF ISCHEMIC CEREBROVASCULAR DISEASE

Objective The-455 G/A (HaeⅢ) polymorphism of β-fibrinogen gene influences levels of plasma fibrinogen. We further investigated whether it influences the risk of isehemie cerebrovaseular disease. Methods We accumulated 134 acute isehemic eerebrovaseular disease (ICVD) eases and compared their -455 G/A status with a control group (n=166). The β-fibrinogen gene -455 G/A polymorphism was analyzed for all subjects by PCR-RFLP with the restrictive enzyme HaeⅢ. Results Plasma fibrinogen was higher in AA homozygous participants (341mg/dL) than in participants carrying the G allele: GA (290mg/dL), GG (298mg/dL) in the control group. Plasma fibrinogen was also higher in AA homozygous patients (353mg/dL) than in eases carrying the G allele: GA (287mg/dL), GG (302mg/dL) in the ICVD group. However, there was no significant association between β-fibrinogen gene -455 G/A polymorphism and ICVD group. Conclusions Although a small effect cannot be excluded, β-fibrinogen gene -455 G/A polymorphism is an independent predictor of plasma fibrinogen, but not of isehemie cerebrovaacular disease.     

A Meta-analysis of β-fibrinogen Gene-455G/A Polymorphism and Plasma Fibrinogen Level in Chinese Cerebral Infarction Patients

Objective To evaluate the correlation between the β-fibrinogen gene-455G/A polymorphism and cerebral infarction in Chinese population by means of meta-analysis. Methods Genetic association studies on evaluating the β-fibrinogen gene -455G/A polymorphism and cerebral infarction involving Chinese population published before December 2005 were collected from database of PubMed, EMBASE, and CNKI. All the data in literature were abstracted based on the defined selection criteria by two independent investigators. Publication bias was tested by funnel plot and the odd ratios of all studies were combined dependent on the result of heterogeneity test among the individual studies. The software Review Manager (Version 4.2) was used for meta-analysis. Results Eleven studies including 1405 patients and 1600 controls met the selection criteria. There was no publication bias in 11 reviewed studies. Heterogeneity test of reviewed studies showed statistically significant differences (χ2=24.58, P=0.006) among the ORs of individual studies. The combined OR of 11 studies of susceptibility to cerebral infarction in –455A allele carriers compared with the -455G/G wild homozygotes was 1.33 (95%CI 1.04-1.71, P=0.02). In the patients with cerebral infarction in 6 studies, the summarized average plasma fibrinogen level of allele A carrier was 0.29 g/L (95%CI 0.14-0.44, P=0.0002) higher than that of -455G/G homozygous ones. Conclusions β-fibrinogen gene -455G/A polymorphism might contribute to susceptibility of cerebral infarction in Chinese population; allele A increases the individual susceptibility to the disease.     

Levels of plasma fibrinogen and D-dimer in subjects with subclinical hyperthyroidism.

BACKGROUND: During the last 15 years, several risk markers for atherosclerosis, such as fibrinogen and D-dimer, have been identified. The role of elevated fibrinogen levels as an independent risk factor for coronary, cerebral, and peripheral vascular disease is well established on the basis of clinical and epidemiological studies. Increased D-dimer levels are associated with increased risk of future myocardial infarction, stroke, and peripheral vascular disease. The aim of this study was to evaluate the alterations in fibrinogen and D-dimer, which indicates overall thrombotic activity, in subjects with subclinical hyperthyroidism. MATERIAL/METHODS: Thirty-six subclinical hyperthyroidic subjects and 36 euthyroidic control subjects matched for age, gender, and body mass index were selected. The levels of plasma fibrinogen and D-dimer in all subjects were measured. RESULTS: The level of fibrinogen was significantly higher in the subclinical hyperthyroidic group than in the euthyroidic group (296.9+/-74.3 mg/dl vs. 255.0+/-41.7 mg/dl, p<0.001). The level of D-dimer was significantly higher in the subclinical hyperthyroidic group than in the euthyroidic group (261.9+/-47.8 mg/dl vs. 216.4+/-32.1 mg/dl, p<0.000). CONCLUSIONS: The results suggest that subjects with subclinical hyperthyroidism present a relatively hypercoagulable state. This state could contribute to increased thromboembolic risk in subclinical hyperthyroidism.     

青年缺血性脑卒中与MTHFRC677T、CBS844ins68基因多态性的关系

目的：研究人MTHFR、CBS基因多态性与青年缺血性脑卒中的遗传关联性。方法：采用限制性内切酶片段长度多态性方法（PCR-RFLP）,对98例脑卒中患者（病例组）和116例健康人（对照组）MTHFR C677T及CBS844ins68多态性位点进行检测。结果：病例组MTHFR基因T、C等位基因频率分别为54.09%和45.91%,对照组为37.93%和62.07%,两组比较差异有显著性（P<0.05）。TT型携带者与CC型携带者罹患脑卒中比较相对危险度为2.83,T等位基因携带者与C等位基因携带者罹患脑卒中比较相对危险度为1.93。CBS844ins68多态性位点在病例组与对照组之间D/I 2种等位基因及基因型分布频率差异无显著性(P>0.05)。Logistic回归分析显示MTHFRC677T是青年缺血性脑卒中的一个独立危险因子,且吸烟及高血压也与之有关联(P<0.01)。结论：汉族人群MTHFR C677T位点多态性与青年缺血性脑卒中有相关性,MTHFR基因可能是青年缺血性脑卒中的一个易感基因。CBS844ins68多态性位点与青年缺血性脑卒中无关联。     

血清脂蛋白(a)水平与青年缺血性卒中CISS分型及严重程度的关系

目的 探讨血清脂蛋白(a)[Lp(a)]与不同中国缺血性卒中亚型(CISS分型)青年缺血性卒中之间的关系,为其防治提供依据.方法 收集蚌埠医学院第一附属医院2017年4月-2019年12月收治的122例青年缺血性卒中患者的临床资料作为青年卒中组,随机选取同期入院治疗的年龄≥45岁缺血性卒中患者122例作为中老年卒中组,...     

A meta-analysis of relationship between β-fibrinogen gene -148C/T polymorphism and susceptibility to cerebral infarction in Han Chinese

Objective The results of studies on association between -148C/T polymorphism in promoter region of β-fibrinogen gene and susceptibility to cerebral infarction in Chinese population are controversial. In this study, we summarize the results of published works in this field by a meta-analysis. Data sources Genetic association studies evaluating the β-fibrinogen gene -148C/T polymorphisms and cerebral infarction involving Chinese population published before December 2005 were collected from PubMed, EMBASE and CNKI. Study selection Case control studies involving unrelated, Han subjects aged from 18 to 80 years, and the internationally recognized diagnostic standard of cerebral infarction and genotype frequencies in control group consistent with Hardy-Weinberg equilibrium were used. Publication bias was tested by funnel plot and the odds ratios of all studies were combined dependent on the result of heterogeneity test among the individual studies. The software Review Manager (Version 4.2) was used for meta-analysis. Results Eleven studies including 1223 patients and 1433 controls met the selection criteria. There was no heterogeneity among the odds ratios (ORs) of individual studies (χ(2)=17.82, P=0.06). The combined OR of susceptibility to cerebral infarction in -148T allele carriers compared to the wild homozygote was 1.32 (95%CI 1.12 to 1.55, P=0.0008). In the patients with cerebral infarction, the average plasma fibrinogen level of allele T carrier was 0.42 g/L (95%CI 0.29 to 0.54, P&lt;0.001), higher than that of -148C/C homozygous ones. Conclusions β-fibrinogen gene -148C/T polymorphism might contribute to susceptibility to cerebral infarction in Han Chinese. To reach a definitive conclusion, further gene to gene and gene to environment interactions studies on β-fibrinogen polymorphisms and cerebral infarction with large sample size are required.     

High-density lipoprotein cholesterol and ischemic stroke in the elderly: the Northern Manhattan Stroke Study

CONTEXT: Elevated high-density lipoprotein cholesterol (HDL-C) levels have been shown to be protective against cardiovascular disease. However, the association of specific lipoprotein classes and ischemic stroke has not been well defined, particularly in higher-risk minority populations. OBJECTIVE: To evaluate the association between HDL-C and ischemic stroke in an elderly, racially or ethnically diverse population. DESIGN: Population-based, incident case-control study conducted July 1993 through June 1997. SETTING: A multiethnic community in northern Manhattan, New York, NY. PARTICIPANTS: Cases (n = 539) of first ischemic stroke (67% aged >/=65 years; 55% women; 53% Hispanic, 28% black, and 19% white) were enrolled and matched by age, sex, and race or ethnicity to stroke-free community residents (controls; n = 905). MAIN OUTCOME MEASURE: Independent association of fasting HDL-C levels, determined at enrollment, with ischemic stroke, including atherosclerotic and nonatherosclerotic ischemic stroke subtypes. RESULTS: After risk factor adjustment, a protective effect was observed for HDL-C levels of at least 35 mg/dL (0.91 mmol/L) (odds ratio [OR], 0.53; 95% confidence interval [CI], 0.39-0.72). A dose-response relationship was observed (OR, 0.65; 95% CI, 0.47-0.90 and OR, 0.31; 95% CI, 0.21-0.46) for HDL-C levels of 35 to 49 mg/dL (0.91-1.28 mmol/L) and at least 50 mg/dL (1.29 mmol/L), respectively. The protective effect of a higher HDL-C level was significant among participants aged 75 years or older (OR, 0.51; 95% CI, 0.27-0.94), was more potent for the atherosclerotic stroke subtype (OR, 0.20; 95% CI, 0.08-0.50), and was present in all 3 racial or ethnic groups studied. CONCLUSIONS: Increased HDL-C levels are associated with reduced risk of ischemic stroke in the elderly and among different racial or ethnic groups. These data add to the evidence relating lipids to stroke and support HDL-C as an important modifiable stroke risk factor.     

TIMP-2基因-418G/C多态性与房颤性脑梗死的关系研究

目的 心房颤动引起的梗死是目前缺血性卒中患者高死亡率的主要原因之一,基于基质金属蛋白酶抑制因子(TIMP)在房颤心肌维化过程中重要作用,本文探讨了TIMP-2基因启动子-418G/C多态性与房颤引起脑梗死的关系。方法 采用聚合酶链反应-限制性片段长多态性法对2016年1月—2018年6月浙江省台州医院神经内科首次因房颤性脑梗死住院患者204例(观察组)及非心源性脑梗死248例(对照组)进行TIMP-2基因启动子区-418G/C多态性检测,并对2组患者的一般情况及基因型、等位基因等进行比较。结果 观察组和对照组性别、年龄、吸烟、饮酒、入院时收缩压及舒张压、空腹血糖、甘油三酯、总胆固醇、低密度脂蛋白胆固醇、纤维蛋白原、同型半胱氨酸等差异均无统计学意义(均P>0.05)。观察组GC+CC基因型共94例(46.1%),对照组GC+CC基因型共90例(36.3%),2组比较差异有统计学意义(P=0.043,95%CI:1.017～1.585),观察组C等位基因115例(28.2%),与对照组[106例(21.4%)]比较差异有统计学意义(P=0.020,95%CI:1.049～1.658)...     

The effect of foods containing refined Konjac meal on human lipid metabolism

A total of 110 elderly people with hyperlipidemia were randomly assigned to one of two groups. The experimental group consumed an ordinary diet plus foods containing refined Konjac meal, and the control group consumed only the ordinary diet. The experiment was carried out for 45 days. The results indicate that for the experimental group blood levels of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were significantly lowered (P less than 0.01) at the end of the trial, whereas high-density lipoprotein cholesterol (HDL-C) and apoprotein (AI) levels were significantly elevated (P less than 0.01). In contrast, for the control group, the changes in the above parameters were insignificant. The differences in TC, TG, LDL-C, and HDL-C levels between the two groups were statistically significant. The effects of refined Konjac meal on lipid levels in the blood were somewhat different between patients with hyperlipidemia and subjects with risk critical values only. For the former, TG and TC were decreased by 83.8 +/- 133.5 mg/dl, and 42.4 +/- 23.4 mg/dl, respectively; but for the latter, they are decreased only by -1.1 +/- 23.1 mg/dl and 8.3 +/- 18.2 mg/dl, respectively; the difference mentioned above is statistically significant (P less than 0.01).