[Detection of gene mutations of SCN5A in 7 patients with Brugada syndrome].

OBJECTIVE: Brugada syndrome is linked to sodium channel mutations and could induce arrhythmias that even lead to sudden death. The purpose of this study was to detect if there was gene mutation of SCN5A in 7 patients with Brugada syndrome and explore the molecular genetic characteristics of this disease. METHOD: Genomic DNA was extracted from peripheral blood of all 7 patients with Brugada syndrome and 41 pairs of PCR primers were designed to amplify all the 28 exons of SCN5A. RESULT: There was no novel mutation in exons of Gene SCN5A in these patients with Brugada syndrome. CONCLUSION: Brugada syndrome might associated gene mutation or other mechanisms independent of SCN5A gene mutation.

Resection of inferior pubic ramus tumors through a femoribus internus-perineal approach.

An operative approach to the inferior pubic ramus that was utilized in four patients with various bone tumors in the inferior pubic ramus is described here. These patients were successfully managed though a femoribus internus (inner thigh)-perineal approach. Data concerning preoperative and postoperative symptoms, surgical procedures, and outcomes are presented. There was no recurrence in the four cases and the pain associated with an initial pelvic floor had completely resolved except one case. The slight limitation in range of motion of the left hip joint and pain were performed in the same case postoperatively. The Musculoskeletal Tumor Society scores were 28, 15, 25, and 18 at the final follow-up. A typical case is described in full and our experience concerning surgical indications, and intraoperative issues in tumor patients discussed. The purpose of this paper is to recommend that the femoribus internus-perineal approach be used to resect the inferior pubic ramus, whether affected by osteomyelitis, bone tumor, or tuberculosis, but especially in patients with tumors.

[Risk factors for early postoperative death after total correction of tetralogy of Fallot: analysis of 20 cases].

OBJECTIVE: To identify the risk factors of early postoperative death after total correction of tetralogy of Fallot (TOF). METHODS: A retrospective analysis was conducted among 356 patients undergoing total correction of TOF by opening heart surgery and cardiopulmonary bypass. Of these patients, 20 died in the early postoperative period, and the possible risk factors for early postoperative death were analyzed in view of the surgical indication, surgical approaches, myocardial protection and postoperative management. RESULTS: Of the 20 fatal cases, death occurred due to low cardiac output syndrome in 11 cases, respiratory failure in 4 cases, kidney failure or multiple organ failure in 3 cases, acute left heart failure in 1 case, and cerebrovascular accident in 1 case. CONCLUSION: Young age at repair and poor development of the pulmonary vessels and left ventricle are high risk factors for postoperative low cardiac output syndrome. Postoperative death following surgical correction of TOF is associated mainly with the surgical skills and approaches. Appropriate cardiopulmonary bypass and effective measures for myocardial protection are critical to ensure the surgical success, and proper postoperative management and close monitoring may help reduce postoperative death in surgical patients with TOF.

[Time course change in the high mobility group box-1 after myocardial infarction in rats].

OBJECTIVE: To investigate the time course change in myocardial high mobility group box-1 (HMGB1) after myocardial infarction in rats. METHODS: Myocardial infarction (MI) was induced in SD rats by ligation of the anterior descending coronary artery. At 1, 2, 4, and 8 weeks after MI, the cardiac function of the rats was examined, and the expressions of HMGB1 at mRNA and protein levels in the myocardium were detected using real-time RT-PCR and Western blotting, respectively. RESULTS: Cardiac function test confirmed that the MI model was successfully induced. The expression of HMGB1 mRNA was increased in early stage (1 week) after MI, while significantly down-regulated in later stage (4-8 weeks after MI). HMGB1 protein showed a similar biphasic pattern of changes, and was up-regulated early (1-2 weeks) after MI (P<0.05) and decreased markedly (P<0.01) at 8 weeks. CONCLUSIONS: As an inflammatory regulator, HMGB1 can modulate inflammatory response early time after MI and functions later as a transcriptional modulator, thus contributing to the myocardial repair after MI. Interventions targeting HMGB1 in different stages after MI may prove helpful in reducing the complications, improving the prognosis and promoting long-term survival.