Objective To discuss the accuracy and objectivity of student standardized patients (SSP) in objective structured clinical examination(OSCE). Methods On March 30 and 31, 2013, 168 seven-year program medical students of class 2006 and 2007 took part in OSCE. Differences in as-sessment results between SPP and those given by professional doctors at 3 SP sites(angina pectoris SSP station, acute cholecystitis SSP station, depression SSP station) were analyzed. Each site had 4 items for assessment, with a total score of 100. Scores were given in strict accordance with a set of unified scoring rules. Counting data were presented as x±s. Data were verified using t test. P<0.05 was considered statis-tically considerable. Results At angina pectoris station, respective scores of SSP and professional physi-cians were 85.2±7.1 and 85.5±6.6, P=0.688. At acute cholecystitis station, respective score of SSP and professional physicians were 89.1±5.2 and 88.2±6.2, P=0.150. At depression station, respec-tive score of SSP and professional physicians were 79.8±7.5 and 78.2±7.0, P=0.078. Conclusion There is no statistical difference between scores given by SSP and those given by the physicians in OSCE. This proves that SSP who received standardized training delivers fair and accurate results in OSCE , and therefore is recommended for future application.

Utilizing standardized patient(SP) for classroom simulation is common in current medical education. In this paper, incentive measures and combination of SP with theoretical examination, simulated people and clinical practice were proposed after in-depth analysis of advantages and disadvan-tages of using medical students as SP in terms of recruitment, training, and application. All these mea-sures were intended to promote the development of simulative medical education that in turn to cultivate students to be competent in practice.

Aim To study the preventative effects of noninvasive delayed limb ischemic preconditioning ( NDLIP) on sudden cardiac death in rats with myocar-dial infarction. Methods Thirty healthy SD male rats weighting ( 250 ± 10 ) g were randomly divided into 3 groups:① myocardial infarction ( MI ) group: animal model of MI was established by making surgical ligation of animal LAD. ② MI plus NDLIP group: after the success of the animal model of MI, NDLIP was carried out every other day until 4th week. ③Sham group:as the negative control group, animals were taken heart LAD threading but no ligation. All rats were fed con-ventionally. At the end of 4 weeks, three groups of rats were administered with metaraminol ( 0. 2 mg · min-1 ) . ECG, drug cumulant of sudden death and death onset time were recorded. After sudden death, blood samples were withdrawn from abdominal aorta and serum was separated via centrifugation. ELISA method was used to measure serum caspase-3 , HSP70 and SOD concentration. Results While metaraminol led animal cardiac sudden death, the rats heart rate ( HR) kept declining with the increase of dosage of metaraminol during the administration period. Rat HR of MI+NDLIP group [ ( 479 ± 8 ) vs ( 416 ± 19 ) beat ·min-1 , ( 446 ± 32 ) vs ( 370 ± 20 ) beat · min-1 , (376 ± 53) vs (305 ± 29) beat·min-1, (307 ± 63) vs (244 ± 33) beat·min-1, (283 ± 45) vs (121 ± 35 ) beat · min-1 , P <0. 01 ] was markedly higher than that of MI group at 0 , 5 , 10 , 30 , 50 min before death. Compared with MI group, drugs cumulant to sudden death and death onset time of MI + NDLIP group [ ( 14. 58 ± 3. 03 ) vs ( 10. 76 ± 2. 73 ) mg, (72. 9 ± 15. 2 ) vs ( 53. 8 ± 13. 6 ) min, P <0. 01 ] were significantly increased. Compared with MI group, serum caspase-3 content of MI+NDLIP group was sig-nificantly reduced [ ( 2. 01 ± 0. 52 ) vs ( 2. 34 ± 0. 38 )μg·L-1 , P<0. 01 ]; HSP70 levels were remarkably increased [ ( 3. 01 ± 0. 58 ) vs ( 2. 70 ± 0. 43 ) μg · L-1 , P <0. 05 ]; SOD levels were significantly im-proved [(1. 99 ± 0. 65) vs (1. 70 ± 0. 58) mg·L-1, P<0. 01 ] . Conclusion NDLIP can prevent sudden cardiac death after myocardial infarction in rats, which may be mediated by reducing the myocardial cell apop-tosis, increasing protective protein expression and en-hancing antioxidant capacity.

AIM:To study the effects of noninvasive delayed limb ischemia preconditioning ( NDLIP) on ani-mal cardiac function , myocardial morphology and myocardial apoptosis after myocardial infarction ( MI ) .METHODS:Healthy SD male rats [n=45, weighing (250 ±10) g] were randomly divided into 3 groups:MI group:the animal model of MI was established by surgical ligation of left anterior descending artery ( LAD) after 2 weeks;NDLIP group:after the success of the MI animal model , NDLIP was carried out every other day until the 4th, 6th and 8th weeks;sham group:as the negative control group , the animals were taken heart LAD threading but no ligation .All rats were fed conventionally .At the end of the 4th, 6th and 8th weeks, all rats were made ventricular intubation , and then the hemodynamic parameters were recorded .The blood samples were withdrawn from the abdominal aorta and the serum was separated via centrifugation . The serum contents of Bcl-2 and Bax were measured by ELISA .Left ventricular anterior wall was homogenized .The mito-chondrial respiratory chain complexes Ⅰ,Ⅱ,Ⅲand Ⅳin the myocardial tissues were detected by ELISA .RESULTS:At the end of the 4th, 6th and 8th weeks, compared with MI group, left ventricular systolic pressure in NDLIP group was significantly increased , while left ventricular end-diastolic pressure in NDLIP group was significantly decreased ( both P<0.05).Mitochondrial respiratory chain complexesⅠ, Ⅱ, Ⅲ and Ⅳ in NDLIP group were significantly increased (P<0.05).The serum level of Bcl-2 in NDLIP group was significantly increased and Bax level was reduced remarkably (both P<0.01) .CONCLUSION:NDLIP improves the hemodynamic indexes , promotes the mitochondrial respiratory function and inhibits cell apoptosis , thus improving the prognosis of MI .

Objective To analyze the characteristic of Yunnan unexpected sudden death (YUSD) cases by pathological diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC),in order to offer clue for ARVC etiologic research of YUSD.Methods The pathological diagnosis results of 9 cases of sudden death of ARVC in Yunnan,as well as epidemiological investigation data,were used to comprehensively analyze the pathological features of the pathological diagnosis of ARVC in Yunnan.Results The 9 cases including 8 females and 1 male,aged 16-47 years.The sudden death time was from June to August,mainly distributed in 8 families from the disease seriously ridden 7 villages.Three of them had a genetic history of family YUSD,2 cases had a history of mental stimulation,1 case had eaten Trogia venenata;and acute symptoms and signs were palpitation,chest tightness,shortness of breath,and loss of consciousness.Pathological observations were the typical ARVC change,mainly right ventricular lesions,with different degrees of cardiac enlargement and extensive adipose tissue infiltration in the ventricular wall.Among them,6 cases of fat infiltration almost reached the full thickness of the heart wall.In addition to the pathological changes of ARVC,8 cases were accompanied by one or several pathological changes in myocarditis,cardiac dysplasia,nephropathy,pulmonary edema,pneumonia and pancreatitis.Of the 9 cases,5 cases were diagnosed with ARVC,2 cases with ARVC and pulmonary edema,1 case with ARVC and acute hemorrhagic necrotizing pancreatitis,and 1 case with ARVC and Trogia venenata poisoning.The clinical examination abnormalities of the family members of the cases mainly showed arrhythmogenic electrocardiography changes and abnormal myocardial enzymes.Conclusions The nine cases have showed typical epidemiology characteristics of YUSD,and cardiachistological changes are consistent with the ARVC pathological diagnostic criteria.A part of YUSD cases may be caused by ARVC,and the inference will be proved by cadaveric pathologic examination and related pathogenic gene detection.

Objective To study the desmosomal protein plakophilin-2(PKP2)gene mutation of arrhythmogenic right ventricular cardiomyopathy (ARVC) in different populations of Yunnan unexplained sudden death (YUSD) areas,and explore the relationship between PKP2 gene mutation and YUSD.Methods Heart blood samples of YUSD cases (n =7) and venous blood samples of YUSD immediate family (n =30) and other family (n =11) members were collected.Basic situation and genetic relationship of YUSD immediate family and other family were investigated,and electrocardiography (ECG) was examined.DNA from blood samples was extracted and 15 exons of PKP2 gene were sequenced to analyze the mutation of PKP2 gene in different populations.Results A total of 10 people carried 11 PKP2 gene mutation sites with a mutation rate of 20.83％ (10/48).Two mutation sites were novel (p.G247R,p.T298N),and the new mutation sites were carried by two YUSD cases.Eight missense mutations were heterozygous mutations,two of the three synonymous mutations were heterozygous mutations,and one was homozygous synonymous mutation.The mutation sites were significantly concentrated in 4 exons,which were No.1 097 base of exon 4,No.819 and 893 bases of exon 3.2,No.739 base of exon 3.1,and No.156 base of exon 1.One YUSD case of ARVC pathological change carried exon 3.1 (p.G247R) and exon 4 (p.L366P) compound heterozygous mutations,the other YUSD case carried exon 3.2 (p.T298N) heterozygous mutation.The YUSD cases and immediate family with PKP2 gene mutations showed obvious family genetic relationships,and they were all first-degree and second-degree relatives.The abnormal ECGs of YUSD immediate family and other family mainly were conduction block,arrhythmia and premature beat.Conclusion There is a high PKP2 gene mutation rate in different populations of YUSD areas,and there may be a certain etiological connection between PKP2 gene mutations and YUSD.

Objective:To expound the pathogenesis relationship between Yunnan unexplained sudden death (YUSD) and desmosomal protein gene mutations of arrhythmogenic right ventricular cardiomyopathy (ARVC).Methods:Four YUSD cases families by ARVC pathological diagnosis were selected, to collect heart blood samples of YUSD cases by ARVC pathological diagnosis( n=3), venous blood samples of immediate relatives with genetic relationship (case relatives, n=4) and control population without genetic relationship ( n=7). DNA was extracted for PCR amplification and sequencing of a total of 97 exons of the ARVC desmosomal protein genes plakophilin 2 (PKP2), desmoplakin (DSP), desmoglein 2 (DSG2), desmocollin 2 (DSC2), and junction plakoglobin (JUP), and the mutations of the 5 genes were analyzed in combination with the genetic family. Results:DSP gene mutations were found in all YUSD cases by ARVC pathological diagnosis and case relatives, and PKP2, DSG2, DSC2 and JUP genes mutations were found in 1 person each. The same person carried 1-3 genes mutations. DSP gene existed 4 exon mutation sites, and 1 of which was a newly discovered heterozygous synonymous mutation c.4014 C>A (p.A1338A). PKP2 gene existed 2 exon missense mutation sites in 1 YUSD case by ARVC pathological diagnosis, and 1 of which was a newly discovered heterozygous mutation c.739 G>C (p.G247R). One heterozygous missense mutation site c.799 G>A (p.A267T) of JUP gene was newly discovered, and the predictive value of protein function was 0.963, the possibility of abnormal changes in protein function was high. DSG2 and DSC2 genes each had one mutation site. However, no mutation was found in control population.Conclusions:Both YUSD cases by ARVC pathological diagnosis and case relatives carry ARVC desmosomal protein genes DSP, PKP2, DSG2, DSC2 and JUP mutations. There may be a certain pathogenesis relationship between YUSD and ARVC desmosomal protein gene mutations.

Objective:To explore the relationship between arrhythmogenic right ventricular cardiomyopathy (ARVC) desmosomal protein gene mutations and Yunnan unexplained sudden death (hereinafter referred to as Yunnan sudden death) by detecting 5 common ARVC desmosomal protein gene mutations of Yunnan sudden death cases and their relatives in Heqing County, Yunnan Province.Methods:In January 2021, the autopsy heart cavity blood was collected from Yunnan sudden death cases in 8 villages in Heqing County, and peripheral venous blood samples of relatives of the cases were collected. Blood samples' DNA was extracted, after PCR amplification, 97 exons of 5 desmosomal protein genes [desmoplakin (DSP), desmoglein-2 (DSG2), plakophilin-2 (PKP2), junction plakoglobin (JUP) and desmocollin-2 (DSC2)] were sequenced by Sanger method to analyze gene mutations.Results:Three blood samples of Yunnan sudden death cases and 36 blood samples of relatives were collected. A total of 26 gene mutation sites were detected in 39 blood samples, with a total mutation rate of 26.80% (26/97). There were 13, 5, 3, 3 and 2 mutation sites in DSP, DSG2, PKP2, JUP and DSC2 genes, respectively. Among them, 19 were reported mutations and 7 were new mutations: DSP gene exon 3 c.372G>A, exon 15 c.2090A>G, exon 17 c.2371C>A, exon 24-I c.8458T>G; DSG2 gene exon 8 c.861C>T; PKP2 gene exon 3 c.892C>A, exon 8 c.1725G>T. Three Yunnan sudden death cases and 36 relatives were all carriers of compound gene mutation, and the same person carried 3 - 9 gene mutation sites at the same time.Conclusion:Mutations of ARVC desmosomal protein genes DSP, DSG2, PKP2, JUP and DSC2 exist in Yunnan sudden death cases and their relatives, which may be the genetic background factors of some Yunnan sudden death.

Objective:To explore the cause of death of 2 suspected Yunnan sudden unexplained death (YNSUD) cases in Dayao County, Yunnan Province.Methods:The field epidemiological investigation and autopsy of 2 cases of YNSUD in Dayao County from June 15 to 20, 2020 were conducted; and blood and tissue samples were collected for qualitative analysis of common poisons and drugs.Results:The areas where the two cases were located were all seriously ill villages with a history of YNSUD, and the time of death occurred in the onset season of YNSUD. There was no blood relationship between the 2 cases, no obvious abnormal symptoms before death, no special diet, no history of exposure to pesticides and other toxic chemicals, and the test results of common poisons were all negative. Autopsy pathological examination results showed that case 1 died of acute cardiac dysfunction caused by sudden acute myocardial infarction of coronary heart disease, and case 2 died of central respiratory and circulatory failure caused by spontaneous subarachnoid hemorrhage.Conclusions:The two cases are excluded from YNSUD through autopsy, and the cause of death is determined. It is suggested that emergency response should be taken as soon as possible for YNSUD cases, and autopsy should be actively carried out to clarify the cause of death from a pathological point of view.

Objective:To investigate the mutation of desmosomal protein gene of arrhythmogenic right ventricular cardiomyopathy (ARVC) in people from Yunnan unexplained sudden death (YUSD) area in Xiangyun County, Dali Prefecture, Yunnan Province, and to explore the etiological relationship between the mutation of ARVC desmosomal protein gene and YUSD.Methods:The autopsy cardiac blood sample of YUSD case ( n = 1) and the peripheral venous blood samples of the same time case ( n = 1) and relatives of YUSD case ( n = 16) were collected in Xiangyun County. Blood DNA was extracted for PCR amplification and sequencing of a total of 97 exons of the ARVC desmosomal protein genes [plakophilin 2 (PKP2), junction plakoglobin (JUP), desmoplakin (DSP), desmoglein 2 (DSG2) and desmocollin 2 (DSC2)] were conducted by Sanger method. At the same time, basic information and genetic family of YUSD case, the same time case and relatives of YUSD case were investigated, and gene mutations were comprehensively analyzed. Results:The YUSD case and the same time case carried JUP, DSP and DSG2 gene mutations. Among the relatives of YUSD case, 2, 14, 16, 15 and 4 cases had mutations in PKP2, JUP, DSP, DSG2 and DSC2 genes, respectively. The YUSD case, the same time case and the relatives of YUSD case carried 6 identical mutation sites: JUP gene exon 3 c.213 T>C synonymous mutation, exon 14 c.2089 A>T missense mutation; DSP gene exon 19 c.2631 G>A synonymous mutation, exon 24 c.8472 G>C synonymous mutation; DSG2 gene exon 8 c.861 C>T synonymous mutation, and exon 15 c.3321 T>C synonymous mutation.Conclusion:In Xiangyun County, six identical mutation sites (JUP gene c.213 T>C and c.2089 A>T, DSP gene c.2631 G>A and c.8472 G>C, DSG2 gene c.861 C>T and c.3321 T>C) carried by YUSD case, the same time case and the relatives of YUSD case may be related to the incidence of some YUSD cases.