目的掌握珠海市户籍0~14岁儿童伤害死亡流行特征及变化趋势,为伤害干预提供科学依据。方法数据来源于珠海市死因监测系统,应用国际疾病分类标准(international classification of diseases,ICD-10)分析珠海市0~14岁儿童伤害死亡率及分...目的掌握珠海市户籍0~14岁儿童伤害死亡流行特征及变化趋势,为伤害干预提供科学依据。方法数据来源于珠海市死因监测系统,应用国际疾病分类标准(international classification of diseases,ICD-10)分析珠海市0~14岁儿童伤害死亡率及分布特征。结果2006—2017年珠海市0~14岁儿童伤害死亡159例,占0~14岁儿童总死亡的比例为15.46%,12年间平均伤害死亡率为8.15/10万,男童伤害死亡率(9.78/10万)高于女童(6.24/10万)(P<0.01);农村儿童伤害死亡率(11.58/10万)高于城市儿童(5.66/10万)(P<0.01)。前5位伤害死因顺位为溺水死亡(35.86%)、道路交通伤害(19.50%)、跌倒(10.06%)、窒息(7.55%)、中毒(6.92%)。结论伤害死亡是珠海市0~14岁儿童的第3位死因,是1~14岁儿童首位死因。近年来儿童伤害死亡率有逐年下降的趋势。应根据不同地区、性别、年龄的儿童伤害特点,采取有针对性的儿童伤害预防策略和措施。展开更多
Background Estrogen might play an important role in type 2 diabetes mellitus pathogenesis. A number of polymorphisms have been reported in the estrogen receptor alpha （ERα） gene （also named ESR1）, including the ...Background Estrogen might play an important role in type 2 diabetes mellitus pathogenesis. A number of polymorphisms have been reported in the estrogen receptor alpha （ERα） gene （also named ESR1）, including the XbaⅠ and PvuⅡ restriction enzyme polymorphisms of ESR1, which may be involved in disease pathogenesis. The aim of this study was to determine whether ER0t gene polymorphisms are associated with type 2 diabetes mellitus and serum lipid level. Methods Two hundred and ninety-nine patients with type 2 diabetes mellitus were compared with three hundred and forty-one health controls of Guangzhou in China, both were male and postmenopausal female residents at 51--70 years. ESR1 genotyping was performed using polymerase chain reaction （PCR） and PvulI and XbaI restriction fragment length polymorphism （PCR-RFLP） analysis. Results ESR1 allelic frequencies of P, p and X, x alleles were 0.408, 0.592; 0.360, 0.640 in the type 2 diabetes mellitus group and 0.318, 0.682; 0.328, 0.672 in the control group, respectively. In case-control study, there was significant difference in PvuⅡ, but not XbaⅠ, allele frequency between the type 2 diabetes mellitus and control groups （P=0.001 and P=0.122）. When the group was separated into men and women, the difference was significant in women （P〈0.001） but not in men （P=0.854） with the PvulI genotype, and the effect of PvulI variant on the development of type 2 diabetes mellitus was improved with aging. In addition, PvulI genotype was associated with blood glucose [fasting blood glucose （FBG）, postprandial blood glucose （PBG）] and serum lipid [total cholesterol （TC） and low density lipoprotein （LDL）-c] concentration in healthy women. Conclusions PvuII polymorphism of ESRI increases susceptibifity to type 2 diabetes mellitus in Chinese Guangzhou women. ESR1 variants may also impact serum lipid metabolism, which might provide a mechanism connecting ESR1 to type 2 diabetes.展开更多
Background Increased risk of bladder cancer has been reported in diabetic patients. This study was to investigate the roles of mitogen-activated protein kinase kinase （MEK） 1 and 2 in the regulation of human insulin...Background Increased risk of bladder cancer has been reported in diabetic patients. This study was to investigate the roles of mitogen-activated protein kinase kinase （MEK） 1 and 2 in the regulation of human insulin- and insulin glargine-induced proliferation of human bladder cancer T24 cells. Methods In the absence or presence of a selective inhibitor for MEK1 （PD98059） or a specific siRNA for MEK2 （siMEK2）, with or without addition of insulin or glargine, T24 cell proliferation was evaluated by cell counting kit （CCK）-8 assay. Protein expression of MEK2, phosphorylation of ERK1/2 and Akt was analyzed by Western blotting. Results T24 cell proliferation was promoted by PD98059 at 5-20 IJmol/L, inhibited by siMEK2 at 25-100 nmol/L. PD98059 and siMEK2 remarkably reduced phosphorylated ERKI/2. Insulin- and glargine-induced T24 cell proliferation was enhanced by PD98059, suppressed while not blocked by siMEK2. Insulin- and glargine-induced ERKI/2 activation was blocked by PD98059 or siMEK2 treatment, whereas activation of Akt was not affected. Conclusion MEK1 inhibits while MEK2 contributes to normal and human insulin- and insulin glargine-induced human bladder cancer T24 cell proliferation.展开更多
文摘目的掌握珠海市户籍0~14岁儿童伤害死亡流行特征及变化趋势,为伤害干预提供科学依据。方法数据来源于珠海市死因监测系统,应用国际疾病分类标准(international classification of diseases,ICD-10)分析珠海市0~14岁儿童伤害死亡率及分布特征。结果2006—2017年珠海市0~14岁儿童伤害死亡159例,占0~14岁儿童总死亡的比例为15.46%,12年间平均伤害死亡率为8.15/10万,男童伤害死亡率(9.78/10万)高于女童(6.24/10万)(P<0.01);农村儿童伤害死亡率(11.58/10万)高于城市儿童(5.66/10万)(P<0.01)。前5位伤害死因顺位为溺水死亡(35.86%)、道路交通伤害(19.50%)、跌倒(10.06%)、窒息(7.55%)、中毒(6.92%)。结论伤害死亡是珠海市0~14岁儿童的第3位死因,是1~14岁儿童首位死因。近年来儿童伤害死亡率有逐年下降的趋势。应根据不同地区、性别、年龄的儿童伤害特点,采取有针对性的儿童伤害预防策略和措施。
文摘Background Estrogen might play an important role in type 2 diabetes mellitus pathogenesis. A number of polymorphisms have been reported in the estrogen receptor alpha （ERα） gene （also named ESR1）, including the XbaⅠ and PvuⅡ restriction enzyme polymorphisms of ESR1, which may be involved in disease pathogenesis. The aim of this study was to determine whether ER0t gene polymorphisms are associated with type 2 diabetes mellitus and serum lipid level. Methods Two hundred and ninety-nine patients with type 2 diabetes mellitus were compared with three hundred and forty-one health controls of Guangzhou in China, both were male and postmenopausal female residents at 51--70 years. ESR1 genotyping was performed using polymerase chain reaction （PCR） and PvulI and XbaI restriction fragment length polymorphism （PCR-RFLP） analysis. Results ESR1 allelic frequencies of P, p and X, x alleles were 0.408, 0.592; 0.360, 0.640 in the type 2 diabetes mellitus group and 0.318, 0.682; 0.328, 0.672 in the control group, respectively. In case-control study, there was significant difference in PvuⅡ, but not XbaⅠ, allele frequency between the type 2 diabetes mellitus and control groups （P=0.001 and P=0.122）. When the group was separated into men and women, the difference was significant in women （P〈0.001） but not in men （P=0.854） with the PvulI genotype, and the effect of PvulI variant on the development of type 2 diabetes mellitus was improved with aging. In addition, PvulI genotype was associated with blood glucose [fasting blood glucose （FBG）, postprandial blood glucose （PBG）] and serum lipid [total cholesterol （TC） and low density lipoprotein （LDL）-c] concentration in healthy women. Conclusions PvuII polymorphism of ESRI increases susceptibifity to type 2 diabetes mellitus in Chinese Guangzhou women. ESR1 variants may also impact serum lipid metabolism, which might provide a mechanism connecting ESR1 to type 2 diabetes.
基金This work was supported by a grant from the National Natural Science Foundation of China （No. 81070598）.
文摘Background Increased risk of bladder cancer has been reported in diabetic patients. This study was to investigate the roles of mitogen-activated protein kinase kinase （MEK） 1 and 2 in the regulation of human insulin- and insulin glargine-induced proliferation of human bladder cancer T24 cells. Methods In the absence or presence of a selective inhibitor for MEK1 （PD98059） or a specific siRNA for MEK2 （siMEK2）, with or without addition of insulin or glargine, T24 cell proliferation was evaluated by cell counting kit （CCK）-8 assay. Protein expression of MEK2, phosphorylation of ERK1/2 and Akt was analyzed by Western blotting. Results T24 cell proliferation was promoted by PD98059 at 5-20 IJmol/L, inhibited by siMEK2 at 25-100 nmol/L. PD98059 and siMEK2 remarkably reduced phosphorylated ERKI/2. Insulin- and glargine-induced T24 cell proliferation was enhanced by PD98059, suppressed while not blocked by siMEK2. Insulin- and glargine-induced ERKI/2 activation was blocked by PD98059 or siMEK2 treatment, whereas activation of Akt was not affected. Conclusion MEK1 inhibits while MEK2 contributes to normal and human insulin- and insulin glargine-induced human bladder cancer T24 cell proliferation.
