Objective To explore the changes of PH values of N,O-CMC/β-TCP compositive materials with different mass fractions in simulated body fluids (SBF)and their influence in the growth of MG63 cells, and to illustrate their mechanisms, and to provide reference for the further research on the bone repair materials. Methods The N,O-CMC/β-TCP with mass fractions of 2/1,1/1 and 1/2 were used as experimental groups,and the collagen nano calcium phosphate bone repair material as control group. The materials with different mass fractions were immersed in SBF and the pH values were measured by pH meter after soaking for 7,14,21 and 28d,respectively.The MG63 cells with the concentration of 1 × 105 mL-1 were inoculated and co-cultured in experimental and control groups,the adhesion and morphological changes of MG63 cells in each group were observed by scanning electron microscope and the cell proliferation was detected by MTT method after co-culturing for 2,4 and 6 d.Results The pH values were 6.70-7.25 in N,O-CMC/β-TCP (1/2)group and N,O-CMC/β-TCP (2/1)groups and the pH value in N,O-CMC/β-TCP (1/1)group was basically 7.15. The cells in N,O-CMC/β-TCP (2/1)group formed owe full,spreading face small and less secretion,but the cells in N,O-CMC/β-TCP 1/2 and 1/1 groups formed in full, pseudopodia interconnection, widely spreading and more secretions under electron microscope. The proliferation rate of the cells in N,O-CMC/β-TCP with (1/1 ) and N,O-CMC/β-TCP (2/1)groups had no statistical difference compared with control group (P>0.05),but there was significant difference between control group and N,O-CMC/β-TCP (1/2)group (P<0.05).Conclusion The changes of pH values of N,O-CMC/β-TCP materials with different mass fractions in SBF are small and the pH values are neutral;the order of the mass fraction of N,O-CMC/β-TCP to promote the growth of MG63 cells is 1/1,2/1,and 1/2.

To investigate the mutation site of pathogenic gene in patients with hypertrophic cardiomyopathy (HCM) and to analyze the relationship between the genotype and clinical phenotype. Methods: Targeted exon capture sequencing was conducted in a HCM proband for 30 coding exons related HCM gene by all exon amplification and high-throughput sequencing. Furthermore, Sanger sequencing was performed in other family member and in 200 healthy volunteers for verification. The familial investigation included in clinical presentation, physical examination, electrocardiogram and echocardiography. Results: There were 3/6 blood relatives carrying cardiac myosin-binding protein gene MyBPC3 G772A heterozygous mutation, the mutation site was at 258 amino acid of MyBPC3 as glutamic acid (Glu) was substitute to lysine (Lys), such mutation was not found in rest of family member and not in healthy volunteers. The onset of proband and her daughter was rather late, they had palpitation and chest tightness; echocardiography showed interventricular septum basal segment thickening (16-18) mm. Proband was complicating paroxysmal ventricular tachycardia, malignant arrhythmia and heart failure, the maximum pressure gradient of left ventricular outflow was 56 mmHg, which with the high risk for sudden death. Conclusion: Comprehensive gene test has been helpful for clinical stratification, early diagnosis and treatment. MYBPC3 site mutation c.G772A might be the pathogenic mutation in that specific HCM family.