Objective To investigate the occurrence situation and related influencing factors of obesity among children aged 6-17 years old in Chengde City.Methods The random sampling method was adopted to extract 16 811 children from 10 primary and middle schools in urban and rural areas of this city.The physical examinations were carried out.The incidence rates of over weight and obesity in different ages,sexes and areas were calculated.The risk factors for childhood obesity were preliminarily screened through questionnaire.And the Logistic regression analysis was conducted for further analyzing the risk factors for childhood obesity.Results Among 16 811 sampled children,the overweight rate was 13.09％ and the obesity rate was 12.1％.The overweight rate and obesity rate in boys were higher than those in girls;which had no statistically significant difference between urban and rural areas(P＞0.05);the incidence rates of overweight and obesity in adolescence were higher than those in preadolescence.The multivariate Logistic regression analysis showed that parental overweight,like to drink sugary drinks and watching television for long time might be the risk factors for childhood obesity.Conclusion The overweight rate and obesity rate among children aged 6-17 years old in this city are higher.Reasonable diet,correct life style and increasing exercise can partially reduce the incidence of children obesity.

Objective: To explore the antagonistic effect of quercetin on fine particulate matter (PM2.5)-induced embryonic developmental toxicity in vitro.Methods: PM2.5 was collected on glass fiber filters by PM2.5 samplers during the heating period of Dec.2015 to Mar.2016 in an area of Haidian District, Beijing City.The sampled filters were cut into 1 cm×3 cm pieces followed by sonication.The PM2.5 suspension was filtered into a 10 cm glass dish through 8 layers of sterile carbasus and stored at-80 ℃ until freeze drying.Frozen PM2.5 suspension was dried by vacuum freeze-drying.In vitro post-implantation whole embryo culture was used in this study.Pregnant rats with 9.5 gestation days (GD) were killed by cervical dislocation and the uteri were removed into sterile Hank's solution.The embryos with intact yolk sacs and ecto placental cones were induced by PM2.5, and then subjected to intervention of quercetin at the doses of 0.1 μmol/L, 0.5 μmol/L, 1.0 μmol/L and 5.0 μmol/L, respectively.At the end of the 48 h culture period, the cultures were terminated, and all embryos were removed from the culture bottles and placed in prewarmed Hank's solution for evaluation.Morphological evaluation of the embryos was conducted under a stereomicroscope using the morphologic scoring system by Brown and Fabro.The mitochondrial reactive oxygen species (ROS) level was detected by FACSCalibur flow cyto-metry using MitoSOXTM Red staining.Results: An obvious antagonistic effect was achieved through querce-tin at the dose of 1.0 μmol/L, which could result in an increase of visceral yolk sac (VYS) diameter, crown-rump length and head length, somite number, and the differentiation of visceral yolk sac vascular vessels.The scores of allantois, flexion, heart, hind brain, midbrain, forebrain, auditory system, visual system, olfactory system, branchialarch, maxillary process, forelimb bud and hindlimb bud also revealed a significant increase and the relative mitochondrial ROS level of embryonic cells was significantly decreased when compared with PM2.5 group.Although quercetin at the doses of 0.1 μmol/L, 0.5 μmol/L, 5.0 μmol/L also exhibited protective effects against PM2.5-induced embryonic developmental toxicity, the protective effect was weaker when compared with the dose of 1.0 μmol/L.Conclusion: Quercetin at proper dose may be of great benefit for the development of embryos exposed to PM2.5 in the uterus of the rats.Quercetin provides an effective strategy for the prevention of PM2.5-induced embryonic developmental toxicity.Clearance of mitochondrial ROS may be one of its mechanisms.

ObjectiveTo investigate the relationship between HLA-DRB1 alleles and chronic urticaria with positive autologous serum skin test (ASST) in Guangxi Zhuang Autonomous Region.MethodsASST was conducted in 144 patients with chronic urticaria,who were subsequently divided into two groups according to the test result:positive group (n =62) and negative group (n =82).PCR amplification with sequence-specific primers was used to determine the genotypes of HLA-DRB1 alleles in the patients and 199 normal human controls.Chi-square test was performed to analyse the difference in the frequency of HLA-DRB1 alleles between the 3 groups by using the SPSS 13.0 statistical software package.ResultsThere were significant differences in the frequency of HLA-DRB1*01,*1401 and *16 alleles among the patients with positive and negative ASST and the controls (x2 =10.92,Pc =0.032;x2 =35.34,Pc ＜ 0.01 ;x2 =12.69,Pc =0.032).Paired comparison revealed significant differences in the frequency of HLA-DRB1*1401 allele between the patients with positive ASST and controls(RR =17.09,Pc ＜ 0.01 ) as well as between the patients with positive and negative ASST (RR =7.20,Pc ＜ 0.01).ConclusionHLA-DRB1*1401 allele may be,or be linked to,the predisposing gene of chronic urticaria with positive ASST in Guangxi Zhuang Autonomous Region.

Objective: To study the incidence of ventricular arrhythmia (VT) in heart failure (HF) patients after cardiac resynchronization therapy (CRT-D) and identify the influencing factors for VT occurrence, to explore the impact of CRT-D shocks on mortality and the management of appropriate shocks. Methods: A total of 42 patients with successfully implanted CRT-D in our hospital from 2009-01 to 2015-04 were studied. There were 2 groups of patients: Ischemic cardiomyopathy group,n=12 including 8 patients for primary prevention and 4 for secondary prevention; Non-ischemic cardiomyopathy group,n=30 including 19 patients for primary prevention and 11 for secondary prevention. The patients with appropriate shocks received four step-wise therapy as drug, equipment parameter adjustments, revascularization and radiofrequency ablation (RA). Results: The patients in Ischemic cardiomyopathy group were followed-up for (38.1±24.0) months, 7 patients suffered from post-operative VT, 5 patients had CRT-D appropriate shocks. The patients in Non-ischemic cardiomyopathy group were followed-up for (27.5±17.8) months, 11 patients suffered from post-operative VT, 10 patients had CRT-D appropriate shocks. The occurrence rates of post-operative VT and CRT-D appropriate shocks were similar between 2 groups,P>0.05; the success rate for ATP treating VT was higher in Ischemic cardiomyopathy group (69% vs 55%),P<0.05. Cox regression analysis indicated that CRT-D as secondary prevention was the independent influencing factor for VT occurrence,P=0.001. During follow-up period, 9 patients with shocks died; the mortality in patients with shocks was higher than those without shocks (43% vs 0%),P<0.05. With four step-wise therapy, 80% patients in Ischemic cardiomyopathy group had no more shocks; with three step-wise therapy as drug, equipment parameter adjustments and RA, 90% patients in Non-ischemic cardiomyopathy group had no more shocks, 10% patients had reduced shocks. Conclusion: CRT-D as secondary prevention was the independent impact factor for post-operative VT occurrence, no matter appropriate or inappropriate shocks would elevate the risk of death in HF patients. Step-wise therapy was important to reduce appropriate shocks.

Objective:To evaluate the immunomodulating effect of oyster peptide on immunosup-pressed mice.Methods:ICR mice injected with cyclophosphamide (CTX)were adopted as the module group,with mice without treatment as the control group,and different dosages of oyster peptide (0.5 g/kg,1 .0 g/kg,and 2.0 g/kg)were given to the low,middle,and high groups for 1 5 days.The body weight,spleen,and thymus weight of the mice,structures under the microscope of the immune organs, numbers of white blood cells,ratios of T lymphocyte subsets,immune cytokines and numbers of nuclear cells,and DNA content in bone marrow were all assessed.Results:Compared with the control group, the structures of thymus and spleen of the mice in the CTX group appeared obscure and shrunk when ob-served under microscope,the number of their white blood cells declined (P =0.04),the proportion of their CD3 +T cells in peripheral blood declined (P =0.003),the proportion of their CD8 +T cells in pe-ripheral blood declined (P =0.002),the concentration of their IL-5 in peripheral blood significantly in-creased (P <0.01 ),the concentration of their nucleated cells and DNA density in bone marrow de-creased (P =0.04,P <0.01 ).Oyster could improve the structures of thymus and spleen of the immuno-suppressed mice.Compared with the CTX group,the number of white blood cells in 2.0 g/kg group in-creased (P =0.003),the proportion of CD3 +T cells in peripheral blood in 1 .0 g/kg group (P =0.04) and 2.0 g/kg group (P =0.02)increased,the proportion of CD8 +T cells in peripheral blood in 2.0 g/kg group increased (P =0.002),the concentration of IL-5 in peripheral blood in all the oyster treated groups increased (P <0.01 in 0.5 g/kg,1 .0 g/kg,and 2.0 g/kg groups),the concentration of IL-1 7 in peripheral blood in 2.0 g/kg group decreased (P =0.03),the concentration of nucleated cells in bone marrow of all the oyster treated groups increased (0.5 g/kg vs.CTX,P =0.04;1 .0 g/kg vs. CTX,P =0.02;2.0 g/kg vs.CTX P =0.01 ),the DNA content in bone marrow of all the oyster treated groups increased (P <0.01 in the 0.5 g/kg,1 .0 g/kg,and 2.0 g/kg groups).Conclusion:Oyster peptide could improve the structures of immune organs of the CTX-induced immunosuppressed mice,re-cover the imbalances of T lymphocyte subsets,improve the immune cytokines and increase numbers of nucleated cells and DNA content in bone marrow,thus improving the immunologic function.

Background Atrial electrical remodeling(AER)plays an important role in the pathogenesis and maintenance of atrialfibrillation.However,little is known about modulation of vagal activilty to AER.This study aimed to investigate the relationshipbetween vagal moduation and AER. Methods Twenty four adult mongrel dogs under general anesthesia were randomized into 3groups.Sympathetic activity was blocked by administration of metoprolol in 3 groups.The changes in vagal modulation to atria afterAER were observed in 10 dogs without vagal interruption in group A.The effects of vagal intervention on AER were investigated in 8dogs with administration of atropine in group B.The impact of aggressively vagal activity on AER was studied in 6 dogs with bilateralcervical vag sympathetic trunLks stimulation during AER in group C.Bilateral cervicall vagosympathetic trunks were decentralized.Multipolar catheters wereplaced into high right atria(RA),coronary sinus(CS)and rightventricle(RV).AER was induced by 600 bpmpacing through RA catheter for 30 minutes.Attial effective refractory period(ERP)and vulnerability window (VW)of atrial fibrillationwere measured with and without vagal stimulation before and after AER.Results In group A,ERP decreased significantly at baselineand during vagal stimulation after AER compared with that beforeAER(all P＜0.05).In group B,ERP remaind unchanged at baselineand vagal stimulation after AER compared with tbat before AER (all P＞0.05).In group C,ERP shortened significantly at baseline andvagal stimulation after AER compared with that before AER(all P＜0.05).ERP shortening after AER in Groups A and C increasedsignificantly than that in group B (all P＜0.05).Atrial fibrillation could not be induced at baseline(VW close to 0) before and after AERin three groups.VW became widen significantly during vagal stimulation after AER compared with that before AER in Groups A and C(all P＜0.05),while VW remained unchanged in group B (VW close to 0).Conclusions Short-term AER results in the decrease inERP.AER is accompanied by the increases in atrial vagal modulation.The increased vagal activity and vagal stimulation promote AER,thereby increase the susceptibility to atrial fibrillation.The interrupted vagal activity attenuates AER.thereby suppresses the atriaIfibrillation mediated by vagal stimutlation.

Objective: To examine the regulatory effect of ginsenoside Rg1 (G-Rg1) on endoplasmic reticulum stress and its effect on hepatocellular apoptosis in carbon tetrachloride (CCl₄)-induced acute liver failure (ALF). Methods: Forty healthy, adult male C57/BL mice were randomly divided into normal saline control (NS) group, G-Rg1 blank control (G-Rg1) group, CCl₄ model (CCl₄) group, and G-Rg1 preventive treatment (CCl₄+G-Rg1) group, and an ALF mouse model was established by CCl₄ induction. Blood and liver specimens were collected from all mice upon sacrifice at 12 hours post-intraperitoneal injection. Serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST) and total bilirubin (TBil) levels were determined using commercial test kits. The mRNA expression of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) was measured using real-time PCR. The protein expression of GRP78, CHOP, caspase12, and caspase3 were measured by Western blot. Histological changes in the liver were assessed by hematoxylin-eosin staining, and the expression of GRP78 and caspase3 was detected by immunohistochemistry. Hepatocyte apoptosis was determined using terminal transferase dUTP nick end labeling. Quantitative data were analyzed using one-way ANOVA, and subsequent pairwise comparisons were performed using the LSD-t method. Results: Serum ALT, AST, and TBil levels in the CCl₄+G-Rg1 group were significantly reduced compared with those in the CCl₄ group (ALT: 691.30 ± 108.06 U/L vs 980.66 ± 110.29 U/L, F = 365.07, P < 0.05; AST: 195.40 ± 15.41 U/L vs 319.44 ± 89.32 U/L, F = 115.64, P < 0.05; TBil: 1.09 ± 0.11 mg/dl vs 1.56 ± 0.12 mg/dl, F = 211.29, P < 0.05). The relative mRNA expression of GRP78 and CHOP was significantly lower in the CCl₄ + G-Rg1 group than in the CCl₄ group (P < 0.05). The relative protein expression of caspase3, GRP78, caspase12, and CHOP was significantly reduced to different extents in the CCl₄+G-Rg1 group compared with those in the CCl4 group (P < 0.05). The CCl₄ + G-Rg1 group showed reduced liver tissue degeneration and necrosis compared with the CCl₄ group. Furthermore, the CCl₄+G-Rg1 group showed significantly fewer brown granules in the liver than the CCl4 group (P < 0.05), indicating that G-Rg1 preventive treatment reduced CCl₄-induced hepatocyte apoptosis. Conclusion G-Rg1 prophylaxis can inhibit inflammation and reduce hepatocyte necrosis and apoptosis during CCl₄-induced ALF. Its mechanism may involve the suppression of endoplasmic reticulum stress-related signaling molecules to alleviate hepatocyte endoplasmic reticulum stress and apoptosis. The results of this study suggest that G-Rg1 may inhibit liver inflammation and hepatocyte apoptosis through multiple targets to protect liver function.

Gut microbiota provide enzymes and additional biochemical metabolic pathways for the host, which together with the host genome and the external environment, influence the body function. The composition of gut microbiota in infant is closely related to health in later life. However, it is influenced by many factors, including delivery mode, feeding pattern, prenatal diet, pregnancy psychology and antepartum antibiotic treatment. Vaginal delivery and breastfeeding is beneficial for shaping gut microbiota, while cesarean section and formula feeding would reduce the amount of gut dominant bacteria. In addition, inappropriate diet during pregnancy, prenatal stress and antepartum antibiotic treatment alters bacterial colonization of the gut in infant.

OBJECTIVETo observe the effect of Rgl treatment on prognosis of alcoholic hepatitis using a rat model.

METHODSFemale Sprague-Dawley rats were radomly divided into four groups:unmodeled control, untreated model, Rgl-treated model, and dexamethasone (DXM)-treated model. The model groups were generated by intragastric injection of alcohol. The unmodeled control group was given an equal dosage of normal saline by the same route. After model establishment, the Rg1 treatment group and the DXM treatment group were administered a 120-hour treatment of Rgl or DXM; the unmodeled controls were administered normal saline on the same schedule. All rats were then fasted for 120 hours and venous blood samples were collected for detection of serum aspartate aminotransferase (AST), alanine transaminase (ALT), total bilirubin (TBil), albumin (Alb), tumor necrosis factor-alpha (TNFat) and interleukin 6 (IL-6). Markers of liver inflammation were measured by immunohistochemistry, western blotting, and real-time quantitative reverse transcription PCR. Fat and apoptosis indices were assessed by hematoxylin-eosin staining and TUNEL assay, respectively. The t-test and F test were used for statistical analyses.

RESULTSThe model group showed remarkably more liver steatosis (over one-third of the tissue) than the unmodeled control group, indicating proper establishment of alcoholic liver disease in the modeled rats. The AST, ALT, TBil, and IL-6 levels were significantly higher in the untreated model group than in the Rgl-treated group and the DXM-treated group. The values were significantly different between the Rg1-treated group and the DXM-treated group:ALT, 69.19+/-8.00 U/L vs.102.88+/-5.16 U/L; TBil, 0.36+/-0.07 µmol/L vs.1.20+/-0.18 µmol/L; IL-6, 126.50+/-6.50 U/ml vs.169.19+/-7.68 U/ml; TNFa, 268.31+/-13.19 µg/L vs.318.94+/-7.87 µg/L (all P less than 0.05). Expression of caspase3 and caspase8 was significantly higher in the model group than in the Rgltreated group and the DXM-treated group (both P<0.05). The apoptosis index was significantly lower in the Rgltreated group and the DXM-treated group than in the model group (both P<0.05). The mRNA and protein expression of caspase3, caspase8 and NF-kB were significantly lower in the Rgl-treated group and the DXM-treated group than in the model group (allP less than 0.05), and the levels of all were significantly lower in the Rgl-treated group cornered to the DXM-treated group (all P<0.05). Conehision In rats with alcoholic hepatitis, Rg1 can significantly relieve pathological injury, improve liver function by blocking the apoptotic pathway, and inhibit release of inflammatory cytokines.

Alanine Transaminase ; Animals ; Aspartate Aminotransferases ; Bilirubin ; Cytokines ; Disease Models, Animal ; Ethanol ; Female ; Ginsenosides ; Hepatitis, Alcoholic ; NF-kappa B ; Rats ; Rats, Sprague-Dawley

ObjectiveTo review the efficacy and safety in secondary prevention of ischemic stroke with cilostazol or aspirin.Methodswe searched Cochrane Library(the 4th issue, 2009 ), PubMed(1980.1～2009.11), EMBASE(1980.1～2009.11), CBM(1978.1～2009.11), CNKI(1979.1～2009.11) and some other databases, then collected all of the studies describing the outcomes in curing the ischemic stroke after taking cilostazol or aspirin. According to the strict inclusion and exclusion criteria, two reviewers independently selected trials, extracted datas, made cross-checking and methodological quality assessment of the homogeneity studies by using the Cochrane systematic review methods, then made Meta analysis using RevMan 5.0 software.ResultsThis systematic review study included two randomized controlled trials and a cross-over trial, which contained a total of 838 participants. The evidence quality of one of the randomized controlled trials was high, however, the evidence quality of another randomized controlled trial and the cross-over trial was poor. Meta analysis results suggested that the effectiveness of cilostazol and aspirin in the secondary prevention of ischemic stroke performed no significantly statistical difference: primary endpoint(30 d［RR=3.00, 95%CI(0.31,28.70)］; 90 d［RR=1.67, 95%CI(0.40,6.92)］; 180 d［RR=1.25, 95%CI(0.50, 3.13)］; 360 d［RR=0.65, 95%CI(0.33, 1.29)］; 540 d［RR=0.80,95%CI(0.54, 1.18)］); combined endpoint(30 d［RR=4.00, 95%CI(0.45,35.61)］; 90 d ［RR=1.75,95%CI(0.52,5.93)］; 180 d［RR=1.00, 95%CI(0.48, 2.07)］; 360 d ［RR=0.77, 95%CI(0.45, 1.29)］; 540 d［RR=0.66,95%CI(0.40,1.09)］); the recurrence of ischemic stroke: cilostazol group: RR=0.64, 95%CI(0.31,1.30)，aspirin group: RR=0.21, 95%CI(0.04,1.06); PDMP［RR=1.00, 95%CI(0.39, 2.58)］. But in terms of the probability of intracranial hemorrhage (［RR=7.14, 95%CI(0.7,58.33)］) and other safety standards, taking cilostazol performed lower than taking aspirin.ConclusionThe side effects of cilostazol and aspirin in the treatment for ischemic stroke were similar to each other, but in terms of the probability of dizziness, headache, tachycardia and palpitation, taking cilostazol performed higher than taking aspirin, however, taking cilostazol performed lower in the probability of intracranial hemorrhage and other organ hemorrhage than taking aspirin. Since this study included a small amount of studies, in which the evidence quality of one of the randomized controlled trials and the cross-over study was poor, therefore, it would be necessary to make a further validation with lots of high-quality clinical trials.