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Objective:To describe the health-promoting lifestyle of caregivers of children with neurodevelopmental disorders and analyze its influencing factors.Methods:A total of 352 caregivers of children with neurodevelopmental disorders in a hospital in Shenzhen were investigated by questionnaire.The main caregivers were investigated with health-promotion lifestyle scale Ⅱ.Generalized linear model was used to analyze the influencing factors of the health promoting lifestyle score of the caregivers by SPSS 20.0 and R 3.6.0 softwares.Results:The total score of health promotion lifestyle for caregivers of children with neurodevelopmental disorders was (127.66±17.87). The standardized score was (62.05±8.96), with the highest standardized score being (69.62±11.04) for the nutrition dimension and the lowest score being (51.67±11.45) for the physical activity dimension.The difference between the groups was statistically significant ( F=62.780, P<0.01). The results of linear regression analysis showed that the education level ( "junior college" vs "primary and junior high school" : β=14.524, t=3.054, P=0.002; "undergraduate and above" vs "primary and junior high school" : β=18.561, t=3.936, P<0.001), care time ( ">3 years" vs " <1 year" : β=-7.156, t=-3.687, P=0.003), and family income ( "10 000-20 000 yuan/ month" vs "<5 000 yuan/month" : β=14.351, t=3.050, P=0.002) were the influencing factors of health promotion lifestyle of caregivers. Conclusion:The life style of caregivers should be paid attention to.It is necessary to help them improve their health-promoting lifestyle through multiform health promotion methods.
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Objective@#To explore the effect and mechanism of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction.@*Methods@#The acute myocardial infarction (AMI) rat model was established by ligating anterior descending branch of coronary artery for one week.A total of 60 adult male rats in SPF grade with AMI were randomized into the Sacubitril/Valsartan group and the model group, who were gavaged with Sacubitril/Valsartan (68 mg/kg, once daily, n=30) versus with normal saline once daily(n=30) for 4 weeks.Twenty-four hours after the last treatment, the left ventricular cardiac function was examined by echocardiography, and pathological changes of the left ventricle were observed under light microscope.The degree of myocardial fibrosis was quantitatively analyzed by picric acid-sirius scarlet staining.Myocardial cells and fibroblasts from rat pups of the same species were prepared in vitro and were divided into the control group, AngⅡ group, LBQ657 group, valsartan group and LCZ696 group.3[H]-leucine incorporation and 3[H]-proline incorporation were used to detect the myocardial hypertrophy and fibrosis.@*Results@#There was no significant difference in left ventricular function between the the model group and the Sacubitril/Valsartan group before medication (P>0.05). Four weeks after administration of the medications, end-diastolic diameter of left ventricle and end-systolic volume of left ventricle were lower [(9.73±0.26) mm vs.(10.52±0.21) mm, P<0.05; (0.19±0.03) ml vs.( 0.31±0.02) ml, P<0.01], and the left ventricular ejection fraction was higher [(60.17±2.18)% vs.(47.16±5.14)%, P<0.01] in the Sacubitril/Valsartan group than in the model group.The degree of myocardial cell injury in the infarct area was lower, and the area of myocardial fibrosis in the non-infarct zone and peripheral infarcted zone were less in the Sacubitril/Valsartan group than in the model group [(4.0±0.1)% vs. (6.1±0.8)%, P<0.001; (15.7±0.8)% vs. (23.8±1.2)%, P<0.001].3[H]-proline incorporation in cardiac fibroblasts was lower in the Valsartan group than in the Ang Ⅱ group [(152.77±8.46) CPM vs.(221.87±13.41) CPM, P<0.01].3[H]-leucine incorporation in myocardial cells was lower in the Valsartan group than in the Ang Ⅱ group [(113.47±2.33) CPM vs.(127.65±2.38) CPM, P<0.01].3[H]-leucine incorporation in myocardial cells was lower in LBQ657 group than in the Ang Ⅱ group [(119.78±2.98) CPM vs.(127.65±2.38) CPM, P<0.05], and the combined application of valsartan and LBQ657 can further reduce myocardial hypertrophy and fibrosis (P<0.05).@*Conclusions@#Sacubitril/Valsartan can effectively alleviate myocardial remodeling and cardiac dysfunction after myocardial infarction, and the mechanism may be related to reducing AngⅡ-induced myocardial hypertrophy and myocardial fibrosis.
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Objective To explore the effect and mechanism of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction.Methods The acute myocardial infarction (AMI) rat model was established by ligating anterior descending branch of coronary artery for one week.A total of 60 adult male rats in SPF grade with AMI were randomized into the Sacubitril/Valsartan group and the model group,who were gavaged with Sacubitril/Valsartan (68 mg/kg,once daily,n=30) versus with normal saline once daily(n=30) for 4 weeks.Twenty-four hours after the last treatment,the left ventricular cardiac function was examined by echocardiography,and pathological changes of the left ventricle were observed under light microscope.The degree of myocardial fibrosis was quantitatively analyzed by picric acid-sirius scarlet staining.Myocardial cells and fibroblasts from rat pups of the same species were prepared in vitro and were divided into the control group,Ang Ⅱ group,LBQ657 group,valsartan group and LCZ696 group.3 [H]-leucine incorporation and 3[H]-proline incorporation were used to detect the myocardial hypertrophy and fibrosis.Results There was no significant difference in left ventricular function between the the model group and the Sacubitril/Valsartan group before medication (P ＞ 0.05).Four weeks after administration of the medications,end-diastolic diameter of left ventricle and end-systolic volume of left ventricle were lower [(9.73±0.26) mm vs.(10.52±0.21) mm,P＜0.05;(0.19±0.03) ml vs.(0.31±0.02) ml,P＜0.01],and the left ventricular ejection fraction was higher [(60.17±2.18)％vs.(47.16± 5.14)％,P＜0.01] in the Sacubitril/Valsartan group than in the model group.The degree of myocardial cell injury in the infarct area was lower,and the area of myocardial fibrosis in the non-infarct zone and peripheral infarcted zone were less in the Sacubitril/Valsartan group than in the modelgroup[(4.0±0.1)％ vs.(6.1±0.8)％,P＜0.001;(15.7±0.8)％ vs.(23.8±1.2)％,P＜0.001].3 [H]-proline incorporation in cardiac fibroblasts was lower in the Valsartan group than in theAng Ⅱ group [(152.77±8.46) CPM vs.(221.87±13.41) CPM,P＜0.01].3[H]-leucine incorporation in myocardial cells was lower in the Valsartan group than in the Ang Ⅱ group [(113.47 ±2.33) CPM vs.(127.65 ± 2.38) CPM,P＜0.01].3 [H]-leucine incorporation in myocardial cells was lower in LBQ657 group than in the Ang Ⅱ group [(119.78±2.98) CPM vs.(127.65±2.38)CPM,P＜0.05],and the combined application of valsartan and LBQ657 can further reduce myocardial hypertrophy and fibrosis (P ＜ 0.05).Conclusions Sacubitril/Valsartan can effectively alleviate myocardial remodeling and cardiac dysfunction after myocardial infarction,and the mechanism may be related to reducing Ang Ⅱ-induced myocardial hypertrophy and myocardial fibrosis.