Prevalence and Years Lived with Disability for Dental Caries among Children Aged 0-14 Years in China, 1990-2016 / 生物医学与环境科学（英文）

The estimate of dental caries among Chinese children at the microscale level using standard methodology remains unclear. In this study, we assessed and analyzed the disease burden of childhood dental caries in China by extracting data from the Global Burden of Disease, Injuries, and Risk Factors Study 2016 (GBD 2016). In 2016, the number of cases, prevalence, years lived with disability (YLD), and age-standardized YLD rate of dental caries was 93.0 million, 43.0%, 32,200 person years, and 14.8 per 100,000, respectively. Across 33 provincial units, the disease burden was highest in Hubei (YLD rate 28.6 per 100,000), lowest in Macao (9.1 per 100,000), while geographical clustering was not observed. Compared with 1990, the prevalence in 2016 decreased from 46.8% to 43.0%, and the YLD rate decreased from 16.5 per 100,000 to 14.8 per 100,000. Given the slight decrease in dental caries burden, the prevalence and disease burden remained high among Chinese children. Strategies for addressing the spatial inequity of childhood dental caries require geographical targeting.

Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.</p><p><b>METHODS</b>Atrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.</p><p><b>RESULTS</b>The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.</p><p><b>CONCLUSIONS</b>The study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.</p>

Cloning, expression and sequence analysis and tissue distribution of angiotensin-converting enzyme 2 (ACE2) gene in adult mice / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>o clone angiotensin-converting enzyme 2(ACE2) gene, to analyze its amino acids and nucleotides sequence and to investigate tissue distribution of ACE2 in adult mice.</p><p><b>METHODS</b>The full-length ACE2 encoding sequence was amplified from the RNA of mice kidney tissue by RT-PCR technique, cloned into plasmid pGEM-T easy, then subcloned into plasmid pcDNA3.1+. After identification of DNA sequence, the recombinant plasmid pmACE2 was transfected into Cos7 cells with lipofectin reagent. The transient expression of ACE2 molecule was detected by SDS-PAGE. Sequence analysis was conducted with CLUSTALX program. Tissue distribution of ACE2 in mice was detected by RT-PCR.</p><p><b>RESULTS</b>A fragment about 2.6 kb was amplified and the recombinant plasmid pmACE2 was confirmed by two-enzyme digesting and DNA sequencing. The cloned DNA sequence was consistent with that previously reported, except for 3 variations: A701G, T1102C and T1330C. SDS-PAGE proved that expression of a soluble, truncated products form of ACE2 was a glycoprotein of approximately 80 kD in Cos7 cells. The predicted mice ACE2 sequence contained an N-terminal signal sequence (amino acid residues 1-18), a single HHEMGHIQ zinc-binding domain (amino acid residues 373-380) and C-terminal membrane anchor (amino acid residues 738-765). Mice ACE2 showed 84 % identity with that of human, and 90 % identity with that of rat. Expression of ACE2 was the greatest in lungs, hearts and kidneys, and moderate levels were also detected in testes and livers.</p><p><b>CONCLUSION</b>Mice ACE2 gene has been cloned and successfully expressed in vitro. The tissue-specific expression of ACE2 in different species is not identical.</p>

Changes of endothelial progenitor cells from peripheral blood in patients with coronary heart diseases / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate alterations of endothelial progenitor cells (EPCs) from peripheral blood in patients with coronary heart diseases.</p><p><b>METHODS</b>Twenty patients with coronary heart diseases (CHD) and 20 matched control subjects were included in the study. Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After cultured for 7 days, attached cells were cytochemically analyzed. EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin-binding by laser scanning confocal microscope with direct fluorescent staining. EPCs proliferation and migration were measured by MTT assay and modified Boyden chamber assay, respectively. EPCs adhesion assay was performed by replating on fibronectin-coated dishes, then adherent cells were counted.</p><p><b>RESULTS</b>The number of EPCs was significantly reduced in patients with CHD compared with that of age-matched control subjects (31.8+/-7.7 compared with 59.5 +/-10.6 EPCs/x 200 field; P<0.05). In addition, the functional activity of EPCs such as proliferation, migration and adhesive capacity was also impaired in patients with CHD.</p><p><b>CONCLUSION</b>EPCs number and functional activity are significantly decreased in patients with CHD.</p>

A novel splice mutation of HERG in a Chinese family with long QT syndrome / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Congenital long QT syndrome (LQTS) is a genetically heterogeneous disease in which six ion-channel genes have been identified. The phenotype-genotype relationships of the HERG (human ether-a-go-go-related gene) mutations are not fully understood. The objective of this study is to identify the underlying genetic basis of a Chinese family with LQTS and to characterize the clinical manifestations properties of the mutation. Single strand conformation polymorphism (SSCP) analyses were conducted on DNA fragments amplified by polymerase chain reaction from five LQT-related genes. Aberrant conformers were analyzed by DNA sequencing. A novel splice mutation in C-terminus of HERG was identified in this Chinese LQTS family, leading to the deletion of 11-bp at the acceptor splice site of Exon9 [Exon9 IVS del (-12-->-2)]. The mutation might affect, through deficient splicing, the putative cyclic nucleotide binding domain (CNBD) of the HERG K(+) channel. This mutation resulted in a mildly affected phenotype. Only the proband had a history of syncopes, while the other three individuals with long QT interval had no symptoms. Two other mutation carriers displayed normal phenotype. No sudden death occurred in the family. The 4 affected individuals and the two silent mutation carriers were all heterozygous for the mutation. It is the first splice mutation of HERG reported in Chinese LQTS families. Clinical data suggest that the CNBD mutation may be less malignant than mutations occurring in the pore region and be partially dominant over wild-type function.

Single nucleotide polymorphism in SCN5A and the distribution in Chinese Han ethnic group / 生理学报

Mutations in voltage-gated sodium channel type (SCN5A) may evoke severe, life-threatening disturbances in cardiac rhythm, including long QT syndrome, idiopathic ventricular fibrillation (Brugada Syndrome), and isolated cardiac conduction disease. There is increasing awareness of the role of common polymorphisms in altering gene function and in susceptibility to diseases. The aim of the present study was to investigate single nucleotide polymorphism (SNP) in SCN5A gene and the distribution of these identified SNPs in Chinese Han nationality. SCN5A gene was sequenced by fluorescent labeling automatic sequencing method in 120 unrelated samples from Han nationality in South China. Allele frequency distribution was tested by Hardy-Weinberg equilibrium. The results showed that a total of 5 SNPs were identified in SCN5A gene, including three SNPs in code region, one SNP in regulatory region and the other in intron 23 adjacent to donor splicing site. The distribution of the SNPs in SCN5A gene was uneven. These allele frequencies in Han population of South China were as follows: G87A (A29A) 27.5%, A1673G (H588R) 10.4%, 4245+82A>G 32.8%, C5457T (D1819D) 41.3% and G6174A 44.9% respectively. The SNPs G87A (A29A), 4245+82A>G and G6174A were reported for the first time. There was no significant difference in the allele frequency of A1673G (H558R) within different ethical populations (P>0.05). C5457T (D1819D) allele frequency of Han population in South China was similar to that observed in Japanese (P>0.5), but higher than that in American (p<0.005). There was no significant difference in the distribution of the SNPs between male group and female group (all p>0.05). S1102Y and other 10 SNPs identified in other ethnic populations have not been detected in Chinese Han population. The allele distribution of SNPs was in good unity with the Hardy-Weinberg equilibrium. It is suggested that the SNP distribution of SCN5A gene varies within different nationalities. These data will be of use for genetic association studies of acquired arrythmias and investigation of sensitivity to drug therapy.

Single nucleotide polymorphisms of the SCN5A gene in Han Chinese and their relation with Brugada syndrome / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Mutations in the cardiac sodium channel gene (SCN5A) may lead to a broad spectrum of familial arrhythmias, including long QT syndrome (LQTS), idiopathic ventricular fibrillation (IVF), and isolated cardiac conduction diseases. Recent studies have shown that polymorphisms in the SCN5A gene also play an important role in the manifestation of disorders involving cardiac excitability. In this study, we investigated the polymorphisms of the SCN5A gene in Han Chinese and its relation to Brugada syndrome (BS).</p><p><b>METHODS</b>Genomic DNA was isolated from 120 unrelated healthy volunteers and 48 unrelated Brugada syndrome patients by means of standard procedures. All exons including the putative splicing sites of the SCN5A gene were amplified by PCR and sequenced directly or after subcloning using an ABI Prism 377 DNA sequencer.</p><p><b>RESULTS</b>A total of 5 single nucleotide polymorphisms (SNPs) were identified in the Han Chinese population, including 3 novel ones: G87A(A29A), 4245 + 82A > G, and G6174A. The allele frequencies of each SNP in the Han Chinese population were as follows: G87A (A29A) 27.5%, A1673G (H558R) 10.4%, 4245 + 82A > G 32.8%, C5457T (D1819D) 41.3%, and G6174A 44.9%. S1102Y and 10 other SNPs identified in other ethnic populations were not detected in this study. There was no significant difference in the allele frequency of A1673G (H558R) between different ethnic populations (all P > 0.5). On the other hand, the allele frequency of C5457T (D1819D) among Han Chinese was similar to its frequency among Japanese (P > 0.5), but higher than that among Americans (P < 0.005). The allele G1673 (R558) was over-represented in BS patients compared to controls (P < 0.005), but there was no significant difference in genotype frequencies at this locus. There were also no differences in either the allele or genotype frequencies of the 4 other identified SNPs when comparing BS patients with healthy controls.</p><p><b>CONCLUSIONS</b>The distribution of SCN5A SNPs may vary between different ethnicities. The polymorphism of A1673G might be associated with BS and may contribute to a susceptibility to BS in Han Chinese.</p>