Prevalence of diabetes mellitus and impaired fasting glucose of health check-up in a sanatorium of Shanghai in 2003 and 2010 / 中华预防医学杂志

<p><b>OBJECTIVE</b>To examine the prevalence changes of diabetes mellitus (DM) and impaired fasting glucose (IFG) from 2003 to 2010 in the health check-up subjects in Shanghai.</p><p><b>METHODS</b>Health check-up subjects were divided into ten groups by sex and each 5 years old, and the prevalence of crude DM, crude IFG were calculated first. According to Chinese sex and age structure of China Population Statistics Yearbook 2006, sex and age standardized DM and standardized IFG were computed.</p><p><b>RESULTS</b>In the same year, the prevalences of crude DM and IFG increased with increasing age for both male and female, reached the summit at 60 - 69 age group, when at ≥ 70 age group, they had a down trend and were still at higher level. The prevalences of crude DM were 3.99% (986/24 699) in male and 1.61% (176/10 948) in female in 2003, and were 7.85% (3366/42 899) and 2.55% (531/20 820) in 2010. The prevalences of crude IFG were 9.97% (2462/24 699) in male and 5.88% (644/10 948) in female in 2003, and were 30.96% (13 283/42 899) and 17.16% (3573/20 820) in 2010. The prevalences of age standardized DM in 2003 and 2010 were 3.89% and 6.90% for male (χ(2) = 371.89, P < 0.01), 2.12% and 3.23% for female (χ(2) = 29.32, P < 0.01), respectively. The prevalences of age standardized IFG in 2003 and 2010 were 9.51% and 28.55% (χ(2) = 3865.56, P < 0.01) for male, 6.97% and 17.88% (χ(2) = 790.81, P < 0.01) for female. The prevalences of age and sex standardized DM were 3.00% and 5.05% (χ(2) = 385.39, P < 0.01), and prevalences of age and sex standardized IFG were 8.23% and 23.17% (χ(2) = 4480.21, P < 0.01).</p><p><b>CONCLUSION</b>From 2003 to 2010, prevalences of DM and IFG had increased greatly. It concluded that first-level prevention of DM for health check-up subjects should start from youth, and should lay emphasis on population of IFG, especially for male.</p>

Mitochondrial DNA mutations in gastric endothelial cells induced by extract of helicobacter pylori in vitro / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the helicobacter pylori (HP) infection and the genetic instability of mitochondrial DNA (mtDNA) in human gastric adenocarcinoma epithelial cells (AGS).</p><p><b>METHODS</b>After treated with extracts of HP11638 (CagA+, VacA+) or Hp11638 mutant strain (CagA+, VacA-), AGS cells were collected, and mitochondrial DNA was extracted and Cox-I, Cox-II, Cox-III, ATPase6, ATPase8 and Cytb genes and the D-Loop region were amplified by PCR and then sequenced.</p><p><b>RESULTS</b>The mutation rates of the mtDNA in AGS cells were correlated with the extracts of the two HP strains in a concentration- and time-dependent manner. But the mtDNA mutation rate in AGS cells treated with the HP11638 extract was higher than that treated with the Hp11638 mutant extract. Total of 616 mutations in D-Loop region were detected, including 489 point mutations, 81 insertions and 46 deletions. Among them, 70.9% (437/616) belonged to GC to AT and AT to GC transition. Seventeen out of 20 (85%) AGS cells treated with extract of HP had mutations in 303PolyC, 16184PolyC and 514CA regions of mtDNA D-Loop. No mutation was detected in Cox-I, Cox-II, Cox-III, ATPase6 and ATPase8 genes, three point mutations were found in the Cytb gene.</p><p><b>CONCLUSION</b>HP can cause the accumulation of mutations in mtDNA, in particular, in the D-Loop region, and the VacA participated in the process.</p>