Objective To investigate the clinical viability of pre-eclampsia by measuring the level of ?-HCG in blood,blood calcium,hematocrit(HCT)and the mean arterial blood pressure(mABP).The preventive value of calcium supplement was also evaluated. Methods 356 volunteers'(16th～20th gestational weeks)were measured ?-HCG in blood,blood calcium,HCT,meanwhile mABP from the same patients.If blood ?-HCG≥50 632 IU/L,blood calcium≤2.18 mmol/L,HCT≥0.35 and mABP≥85 mm Hg(1 mm Hg=0.133 kPa),a positive conclusion was made.Women with positive results were randomly divided into test group and control group. Results 71 cases turned out to be positive in this serial test.The positive predictive value was 81.82%,negative predictive value was(97.30%),the sensitivity and specificity were 84.38% and 96.77% respectively.In the study group,the incidence of pre-eclampsia was significantly decreased as compared with the control group(P

Objective To discuss the effect of tetrandrine on endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats. Methods 78 rats were randomly divided into 3 groups: control group(n=36), Tet-treated group(n=36), sham-operated group(n=6). Control group and Tet-treated group were adapted with Allen's combat modeling method. Rats in Tet group were injected Ted with a dosage 22.5 mg/kg in 30 minutes, 24 hours and 48 hours after ASCI, and the same dose of saline was injected into injured group as control .Samples were dissected from the spinal cord injury sites at 1 day, 3 days, 1 week, 2 weeks, 3 weeks, 4 weeks after ASCI, and tested by HE staining for morphology and by immunolfuorescence staining for the expression of BrdU and nestin. Results A little Nestin positive cells and BrdU positive cells were found in control group and Tet-treated group at 1 day after injury. A large number of positive cells were found in both groups at 1 week after injury and reached the peak which lasted for 2 weeks and then decreased gradually. The expression of Nestin positive cells and BrdU positive cells in control group and Tet-treated group were decreased significantly at 4 weeks after injury, but were still more than that in sham operation group. The number of Nestin positive cells and BrdU positive cells in Tet-treated group were more than that in control group at each time point after injury. The expression was higher in Tet-treated group than control group at 1 day, 3 days, 1 week, 2 weeks, 3 weeks after injury and had no difference at 4 weeks after injury. Conclusions Tetrandrine could increase the number of Nestin positive cells, BrdU positive cells and endogenous neural stem cells though improving the microenvironment, and it is beneficial for the recovery of spinal cord injury in rats.

AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis in-duced by CoCl 2 .METHODS:NSCs were exposed to CoCl 2 at different doses (200~600μmol/L) for 24 h.The cell via-bility and apoptosis were measured by CCK-8 assay and TUNEL method.The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR.The protein levels of Bcl-2 and Bax were detected by Western blotting .RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05).CoCl2 at concentration of 400μmol/L for 24 h was used to induce apopto-sis and the expression of miR-26a was down-regulated compared with control (P<0.05).Exposure to CoCl2 at concentra-tion of 400μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax , down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05).CONCLUSION:CoCl2 at concentration of 400μmol/L induces the apoptosis of NSCs obviously . CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway .Declining miR-26a may be related to NSC apopto-sis.

Objective To investigate the characteristics of myocardial injury and its underlying mechanism in rats resuscitated from cardiac arrest. Methods Forty-two male Wistar rats were randomly(random number) assigned into the post-resuscitation (PR) 4 h, PR 24 h, PR 48 h, and sham groups. Ventricular fibrillation was induced by transcutaneous electrical epicardium stimulation and untreated for 6 min, followed by cardiopulmonary resuscitation (CPR). Myocardial function, glucose metabolism, myocardial ultrastructure, the status of mitochondrial permeability transition pore (MPTP) and mitochondrial membrane potential (MMP) were evaluated at different time points. Results Myocardial dysfunction was found at 4 h after restoration of spontaneous circulation (ROSC). The ejection fraction and cardiac output were decreased (all P<0.01), the diastole left ventricular posterior wall became thicker (P<0.01), and the end-diastolic volume was reduced (P<0.05). However, cardiac function was recovered almost completely at 48 h after ROSC. The PR 4 h group had a higher SUVmax, a more obvious decreased absorbance, and a lower MMP than the sham group (all P<0.01), but no statistically significant differences were noted between the PR 48 h group and the sham group (P>0.05). At 4 h and 24 h after ROSC, the mitochondria was swollen and the mitochondrial crista was sparse, but the myocardial ultrastructure was complete. Conclusions Post resuscitation myocardial dysfunction occurs after ROSC and the myocardial dysfunction is completely reversible at 48 h after ROSC, which may be related to the reversibility of myocardial injury and the gradual recovery of mitochondrial structure and function.

Objective To compare the effect of transplant islets between the subcutaneous inguinal white adipose tissues and renal capsule in the treatment of type 1 diabetes mellitus in mouse models. Methods The mice with type 1 diabetes mellitus undergoing islet transplantation were divided into the white adipose group (n=10) and renal capsule group (n=10). The islets were isolated, purified and transplanted to the subcutaneous white adipose tissues of inguinal region and renal capsule. The random blood glucose level and glucose tolerance function of the recipient mice in two groups were continuously monitored after operation. Islet grafts of the surviving recipient mice were harvested at postoperative 100 d for histopathological examination. Results In the white adipose group, the blood glucose levels of 6 recipient mice were restored to normal at 1 month after transplantation, whereas the blood glucose levels of the other 4 recipient mice were high, which died before the end of monitoring. In the renal capsule group, the blood glucose levels of 10 recipient mice returned to normal within 10 d after transplantation. Islet grafts of the recipient mice in two groups could lower the blood glucose levels, whereas the islet grafts in the white adipose group required a longer time to exert the effect. The glucose tolerance function of the mice in the renal capsule group was significantly better than that of those in white adipose group (P < 0.05). Histopathological examination demonstrated that the insulin of the islet grafts was normally expressed in two groups. Conclusions The islets transplanted into the subcutaneous white adipose tissues of inguinal region can play an effective role in regulating the changes of blood glucose level. Although the blood glucose-lowering function is slightly weaker than that of the islets graft in the renal capsule, it has multiple advantages resembling the ideal islet transplantation sites, which is a promising replacement site for islet transplantation.

Objective To determine the relationship between brain injury and cerebral glucose metabolism in rat model of cardiac arrest. Methods Asphyxia-induced cardiac arrest model was established. Forty-two male Wistar rats were randomly assigned to sham or experimental groups. Rats in the CA4,CA6 and CA8 group were treated with cardiopulmonary resuscitation(CPR) 4 min, 6 min and 8 min after cardiac arrest, respectively. The maximum standardized uptake value (SUVmax) of glucose was detected by PET, and neural defi cit score (NDS) were evaluated at 24 h and 72 h after ROSC. The numbers of injured neurons and apoptotic cells and the protein level of hexokinase I (HXK I) were measured at 72 h after ROSC. Results SUVmax, NDS and the level of HXK I were all decreased after ROSC, and interestingly, this declination of these markers was correlated with the prolongation of the duration of CA, the longer duration of CA the more declination of these biomarkers. Accordingly, the number of injured neurons and apoptotic cells increased were correlated with duration of CA, and thus CA8 group had greater numbers of those cells than CA6 group and CA4 group (P<0.05),and CA6 group had greater numbers of those cells than CA4 group(P<0.05). In addition, the SUVmaxwas positively correlated with NDS(P<0.05), and negatively correlated with the numbers of injured neurons and apoptotic index(P<0.05). Conclusions The degree of brain injury is associated with cerebral glucose metabolism, and PET may become a novel method to assess the severity of brain damage after CA.

Objective The prevalence of obesity is constantly increasing. Multiple metabolic complications are related to obesity, including type 2 diabetes mellitus and non-alcholic fatty liver disease(NAFLD). Our study aimed to investigate the prevalence of obesity comorbidities and its association with BMI. Methods 765 individuals who visited the multidisciplinary clinic for obesity in Peking University First Hospital from 2015, Jun. to 2018, Sept. were enrolled in this study. The height, body weight, waist circumference, hip circumference were measured during the first visit. Body adipose percentage and basal metabolic rate were recorded. Questionnaires for daily food intake, comorbidity, and lifestyle were recorded. Fasting insulin, C peptide, glucose, HbA1C , uric acid, liver enzymes and lipid profile were measured. Statistical analysis was performed using SPSS 16. 0, and P<0. 05 was considered as statistical significant. Results Daily energy intake was higher in obesity group [ obese vs non-obese, (2136.6±739.4vs1905.7±468.4)kcal/d,P=0.046].Hypertension,NAFLDandgoutriskincreasedsignificantly in obesity group (obese vs non-obese, 36.0％vs 24.5％, P=0.02;76.5％ vs 60.6％, P<0.01;6.9％ vs 1.8％, P=0.04, respectively) . Family history of obesity and diabetes increased in obesity group ( obese vs non-obese, 64.5％vs 53.6％, P=0.03;47.4％vs 37.3％, P=0.048). Fasting insulin and C-peptide levels were higher in obesity group [obese vs non-obese, (24.8 ± 15.3 vs 13.6 ± 9.5)μIU/ml, P<0.01;(3.72 ± 1.40 vs 2.70 ± 1.16)μIU/ml, P<0.01). Liver enzymes increased significantly in obesity group [obese vs non-obese, (47.2±45.4 vs 23.3±21.4)U/L, P<0.01; ( 30. 4 ± 24. 0 vs 19. 9 ± 8. 5 ) U/L, P=0. 001 ] . Conclusions Obesity population had higher risk of hypertension, NAFLD and gout. Fasting insulin, C-peptide, liver enzymes, and UA also increased significantly in these patients. It is critically important to those obese individuals for regular screening of NAFLD and diabetes mellitus.