Objective To observe the effect of rosiglitazone on serum NOS/NO in apolipoprotein(apo) E knockout mice.Methods Twenty eight-week-old apoE knockout mice were intragastrically administrated 0.2 ml 5% sodium carboxymethycellulose for 12 weeks to establish the animal models of atherosclerosis,in which half of mice simultaneously received 10 mg?kg~(-1)?d~(-1) rosiglitazone as treatment.Ten wildtype mice were used as the normal control group.All mice were fed on normal chow diet.After 12 weeks,aorta were used for histomorphometric analysis by means of HE.Vessel blood was collected for plasma lipid,NO and NOS.Results Histomorphometric analysis showed that the area of atherosclerosis plaque in mice receiving rosiglitazone was significantly smaller than the mouse models of atherosclerosis,while the plasm lipid,NO and NOS were higher.Conclusion Rosiglitazone can inhibit the development of atherosclerosis,which mechanism is related to the protection of vascular endothelial function.

Objective To explore the interaction of calcitonin receptor (CTR) gene polymorphisms and environmental factors in the population lived in coal-burning-borne endemic fluorosis areas in Chongqing.Methods A 1 ∶ 1 case-control study was carried out and Duping Township of Wushan County and Xinglong Township of Fengjie County of Chongqing were chosen as the endemic fluorosis areas.The observation subjects were divided into case group 121 cases and internal control group 130 cases.The Alu I polymorphism in the CTR gene was genotyped using the PCR-RFLP procedure.Logistic regression model was used to analyze the environment and genetic factors,and the interaction between genes and environment was determined according to interaction indicators.Results The rate of CC genotype in case group was lower than that of the control group [60.33％ (73/121) vs.74.62％ (97/130)],while the TT genotype was higher than that of the control group[9.09％ (11/21) vs.3.85％(5/130)].Significant differences in Alu I genotypes were observed between groups(x2 =6.57,P =0.037 ＜ 0.05; 95％CI:0.029-0.036).Allele frequencies of CTR genotypes differed significantly between groups(x2 =7.67,P =0.006 ＜ 0.01 ; OR =0.53,95 ％ CI:0.338-0.834).Urinary fluoride level (≥ 1 mg/L) was demonstrated to be a risk factor of fluorosis(OR =1.814,P =0.041 ＜ 0.05).There was a positive interaction(OR =5.530,γ =2.457) between CT + TT genotypes in CTR and the fluorosis environment of the people (urinary fluoride level ≥ 1 mg/L).Conclusions There is a certain type of interaction between CTR gene C/T polymorphism and environmental fluorine content (urinary fluoride ≥ 1 mg/L) in Chongqing population lived in coal-burning-borne fluorosis areas,and the onset of fluorosis is the result of interaction between heredity and environment.

To study the effect of essential MCU regulator (EMRE) on myocardial ischemia injury in experimental mice with underlining mechanism. Methods: Myocardial EMRE expression was up-regulated by EMRE adenovirus (Ad-EMRE) injection in mice myocardium tissue. Our research included in 3 groups: Sham operation group, sham mice received myocardium injection of eGFP adenovirus (Ad-eGFP); Myocardial infarction (MI) control group, the mice received Ad-eGFP injection and 48 hours later had coronary LAD ligation to establish MI model; MI treatment group, MI mice received Ad-EMRE injection. All animals were treated in 3 weeks. Mice cardiac function was examined by ultrasound; cardiomyocyte hypertrophy was evaluated by wheat germ agglutinin (WGA) staining, collagen fibrosis was measured by Masson staining, cell apoptosis was determined by TUNEL assay, protein expressions of EMRE, caspase-3 and caspase-9 were detected by Western blot analysis and mitochondrial reactive oxygen species (ROS) was assayed by MitoSOX fluorescence probe. Results: Compared with MI control group, MI treatment group showed the worse cardiac function, aggravated cardiac hypertrophy and elevated collagen fibrosis; in addition, MI treatment group had obviously increased cardiomyocyte apoptosis and increased protein expressions of Caspase-3, Caspase-9 and more mitochondrial ROS production. Conclusion: Over expressed EMRE can increase mitochondrial ROS production, induce cardiomyocyte apoptosis and therefore, aggravate myocardial ischemia injury in experimental mice.

Objective To investigate the role of tet methylcytosine dioxygenase 2 (TET2) in the regulation of transforming growth factor-β1 (TGF-β1) expression in human glomerular mesangial cells induced by high glucose.Methods Cultured human glomerular mesangial cells were divided into normal control group (5.5 mmol/L glucose) and high glucose group (30.0 mmol/L glucose) which was cultured for 12 h to 72 h.The gene expression of TET2 in mesangial cells were inhibited by small molecule chemical called SC1,and which were divided into high glucose group (30.0 mmol/L glucose+ DMEM),DMSO group (30.0 mmol/L glucose+0.1％DMSO) and SC1 group (30.0 mmol/L glucose+3 μmol/L SC1).The mRNA and protein expression of TGF-β1,TET1 to 3 and α-smooth muscle actin (α-SMA) was detected by quantitative real-time PCR and Western blotting.Methylation of CpG islands in the regulation region of TGF-β1 was detected by bisulfite sequencing PCR (BSP).The activity of mesangial cell proliferation was assessed by colorimetry of thiazolyl blue (MTT).Results Compared with normal control group,the mRNA and protein expression of TET2 in mesangial cells induced by high glucose was increased significantly in a time-dependent manner (all P ＜ 0.05),but the expression of TET1 and TET3 was not affected.Meanwhile methylation rate of 4 CG sites from 24 h to 72 h were decreased in the first exon of TGF-β1 (P ＜ 0.01),but not in the promoter.Compared with high glucose group,when the expression of TET2 was inhibited by SC1,the methylation rate of TGF-β1 was recovered evidently (P ＜ 0.05),the mRNA and protein expression of TGF-β1 and α-SMA was suppressed,and the proliferation of mesangial cells was decreased (all P ＜ 0.05).Conclusions Demethylation of the CpG island mediated by TET2 may play an important role in the expression of TGF-β1 and mesangial cell phenotype transformation induced by high glucose.

Objective To observe the effect of Xingnao Kaiqiao(Brain-resuscitating)Acupuncture plus language rehabilitation training for motor aphasia caused by cerebral infarction.Methods Totally 90 patients with motor aphasia were randomized into acupuncture plus language training group,single acupuncture group,and language training group(control group),with 30 in each.The Western Aphasia Battery(WAB)was adopted to evaluate the speaking functions of the patients.The aphasia quotient(AQ)of the patients,four basic speaking functions including spontaneous talk,spoken language understanding,retelling,and naming,and communicative ability in daily life(CADL)were observed.Results After treatment,AQ,CADL and score of spontaneous talk,spoken language understanding,retelling,and naming of the three groups were all significantly improved(P0.05).Conclusion Xingnao Kaiqiao Acupuncture plus language rehabilitation training for motor aphasia caused by cerebral infarction is effective with the superiority in improving the ability of spontaneous talk,retelling,naming and CADL.

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 evaluate the expression of mitochondrial fission factor (MFF) and its biological effects in the progression of hepatocellular carcinoma (HCC).Methods ①Quantitative real-time PCR (qPCR),Western blotting and immunohistochemistry analysis were used to detect the expression levels of MFF in HCC tumor tissues and cell lines.②The effect of MFF knockdown on proliferation of HCC cells was analyzed by methyl thiazolyl tetrazolium (MrTT) and colony formation assays in siCtrl,si-MFF#1,si-MFF#2 groups.③The effect of MFF knockdown on apoptosis of HCC cells was analyzed by apoptosis assay with Annexin Ⅴ-FITC and PI.Results ①The MFF expression was higher in tumor tissues compared with tumor-adjacent normal tissues [mRNA level M(QR):0.292 (0.443) vs.0.235(0.333),Z=-4.166,P＜0.001;protein level M(QR):5.414 (4.545) vs.3.120 (3.955),Z =-3.961,P ＜ 0.001)].The MFF expression was higher in HCC cell lines compared with normal liver cell line.②RNA interference-mediated knockdown of MFF inhibited proliferation of HCC cells (siCtrl vs.si-MFF#1:5.29 ± 0.34 vs.3.34 ± 0.37,P =0.014;siCtrl vs.si-MFF#2:5.29 ± 0.34 vs.3.09 ± 0.40,P =0.010).RNA interference-mediated knockdown of MFF inhibited colony formation of HCC cells (siCtrl vs.si-MFF#1:95.35 ± 21.20 vs.37.56 ± 10.61,P =0.003;siCtrl vs.si-MFF#2:95.35 ± 21.20 vs.41.23 ± 10.82,P =0.004).③RNA interference-mediated knockdown of MFF induced apoptosis of HCC cells (siCtrl vs.si-MFF#1:9.56％ ± 1.70％ vs.20.08％ ± 2.03％,P ＜ 0.001;siCtrl vs.si-MFF#2:9.56％ ± 1.70％ vs.21.14％ ± 1.38％,P ＜ 0.001).Conclusion MFF is overexpressed in HCC,which accelerates cell proliferation and suppresses apoptosis,indicating that MFF can serve as a potential oncogene and drug target in HCC treatment.

OBJECTIVETo evaluate the effects of acupuncture on post-stroke spastic paralysis.

METHODSA systematic evaluation including all the relavant randomized controlled trials (RCTs) or quasi-RCTs of acupuncture and moxibustion for treatment of post-stroke spastic paralysis were carried out according to the method recommended by the Cochrane Collaboration.

RESULTSNine hundred and seventy-eight patients being included in fourteen papers met the enrolled criteria. However, their methodological quality was relatively poor. Meta-analysis of nine trials indicated that there was no significant difference between the treatment groups and the control groups in Ashworth scores, Carr-Shepherd scores, nerve defect scores and hip adductor tension scores. Whereas the Fugel-Meyer scores in one trial and the Barthel scores in three trials were better in the treatment groups than those of the control group.

CONCLUSIONA reliable conclusion can not be drawn from the present data because of the defects in methodological quality and insufficient numbers of trials, especially lack the long-term terminal outcomes, although it appears a tedency that acupuncture can improve the conditions of post-stroke spastic paralysis. Therefore, it is necessary to perform more multi-central RCTs of high quality in future.

To establish a platform to monitor the immune rejection after abdominal aortic patch suture in a xenotransplantation model.Methods The carotid was excised from wild-type Bama pigs,cut into 2.5 cmx 1.0 cm pieces in shuttle shape and subsequently sutured to the abdominal aorta of cynomolgus monkeys.No immunosuppressive agent was administered.General conditions of the recipient monkeys were observed.The morphological changes of the graft artery were assessed by pathological examination at postoperative 1 year.Before and 7,14,28 and 49 d after surgery,the blood samples were collected from the recipient monkeys.The serum levels of IgM and IgG antibodies were quantitatively measured by the red blood cell and peripheral blood mononuclear cell (PBMC) from Bama pigs.The quantity of lymphocytes in the recipient monkeys was detected by routine blood test and flow cytometry.Results All 3 monkeys undergoing transplantation survived well.At postoperative 1 year,the lateral tissues of the vascular wall at the artery graft were seen in dark red color.Hematoxylin-eosin (HE) staining revealed a large quantity of red blood cell and platelet deposition,accompanied with lymphocyte infiltration.Using porcine red blood cell and PBMC as target cells,the serum levels of anti-pig IgM and IgG antibodies peaked at postoperative 28 d,and slightly declined at postoperative 49 d.The quantity of lymphocytes and T cell subset also peaked at postoperative 28 d and began to decrease at postoperative 49 d.Conclusions Artery patch suture is a simple and reliable xenotransplantation model.The recipients can maintain normal physiological state without the use of immunosuppressive agents.The grafts can effectively activate the immune system of the recipients,induce the production of anti-pig antibodies and provoke cellular immune rejection.Therefore,this model can be utilized to monitor the immune rejection throughout the xenotransplantation process.

Objective To evaluate the features of myocardial perfusion imaging (MPI) in patients with homozygous familial hypercholesterolemia (HoFH) and its influence factors.Methods Forty-two consecutive HoFH patients (21 males,21 females;average age:(14.8±8.4) years) were retrospectively enrolled in this study from June 2010 to November 2016.Diagnosis was proved by clinical and chromosome tests,and all patients underwent ATP stress and rest 99Tcm-methoxyisobutylisonitrile (MIBI) SPECT MPI with a two-day protocol.Summed stress score (SSS) and summed rest score (SRS) were acquired,and summed difference score (SDS;SSS-SRS) was calculated.Relations between SSS,SRS,SDS and age,lipid profile were analyzed.Two-sample t test,x2 test,multiple linear regression analysis and multivariate logistic regression were used to analyze the data.Results There were 24 patients with positive MPI results (SSS≥1),and females (76.2％,16/21) showed more positive MPI results than males (38.1％,8/21;x2=6.22,P＜0.05).Eighteen patients had negative MPI results.There were 6,8,10 patients with MPI positive results in ＜ 10 years group (n =14),10-18 years group (n =14) and ≥ 19 years group,respectively (x2=2.33,P＞0.05).Positive electrocardiograph (ECG) in ATP stress test was observed in 9 females (42.9％,9/21) and 3 males (14.3％,3/21;x2 =4.20,P＜0.05).Sixty-three (8.8％,63/714) abnormal myocardial perfusion segments (SSS≥ 1) were found,which was mainly (60.3％,38/63) distributed in myocardial regions supplied by left anterior descending branch (LAD).SSS was positively correlated with age and high density lipoprotein cholesterol (HDLC).SRS,SDS were positively correlated with HDLC and age respectively.Multivariate logistic regression analysis indicated that the female was the only independent risk factor to predict positive MPI (odds ratio=5.2,95％ CI:1.363-19.774).Conclusions In HoFH patients,abnormal myocardial perfusion had a rising trend with age increasing.Female patients are more likely to have abnormal MPI.Abnormal myocardial perfusion segments are mainly located in myocardial regions supplied by LAD.Age and gender are influence factors of abnormal MPI in HoFH patients.