ABSTRACT
Objective@#To understand the characteristics of injury deaths of children and adolescents aged 0 to 19 years in Kunming during 2010-2019,and to provide injury prevention and control basis.@*Methods@#Injury mortality data in 2010-2019 were from Kunming population based mortality surveillance system. The characteristics of injury death of children and adolescents were analyzed by descriptive statistical analysis, including mortality rate, composition ratio, the annual percent change,etc.@*Results@#Child and adolescent injury mortality was 23.18/10 5,decreasing by year(t=7.13,P<0.05). Male mortality(31.59/10 5) was higher than female(14.27/10 5)(χ2=376.24,P<0.05),the APC of male was -8.82% and -7.48% in female.The injury mortality of male was higher than that of female at all age group. The injury mortality rate of rural children and adolescents(28.65/10 5) was higher than that of urban children(12.37/10 5)(χ2=297.30,P<0.05),the APC was -8.53% in urban areas and -7.78% in rural areas.The top five causes of injury death of children and adolescents were traffic accident drowning, accidental fall, suicide and accidental mechanical suffocation, accounting for 80.88% of the total injury deaths of children and adolescents.In urban and rural areas,injury death by traffic accident, drowning and rural unintentional falls decreased significantly(t urban=3.17,3.20,t rural=5.66,3.12,4.42,P<0.05). The leading cause of death varied by different age groups.@*Conclusion@#The injury mortality rate of children and adolescents in Kunming city is on the decline. Rural children and adolescents, as vulnerable population to injury death, should receive protective strategies according to their specific characteristics of injuries and deaths in different age groups.
ABSTRACT
Objectives: To observe the effect of activated G-protein coupled estrogen receptor 1 (GPER1) on Angiotensin II (AngII)-induced hypertrophy of cultured neonatal rat cardiomyocytes and explore related mechanisms. Methods: Primary cardiomyocytes derived from 2-to 3-day-old neonatal rats were cultured in vitro. Tandem mass tags (TMT) protein mass spectrometry was used to examine protein expressions; relevant bioinformatics analysis was performed to screen the possible regulatory mechanisms. Cardiomyocytes were divided into 6 groups: (1)Blank control group, (2) AngII group, (3)AngII+G1 (GPER1 activator) group, (4)AngII+G1+G15 (GPER1 inhibitor) group, (5)AngII+G1+U0126 (extracellular ERK inhibitor) group and (6)AngII+G1+MK2206 (AKT inhibitor) group (n=3 for each group). Cardiomyocytes GPER1 expressions, mRNA levels of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), protein levels of ERK, AKT with their interactions, autophagy-related proteins LC3II and LC3I were compared among different groups;impact of GPER1 on cardiomyocytes apoptosis was detected by flowcytometry. Results: AngII induced cardiomyocytes hypertrophy and upregulation of ANP and BNP mRNA levels in a dose-dependent manner (P<0.05). GPER1 expression could be detected on cardiomyocytes by Immunofluorescence technique. qRT-PCR results showed that GPER1 was activated by the specific activator G1 and mRNA expressions of ANP and BNP were inhibited in a dose-dependent manner by the specific activator G1 (P<0.05); mRNA levels of ANP and BNP were re-elevated in AngII+G1+G15 group (P<0.05). Western blotting results showed that protein expression of p-ERK and p-AKT was significantly higher in AngII group and AngII+G1 group than in blank control group (P<0.05), significantly reduced in AngII+G1+G15 group compared with AngII+G1 group (P<0.05); decreased expressions of p-ERK, p-AKT and mRNA levels of ANP,BNP were also detected in AngII+G1+MK2206 group (P<0.05). G1 induced protein expression was similar between AngII+G1 group and AngII+G1+U0126 group. Flowcytometry results indicated that cardiomyocytes apoptosis was similar between AngII+G1 group and AngII group (P>0.05). Ratio of LC3II/LC3I was significantly higher and autophagy levels were significantly enhanced in AngII group than in blank control group (P<0.01), these changes could be significantly reversed in AngII +G1 group (P<0.01 vs. AngII). Conclusions: Activation of GPER1 could inhibit neonatal cardiomyocytes hypertrophy, this effect might be related to AKT and ERK signaling pathway and cell autophagy.