Effects of Storage Time and Hydrogen Peroxide on the Formation of Soy Globulin 15S in 11S Dilute Solutions Investigated by Analytical Ultracentrifugation

Two soy protein 11S fractions with different surface sulfhydryl contents were prepared.Utilizing analytical ultracentrifugation,the effects of storage time and hydrogen peroxide at different concentrations(0.5-100 mmol/L)on the two 11S fractions were investigated.Results show that after removing 2-mercaptoethanol(2-ME)by size exclusion chromatography,the 11S fraction with high surface sulfhydryl content(2.0 mol sulfhydryl/mol 11S)progressively formed 15S and 21S in dilute solutions during storage at 4℃ for 82 days.While,the 11s fraction with low surface sulfhydryl content(0.2 mol sulfhydryl/mol 11S)was stable under the same condition.Moreover,after treating the 11s with high surface sulfhydryl content with 1 mmol/L H_(2)O_(2),the weight percentage of 15S reached the maximum value of 20%.The 15S induced by air and H_(2)O_(2)could be totally converted to 11S with the addition of 10 mmol/L 2-ME,which could be attributed to that the disulfide bond linking two 11S molecules is on the surface of the 15S and easily accessible to the reducing agent 2-ME.This study helps us to deeply understand the formation mechanism of 15S and the stability of 11S.

略论《管子》四篇的黄老哲学思想

阐释《管子》一书中《内业》、《白心》、《心术上》和《心术下》四篇文章的思想内容。这四篇文章向来被认为是道家黄老学派的经典文献。结合《老子》、《庄子》、《韩非子》等文献对四篇文章中“道”、“守一”、“名实”、“因应”四个基本概念进行论证和分析。通过对这四篇文章的分疏和解释 ,指明黄老道家与庄子道家的根本差异 。

人心肌肌钙蛋白C两种突变转基因小鼠模型建立与对比分析

目的为建立心肌组织特异性表达人cTnCD145E和cTnCG159D突变基因转基因小鼠,为对比分析两种不同心肌病的发生发展建立模型。方法利用定点突变技术分别制备人cTnC基因的cTnCD145E和cTnCG159D两个突变体,随后插入心肌特异性表达启动子α-MHC下游构建人cTnCD145E和cTnCG159D基因转基因载体。通过显微注射法建立转基因C57BL/6小鼠。利用心脏超声和病理观察对比分析不同年龄转基因小鼠心脏的结构与功能。结果建立了心肌组织高表达人cTnCD145E和cTnCG159D突变基因转基因小鼠,cTnCD145E和cTnCG159D转基因小鼠随年龄增加,有分别向HCM和DCM发展的趋势,12月龄时,cTnCD145E转基因小鼠收缩末期和舒张末期左室容积(left ventricle end-diastolic volume and end-systolic volume,EDV and ESV)与同窝阴性小鼠相比下降,射血分数(ejection fraction,EF)和收缩末期左心室后壁厚度(left ventricle end-systolic posterior wall thickness,ESPWT)增加,而cTnCG159D转基因小鼠EDV和ESV与同窝阴性小鼠相比上升,EF和ESPWT减少。结论心肌组织特异性表达人cTnCD145E突变基因转基因小鼠表现肥厚型心肌病病理表型,而心肌组织特异性表达人cTnCG159D突变基因转基因小鼠表现扩张型心肌病病理表型,二者可作为对比研究由不同发病机制导致的心肌病模型。

心肌酶诊断重症急性胰腺炎并发心功能不全的临床价值

目的探讨心肌酶对重症急性胰腺炎(SAP)并发心功能不全的诊断价值。方法将50例SAP患者按是否并发心功能不全分为心功能不全组14例和无心功能不全组36例,测量血清心肌肌钙蛋白I(cTnI)、肌红蛋白(MYO)、肌酸激酶MB型(CK-MB)、乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST),用ROC曲线评价心肌酶诊断SAP并发心功能不全的敏感性和特异性。记录患者的急性病生理学和长期健康评价(APACHE)Ⅱ分值,并评价心肌酶与APACHEⅡ评分之间的相关性。结果心功能不全组cTnI、LDH、AST水平均明显高于无心功能不全组(P<0.05),MYO、CK-MB与无心功能不全组差异无统计学意义。cTnI的ROC曲线下面积最大为0.940,cut-off值为0.07μg/L,敏感性和特异性分别为0.857和1.000。LDH、AST的ROC曲线下面积大于0.7,但LDH诊断敏感性仅为0.571,AST的特异性仅为0.778。MYO、CK-MB的ROC曲线下面积小于0.7。APACHEⅡ评分与心肌酶中cTnI、CK-MB、LDH呈正相关(r分别为0.639、0.451、0.552,均P<0.05)。结论心肌酶cTnI可作为诊断SAP患者是否并发心功能不全的评价指标,并可反映SAP病情的严重程度。

《管子》的意识论及其修养学说

现代思想对人的关注,已逐渐从对物理世界的关注中挣脱出来.科学的发展使其观察的对象越来越倾向于人自身.人的科学的建立势在必行.科学家们预言,下个世纪将是生命科学的黄金时代.但是。

cTnT和CAVI检测联合预测UAP预后的临床评价

目的探讨血清肌钙蛋白T(cTnT)、心-踝血管指数(CAVI)检测联合预测不稳定型心绞痛(UAP)患者预后的临床评价。方法对150例患者,包括36例非冠心病患者、54例稳定型心绞痛(SAP)和60例不稳定型心绞痛(UAP)患者分别进行血清cTnT、CAVI检测,并对60例UAP患者进行2年随访,观察心脏事件发生率。结果三组中UAP组血清cTnT、CAVI结果均高于非冠心病组和SAP组(P<0.05);在UAP组中,cTnT与CAVI均阳性患者心脏事件发生率也比单一阳性患者及均阴性患者高(P<0.05)。结论 cTnT和CAVI检测联合预测UAP的预后有更好的临床价值。

Optimization of Drying Process for Plasma Protein from Tibetan Sheep

Fresh blood of Tibetan sheep was subjected to protein separation and spray drying, and the effects of drying process on water content, yield and nitrogen soluble index of plasma powder from blood of Tibetan sheep were investigated. The results showed that the optimum separation parameters were a centrifugal speed at 6 000 r/min, centrifugal time of 20 min, a mass fraction of dry matter of 20%, an inlet air temperature at 180 ℃ and a feed rate at 400 ml/h, under which the plasma protein was a pale yellow powdery solid, indicating a good separation effect.

High sensitivity C-reactive protein and cardfiac resynchronization therapy in patients with advanced heart failure

Background The data on the prognostic values of high sensitivity C-reactive protein （hsCRP） levels in patients with advanced symp-tomatic heart failure （HF） receiving cardiac resynchronization therapy （CRT） are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP （〉3 mg/L） prior to CRT was associated with a significant 2.39-fold increase （P=0.006） in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels （–0.5 ± 4.1 mg/L reduction） compared with non-responders （1.7 ± 6.1 mg/L increase, P=0.018）. Com-pared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations （Log-rank P〈0.001）. The echocardio-graphic improvement was also better among patients in whom 6-month hsCRP levels were reduced or remained low compared to those in whom 6-month hsCRP levels were raised or maintained high. Conclusions Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.

H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease

AIM: To determine the overall prevalence of H pylori and CagA positive H pylori infection and the prevalence of other bacterial and viral causes of chronic infection in patients with coronary heart disease (CHD), and the potential role of anti-heat-shock protein 60 (Hsp60) anti- body response to these proteins in increasing the risk of CHD development. METHODS: Eighty patients with CHD and 160 controls were employed. We also compared the levels of anti- heat-shock protein 60 (Hsp60) antibodies in the two groups. The H pylori infection and the CagA status were determined serologically, using commercially available enzyme-linked immunosorbent assays (ELISA), and a Western blotting method developed in our laboratory. Systemic antibodies to Hsp60 were determined by a sandwich ELISA, using a polyclonal antibody to Hsp60 to sensitise polystyrene plates and a commercially available human Hsp60 as an antigen. RESULTS: The overall prevalence of H pylori infec- tion was 78.7% (n = 63) in patients and 76.2% (n = 122) in controls (P = 0.07). Patients infected by CagA- positive (CagA+) H pylori strains were 71.4% (n = 45) vs 52.4% of infected controls (P = 0.030, OR = 2.27). Sys-temic levels of IgG to Hsp60 were increased in H pylori- negative patients compared with uninfected controls (P < 0.001) and CagA-positive infected patients compared with CagA-positive infected controls (P = 0.007). CONCLUSION: CagA positive H pylori infection may concur to the development of CHD; high levels of anti- Hsp60 antibodies may constitute a marker and/or a con- comitant pathogenic factor of the disease.

Losartan reduced connexin43 expression in left ventricular myocardium of spontaneously hypertensive rats

Objective:To assess the effect of angiotensin II type 1(AT1)receptor antagonist losartan on myocardium con- nexin43(Cx43)gap junction(GJ)expression in spontaneously hypertensive rats(SHRs)and investigate possible mechanisms. Methods:Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto(WKY)rats were included in this study.SHRs were randomly divided into two groups to receive losartan at 30 mg/(kg·d)by oral gavage once daily for 8 weeks(SHR-L)or vehicle(0.9%saline)to act as controls(SHR-V);WKY rats receiving vehicle for 8 weeks served as normotensive controls.At the end of the experiment,rats were sacrificed and the hearts were removed.Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65)proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan(30 mg/(kg·d),8 weeks)on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot.Results:Left ventricular(LV)hypertrophy was prominent in SHRs,Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface.Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium.The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment.Conclu- sion:Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy.Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles,possibly through the NF-κB pathway.

Hepatitis C virus proteins

Hepatitis C virus (HCV) encodes a single polyprotein, which is processed by cellular and viral proteases to generate 10 polypeptides. The HCV genome also contains an overlapping +1 reading frame that may lead to the synthesis of an additional protein. Until recently, studies of HCV have been hampered by the lack of a productive cell culture system. Since the identification of HCV genome approximately 17 years ago, structural, biochemical and biological information on HCV proteins has mainly been obtained with proteins produced by heterologous expression systems. In addition, some functional studies have also been confirmed with replicon systems or with retroviral particles pseudotyped with HCV envelope glycoproteins. The data that have accumulated on HCV proteins begin to provide a framework for understanding the molecular mechanisms involved in the major steps of HCV life cycle. Moreover, the knowledge accumulated on HCV proteins is also leading to the development of antiviral drugs among which some are showing promising results in early- phase clinical trials. This review summarizes the current knowledge on the functions and biochemical features of HCV proteins.

Disruption of the 1-deoxy-D-xylulose-5-phosphate reductoisomerase （DXR） gene results in albino, dwarf and defects in trichome initiation and stomata closure in Arabidopsis

1-Deoxy-D-xylulose-5-phosphate reductoisomerase （DXR） is an important enzyme involved in the 2-C-methyi-D- erythritol-4-phosphate （MEP） pathway which provides the basic five-carbon units for isoprenoid biosynthesis. To investigate the role of the MEP pathway in plant development and metabolism, we carried out detailed analyses on a dxr mutant （GK_215C01） and two DXR transgenic co-suppression fines, OX-DXR-L2 and OX-DXR-L7. We found that the dxr mutant was albino and dwarf. It never bolted, had significantly reduced number of trichomes and most of the stomata could not close normally in the leaves. The two co-suppression lines produced more yellow inflorescences and albino sepals with no trichomes. The transcription levels of genes involved in tricbome initiation were found to be strongly affected, including GLABRA1, TRANSPARENT TESTA GLABROUS 1, TRIPTYCHON and SPINDLY, expression of which is regulated by gibberellic acids （GAs）. Exogenous application of GA3 could partially rescue the dwarf phenotype and the trichome initiation of dxr, whereas exogenous application of abscisic acid （ABA） could rescue the stomata closure defect, suggesting that lower levels of both GA and ABA contribute to the phenotype in the dxr mutants. We further found that genes involved in the biosynthetic pathways of GA and ABA were coordinately regulated. These results indicate that disruption of the plastidial MEP pathway leads to biosynthetic deficiency of photosynthetic pigments, GAs and ABA, and thus the developmental abnormalities, and that the flux from the cytoplasmic mevalonate pathway is not sufficient to rescue the deficiency caused by the blockage of the plastidial MEP pathway. These results reveal a critical role for the MEP biosynthetic pathway in controlling the biosynthesis of isoprenoids.

Effect of matrine and carvedilol on collagen and MMPs activity of hypertrophy myocardium induced by pressure overload

Objective： To explore the effect and mechanism of matrine （Mt.） on myocardial interstitial fibrosis induced by pressure overload. Methods： Pressure overloaded myocardial hypertrophy was produced by banding of aorta abdominalis in 67 male Sprague-Dawley rats weighing （200±15） g. The rats were assigned into one of the following groups： sham-operation control, operation control, operation group treated with matrine （15 mg/（kg·d）） and treated with carvedilol （Car.） （3.6 mg/（kg·d）） group. The rats were given drugs one day after operation. Five weeks after treatment, the left ventricular weight （LVW） was measured and the volume of myocardial cells was detected with Hematoxylin-Eosin （H-E） stain and Masson stain was used to assess the level of fibrosis of the myocardial matrix. Myocardial metalloproteinase activity was quantified with zymography, and survival rate was calculated. Results： Survival rate significantly decreased （P〈0.05）, LVW/BW （body weight）, MMP-2 （matrix metalloproteinase-2） activity （P〈0.05）, size of cardiomyocytes and interstitial fibrosis obviously increased in the operation group compared with sham control group. Mr. and Car. treatment can significantly increase survival rate （P〈0.05）, decrease LVW/BW （P〈0.05） and MMP-2 activity （P〈0.05）, decrease size of cardiomyocytes and interstitial fibrosis compared with operation group. But there was difference compared with sham group. Conclusion： Matrine was shown to be able to prevent cardiac remodelling of bypertrophy cardium induced by pressure overload including myocardial hypertrophy and fibrosis which may be associated with the decrease in MMP-2 activity of heart.

Altered serum level of cartilage oligomeric matrix protein and its association with coronary calcification in patients with coronary heart disease

Background Cartilage oligomeric matrix protein （COMP） is mainly found in the skeletal system and vascular smooth muscle cells. Recent researches showed that it had a protective function on blood vessels and could also inhibit vascular calcification. We investigated the serum COMPs in coronary heart disease （CHD） patients, and the relationship between serum COMP and the calcification of coronary artery. Methods A total of 233 consecutive chest pain patients who first underwent coronary angiography followed by multi-slice computed to- mography （MSCT） within six months were recruited and divided into two groups according to the coronary angiography luminal diameter narrowing percentages： CHD group （diameter narrowing 〉 50%, n = 194） and control group （diameter narrowing 〈 50%, n = 39）. The Gen- sini score, Syntax score and coronary artery calcium score （CACs） were calculated. The serum COMP level was determined using ELISA. Results The levels of COMP were significantly higher in the CHD group than in the control group 155.7 （124.5-194.5） ng/mL vs. 128.4 （113.0-159.9） ng/mL, P = 0.019. There were no correlation between COMP, Gensini score, Syntax score, severity of coronary stenosis and the number of coronary artery with stenosis 〉 50%. The serum COMP was correlated with age （r = 0.294, P 〈 0.001）, fasting glucose （r = 0.163, P = 0.015）, HbAlc （r = 0.194, P = 0.015） and CACs （r = 0.137, P = 0.037）. Stepwise linear regression analysis showed that COMP level and age were independent predictors of CACs in the CHD patients （fl = 0.402, t = 2.612, P = 0.015; fl = 0.472, t = 3.077, P = 0.005）. Performance of COMP for predicting CHD was shown as area under curve （AUC）： 0.632, 95% CI： 0.549-0.715 and upper tertile CACs was AUC： 0.602, 95% CI： 0.5264）.678 in receiver operating characteristic （ROC） curve analysis. Conclusion Calcification of coronary artery was an independent predictor of serum COMPs.

POLYMORPHISMS OF THE HUMAN LIPOPROTEIN LIPASE GENE:POSSIBLE ASSOCIATION WITH LIPID LEVELS IN PATIENTS WITH CORONARY HEART DISEASE IN BEIJING AREA

The polymorphisms(Pvu Ⅱand Hind Ⅲ) on the lipoprotein lipase(LPL) gene locus was investigated in a sample of 100 patients surviving previous myocardial infarction and 100 age matched healthy individuals selected from Han Chinese of Beijing area.In patient group a strong association was found between H+allele of Hind Ⅲ polymorphism and raised TG levels(P<0.01).In control group P-P-genotype was observed to be associated with higher TG levels compared with P+P genotype of Pvu Ⅱ polymorphism(P<0.05).Combination of H+H+ genotype with P-P-genotype showed the highest TG levels among all nine kinds of genotype combinations in patient group(P<0.01).However,comparison of distribution of alleles and genotypes of these polymorphisms between patient group and control group demonstrated no significant difference. Our data suggest that the polymorphisms at the LPL gene,as the linkage markers with an aetiologic mutation at or around LPL gene,may constitute one of the genetic determinants for the population variation in plasma TG levels,as well as for the common dyslipidemia in Chinese population.

Hepatic drug transporters and nuclear receptors:Regulation by therapeutic agents

The canalicular membrane represents the excretory pole of hepatocytes.Bile is an important route of elimination of potentially toxic endo-and xenobiotics(including drugs and toxins),mediated by the major canalicular transporters:multidrug resistance protein 1(MDR1, ABCB1),also known as P-glycoprotein,multidrug resistance-associated protein 2(MRP2,ABCC2),and the breast cancer resistance protein(BCRP,ABCG2).Their activities depend on regulation of expression and proper localization at the canalicular membrane,as regulated by transcriptional and post-transcriptional events,respectively.At transcriptional level,specific nuclear receptors(NR)s modulated by ligands,co-activators and co-repressors,mediate the physiological requirements of these transporters.This complex system is also responsible for alterations occurring in specific liver pathologies.We briefly describe the major ClassⅡNRs, pregnane X receptor(PXR)and constitutive androstane receptor(CAR),and their role in regulating expression of multidrug resistance proteins.Several therapeutic agents regulate the expression of relevant drug transporters through activation/inactivation of these NRs.We provide some representative examples of the action of therapeutic agents modulating liver drug transporters, which in addition,involve CAR or PXR as mediators.

Novel biomarkers for cardiovascular risk prediction

Cardiovascular disease （CVD） is the leading cause of death and disability worldwide. The primary prevention of CVD is dependent upon the ability to identify high-risk individuals long before the development of overt events. This highlights the need for accurate risk strati- fication. An increasing number of novel biomarkers have been identified to predict cardiovascular events. Biomarkers play a critical role in the definition, prognostication, and decision-making regarding the management of cardiovascular events. This review focuses on a variety of promising biomarkers that provide diagnostic and prognostic information. The myocardial tissue-specific biomarker cardiac troponin, high- sensitivity assays for cardiac troponin, and heart-type fatty acid binding proteinall help diagnose myocardial infarction （MI） in the early hours following symptoms. Inflammatory markers such as growth differentiation factor-15, high-sensitivity C-reactive protein, fibrinogen, and uric acid predict MI and death. Pregnancy-associated plasma protein A, myeloperoxidase, and matrix metalloproteinases predict the risk of acute cor- onary syndrome. Lipoprotein-associated phospholipase A2 and secretory phospholipase A2 predict incident and recurrent cardiovascular events. Finally, elevated natriuretic peptides, ST2, endothelin-1, mid-regional-pro-adrenomedullin, copeptin, and galectin-3 have all been well validated to predict death and heart failure following a MI and provide risk stratification information for heart failure. Rapidly develop- ing new areas, such as assessment ofmicro-RNA, are also explored. All the biomarkers reflect different aspects of the development ofather- osclerosis.

C-reactive protein aggravates myocardial ischemia/reperfusion injury through activation of extracellular-signal-regulated kinase 1/2

Background Ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP） might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation （OGD/R） in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase （LDH） leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester （TMRE） and mitochondrial permeability transition pore （mPTP） opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 pg/mL CRP, cell viability decreased markedly （82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007）, and the LDH leakage significantly increased （145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122）. CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 pM atorvastatin （Ator） before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase （ERK） 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group （170.4% ± 3.00% v.v. 93.53% ± 1.94%, P 〈 0.0001）. Western blot analysis revealed that Akt expression was markedly activated （184.2% ± 6.96% vs. 122.7% ± 5.30%, P = 0.0003） and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium （mitoKATp） channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.

Restrictive Cardiomyopathy Resulting from a Troponin Ⅰ Type 3 Mutation in a Chinese Family

Objective To identify the pathogenic variant responsible for restrictive cardiomyopathy （RCM） in aChinese family.Methods Next generation sequencing was used for detecting the mutation and results verified bysequencing. We used restriction enzyme digestion to test the mutation in the family members and 200 unrelatednormal subjects without any cardiac inherited diseases when the mutation was identified.Results Five individuals died from cardiac diseases, two of whom suffered from sudden cardiacdeath. Two individuals have suffered from chronic cardiac disorders. Mutation analysis revealed a novelmissense mutation in exon 7 of troponin I type 3 （TNNI3）, resulting in substitution of serine （S） withproline （P） at amino acid position 150, which cosegregated with the disease in the family, which is predictedto be probably damaging using PolyPhen-2. The mutation was not detected in the 200 unrelated subjectswe tested.Conclusion Using next generation sequencing, which has very recently been shown to be successfulin identifying novel causative mutations of rare Mendelian disorders, we found a novel mutation of TNNI3 in aChinese family with RCM.