ABSTRACT
Objective To observe the cardiac structure and function of obese children,so as to evaluate the risk of early pathological changes and severe consequences.Methods One thousand and thirty-four children (aged between 8 and 9,of 520 females) from 5 primary schools in Beijing were recruited and randomly divided into 2 normal groups (206 males and 336 females),2 overweight groups (94 males and 80 females) and 2 obesity groups (214 males and 104 females) according to the sex and body fat percentage (BF％.The cardiac structure and function were measured using echocardiography.Results (1) Compared with the normal groups,significant increase was observed in the left ventricular internal diameter at end-diastole (LVIDd),left ventricular posterior wall dimensions (LVPWd),left ventricular end-diastolic volume (EDV),left ventricular mass (LVM),left ventricular mass index (LVMI),stroke volume (SV) and cardiac output (CO) in the obesity groups (P＜0.01).However,no significant differences were observed between the 2 groups in the ejection fraction (EF) and fractional shortening (FS) (P＞0.05).(2) BF％ was positively correlated with the aortic root dimension,IVSd,LVIDd,LVPWd,EDV,LVM,LVMI,CO and SV (P＜0.01).(3) The prevalence of concentric hypertrophy was 6.1％ among the overweight and obese children aged between 8 and 9.Compared with the normal children,significant increase was found in their BF,BF％,body mass index,LVM,LVMI and RWT,but significant decrease in SV (P＜0.05).Conclusions Screening with BF％,the overweight and obese children between 8 and 9 years old have showed obvious changes in their cardiac structure and function,including higher left ventricular internal diameter at end-diastole,thicker left ventricular wall as well as bigger left ventricular end-diastolic volume,left ventricular mass,left ventricular mass index,stroke volume and cardiac output.Meanwhile,the prevalence of concentric hypertrophy increased with the increase of body fat percentage.
ABSTRACT
<p><b>OBJECTIVE</b>To prepare nanofibrous membranes of poly (vinyl alcohol)/chitosan (PVA/CS) loaded with varied salvianic acid A sodium (SAS) contents.</p><p><b>METHODS</b>Ultrafine fiber mats were prepared with PVA/CS as matrix and SAS as model drug. The structure and morphology of the nanofibrous membranes were characterized by FT-IR and SEM. Drug-loading amount and drug release profiles of these membranes were determined by UV VIS spectra, and the degradation of the membranes was also investigated.</p><p><b>RESULTS</b>Average diameters of PVA/CS/SAS nanofibers with different SAS contents were 280 ≊390 nm. Drug-loading amount of these nanofibrous membranes was high and exhibited sustained and controlled release behavior for SAS.</p><p><b>CONCLUSION</b>The PVA/CS/SAS nanofibrous membrane prepared in this study loads drug uniformly and has remarkably sustained release behavior, which may offer strategies for the research and development of novel topical drug delivery systems.</p>
Subject(s)
Chitosan , Drug Carriers , Membranes, Artificial , Nanofibers , Polyvinyl AlcoholABSTRACT
The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.
Subject(s)
Animals , Mice , Aorta , Metabolism , Disease Models, Animal , Mice, Inbred C57BL , NADPH Oxidases , Genetics , Reactive Oxygen Species , Metabolism , Vaccination , MethodsABSTRACT
The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.