To evaluate the association of ealpain-10 gene UCSNP-43 polyorphism with type 2 diabetes in Chinese Han population.Meta-analysis showed that calpain-10 gene UCSNP-43 polymorphism may be associated with type 2 diabetes in Chinese Han population.Allele G and genotypo GG may be risk factors for type 2 diabetes,while allele A and genotype GA may be the protective factors.

Objective To evaluate the reliability and validity of the Chinese version of the Diabetes,Hypertension and Hyperlipidemia(DHL) Knowledge Instrument in community diabetic patients.Methods A face-to-face interview was conducted among 513 patients with diabetes in the community from January to March 2016 by using the Chinese version of DHL Knowledge Instrument.Forty of them were randomly sampled and reinvestigated 4 weeks later.The analyses on Cronbach's α coefficient,test-retest reliability,content validity,discriminant validity and construct validity were performed to evaluate reliability and validity of the DHL Knowledge Instrument.Results The qualified questionnaires were collected from 488 participants,including 232 males and 256 females with a mean age of (66 ± 6)years.The overall scores of the Chinese version of DHL Knowledge Instrument was 67.7 ± 18.0 and the scores of diabetes,hypertension,hyperlipidemia,medications and general issues sub-scales were 82.0 ± 22.5,65.9 ± 25.2,38.2 ± 34.3,75.5 ± 20.8 and 72.1 ± 22.9,respectively.The standardized Cronbach's α coefficient of the total scale was 0.849 and the test-retest reliability of the total scale was 0.706 (P ＜ 0.01).In term of content validity,the correlation coefficient was from 0.580 to 0.827 among total scale and sub-scales (P ＜ 0.01).In term of discriminant validity,the difference between the high and the low score group on total scale and sub-scales were significant (t value =-13.486 to-35.528,all P ＜ 0.01).In term of construct validity,based on exploratory factor analysis,the scale was revised.According to confirmatory factor analysis of revised scale,four factor model containing 20 items was well fitted (X2 =159.689,df =134,P =0.064);the GFI (goodness of fit index) =0.966,AGFI (adjusted goodness of fit index) =0.952,RMSEA (root mean square error of approximation) =0.020.Conclusion The Chinese version of DHL Knowledge Instrument possesses good reliability and validity and is suitable to evaluate the knowledge of community diabetic patients,and the modified version may work better than the original one.

Objective To evaluate the association of apM1 gene single nucleotide polymorphisms (SNP) with type 2 diabetes mellitus in Chinese population. Methods Odds ratios (OR) of apM1 gene SNP distribution were analyzed. The Meta-analysis software (RevMan 4.3.1) was employed for summarizing the studies,calculating the pooled OR and its 95% CI and testing the overall effects. Egger's test and fail-safe number for P=0.05 (Nfs<,0.05>) were performed for evaluating the publication bias. The sensitivity analysis by different effect models and sample sizes were employed for the reliability of Meta-analysis. Results Nine literatures were obtained, apM1 gene SNP45 showed remarkable heterogeneity among the studies (P<0.10). Sub-group analysis revealed that the discrepancy based on southern Chinese individuals was the main source of the total heterogeneity.The distribution frequencies of apM1 gene SNP45G, SNP45GG, SNP276G and SNP276GG were significantly higher in Chinese type 2 diabetes mellitus group than those in NGT group (P<0.05). Their pooled OR and 95% C/were 1.50[1.12,2.02], 2.15[1.53, 3.02],1.23[1.03, 1.46] and 1.26[1.00,1.59], respectively (all P<0.05). The distribution of apM1 gene SNP45TG and SNP276GT between type 2 diabetes mellitus and normal glucose tolerance group revealed no difference among these studies. The results of publication bias diagnostics and sensitivity analysis accounted for the reliability and stability of this Meta-analysis. Conclusion apM1 gene SNPs are strongly associated with type 2 diabetes mellitus in Chinese population. SNP45G and SNP276G seem to be risk factors for type 2 diabetes mellitus.

ObjectiveTo investigate the in vivo effects of down-regulating the FGF-21 gene expression by shRNA on glucose and lipids metabolism in high fat diet (HFD) fed ApoE-/- mice.MethoedsMale ApoE-/- mice were randomly divided into chow diet (CF)fed group ( NF,n =10),CF fed + pAd-shFGF-21 group ( NFG,n =9),and HFD fed group ( HF,n =10),HFD fed + Adv-null vector ( pAd-GFP ) group ( GFP,n =6) and HFD fed + pAd-shFGF-21 group ( HFG,n =10).Mice were fed for 16 weeks.C57BL/6J mice were set as control group ( NC group,n=10).NFG,HFG,and GFP groups were injected with pAd-shFGF-21or pAd-GFP by tail vein at the end of 15 weeks.The insulin sensitivity and glucoselipid metabolism were assessed by the hyperinsulinemic- euglycemic clamp technique using 3-[ 3 H] glucose as a tracer at the end of 16 week.ResultsThe plasma FGF-21 levels in NFG and HFG groups were significantly degraded than those in NF and HF groups(20％-27％,P＜0.05),respectively.In the basal state,the fasting blood glucose,fasting plasma insulin,free fatty-acids,triglycerides,total cholesterol,and LDL-C were significantly higher,while the HDL-C was lower in NFG and HFG groups compared with those in NF and HF groups,respectively (P＜0.05 or P＜0.01 ).During the steady-state of clamp,FFA was suppressed in all groups,but it was still higher in NFG and HFG groups than NF and HF groups ( P＜0.05or P＜0.01 ).The glucose infusion rate (GIR)and glucose disappearance rate (GRd)in NFG and HFG groups were significantly decreased compared with NF and HF groups (all P＜0.01 ).In addition,insulin's ability to suppress hepatic glucose production (HGP) during clamps was significantly decreased in HFG and NFG group compared with HF and NF groups (49％ and 20％,respectively; all P＜0.01 ).ConclusionFGF-21 knockdown and low FGF-21 level facilitate the development of metabolic disorder and insulin resistance.

Eighty-two newly-diagnosed type 2 diabetic patients with poor glycemic control were treated by mitiglinide calcium for 16 weeks.Plasma fibroblast growth factor-21 ( FGF-21 ) level were evaluated.The relationship of plasma FGF-21 levels with body mass index,body fat,waist-to-hip ratio,lipid,blood glucose,HbA1c,and free fatty-acid were analyzed.Plasma FGF-21 was decreased significantly by treatment with mitiglinide calcium in type 2 diabetic patients,and it may play a role in the pathogenesis of type 2 diabetes mellitus.

Objective To investigate the effects of liraglutide on gene expression related to cholesterol metabolism in ApoE-/-mice with adiponectin deficiency. Methods Thirty six ApoE-/-mice fed with the high-fat diet were subdivided into four groups. One group was given 100 μl(1×109PFU) of adenoviral pAd-U6-GFP(GFP group, n=6). The second group received 100 μl of adenoviral pAd-U6-Acrp30(ADI group, n=10). The third group was given 100 μl of adenoviral pAd-U6-Acrp30 and liraglutide(HEA group, n=10) and the fourth group was given only 100 μl sterile saline(HF group, n=10). Insulin sensitivity and glucose metabolism were assessed by the hyperinsulinemic-euglycemic clamp technique using 3-[3H] glucose as a tracer. Plasma adiponectin level was evaluated using a commercially available ELISA kit. The mRNA expressions of genes involved in cholesterol metabolism were measured by quantitative realtime PCR. Results Fasting blood glucose(FBG), free fatty acids(FFA), total cholesterol, triglyceride, low density lipoprotein cholesterol, adiponectin, and fasting plasma insulin(FINS) in ADI mice were significantly higher than those in the other groups(P＜0.01), while high density lipoprotein cholesterol was significantly lower(P＜0.05). During the clamp, glucose infusion rate(GIR) in ADI group was significantly lower than the other groups(P＜0.01), and hepatic glucose production(HGP) significantly higher in ADI group(P＜0.01). The mRNA expressions of INSIG2 and LDLR in ADI group were significantly down-regulated in HEA group(P＜0.01 or P＜0.05), while HMGCR and SREBP-2 were significantly up-regulated in HEA group(P＜0.01 or P＜0.05). Conclusions Liraglutide regulates a number of genes involved in cholesterol metabolism and ameliorates hypercholesterolemia by elevating plasma adiponectin level.

OBJECTIVETo investigate the effects of Qili Qiangxin capsules on the amino-terminal pro-brain natriuretic peptide (NT-proBNP) level and cardiac function in patients with silicosis.

METHODSHospitalized silicosis patients with heart failure were divided into treatment group (41 cases) and control group (30 cases) according to their own will. Both groups received comprehensive symptomatic treatment; in addition, the treatment group received Qili Qiangxin capsules. The treatment lasted 6 months. The observed items included NT-proBNP level, 6-minute walk test, ultrasonic cardiogram, and NYHA classification before and after treatment.

RESULTSAccording to NYHA classification, the response rate was 29.27%in the treatment group and 10.00%in the control group; there was a significant difference between the two groups (P < 0.05). The average walk distance in the treatment group was increased from 150.96±73.12 m before treatment to 169.32±77.04 m after treatment, and the improvement was statistically significant (P < 0.05). The average NT-proBNP level in the treatment group was reduced from 1154.44 ± 480.79 ng/L before treatment to 494.49 ± 342.61 ng/L after treatment, and the reduction was statistically significant (P < 0.01). Left ventricular ejection fraction was significantly improved in the treatment group (P < 0.05).

CONCLUSIONQili Qiangxin capsules in addition to comprehensive symptomatic treatment can significantly reduce NT-proBNP level and improve cardiac function in silicosis patients, and thereby improve patients' quality of life.

Capsules ; Drugs, Chinese Herbal ; pharmacology ; Echocardiography ; Heart Failure ; physiopathology ; Humans ; Natriuretic Peptide, Brain ; drug effects ; metabolism ; Peptide Fragments ; drug effects ; metabolism ; Quality of Life ; Silicosis ; drug therapy ; physiopathology

Objective: To study the molecular features of metanephric adenoma (MA) and discuss their values in differential diagnosis. Methods: BRAF V600E immunohistochemistry (IHC) using the mutation-specific VE1 monoclonal antibody and Sanger sequencing of BRAF mutations were performed on 21 MAs, 16 epithelial-predominant Wilms tumors (e-WT) and 20 the solid variant of papillary renal cell carcinomas (s-PRCC) respectively. p16 protein was detected by IHC also. Fluorescence in situ hybridization (FISH) analyses using centromeric probes for chromosome 7 and 17 were performed on the three renal tumors in parallel. Results: Fourteen (14/21, 66.7%) of 21 MA cases demonstrated diffuse, moderate to strong cytoplasmic BRAF V600E IHC staining and the BRAF V600E protein expression was detected in 2 (2/16) of 16 e-WT cases for the first time, whereas all s-PRCCs were negative (P<0.05). All cases (including 14 MAs and 2 e-WTs) with diffuse, moderate to strong cytoplasmic BRAF V600E IHC staining were confirmed to harbor BRAF V600E missense mutations using Sanger sequencing, and no BRAF mutations were detected in cases with negative BRAF V600E protein expression. One case (1/21, 4.8%) showed trisomy of chromosome 7 alone, and another one (1/21, 4.8%) showed trisomy of chromosome 17 alone in 21 MAs. Two cases (2/16) of 16 e-WTs showed trisomy of chromosome 17 alone. In 20 s-PRCCs, trisomy of chromosomes 7 alone was reported in 2 cases (2/20), trisomy of chromosome 17 alone in 3 cases (3/20) and trisomy of chromosome 7 and 17 in 14 cases (14/20). The total positive rates of trisomy of chromosome 7 and/or 17 in MAs, e-WTs and s-PRCCs were 9.6% (2/21), 2/16 and 95.0% (19/20). p16 protein was positive in 81.0% (17/21) MAs, whereas the positive rates in e-WTs and s-PRCCs were 2/16 and 5.0% (1/20). Conclusions Most MAs harbor BRAF V600E mutations, and MAs lack the gains of chromosome 7 and 17 that are characteristic of papillary renal cell carcinoma. These molecular features can be used to distinguish MA from its mimics. BRAF V600E IHC using the mutation-specific VE1 monoclonal antibody provides an effective method in BRAF V600E mutations detection of renal tumors. p16 is overexpressed in MA, and the finding suggests that the low proliferative rate of the tumor might be attributed to BRAF V600E-induced senescence mediated by p16.

Objective:To explore the feasibility of estimating adenoma detection rate (ADR) based on polyp detection rate (PDR) in colonscopy.Methods:In the present single-center retrospective study, the conversion coefficient was calculated based on the total colonoscopy cases in 2017. ADR of each colonoscopists was estimated based on PDR and conversion coefficient, which was then verified compared with the actual ADR for consistency.Results:A total of 25 112 colonoscopies with 20 experienced colonoscopists were included. The overall conversion coefficient was 0.483. The intraclass correlation coefficient of the actual ADR and the estimated ADR was 0.818 (95% CI: 0.596-0.924, P<0.01). Conclusion:It is feasible to estimate ADR based on PDR, but this method is only an expediency. More attention should be paid to the establishment of a standardized electronic database.

The objective was to investigate the effect of kinsenoside (Kin) treatments on macrophage polarity and evaluate the resulting protection of chondrocytes to attenuate osteoarthritis (OA) progression. RAW264.7 macrophages were polarized to M1/M2 subtypes then administered with different concentrations of Kin. The polarization transitions were evaluated with quantitative real-time polymerase chain reaction (qRT-PCR), confocal observation and flow cytometry analysis. The mechanism of Kin repolarizing M1 macrophages was evaluated by Western blot. Further, macrophage conditioned medium (CM) and IL-1 were administered to chondrocytes. Micro-CT scanning and histological observations were conducted on anterior cruciate ligament transection (ACLT) mice with or without Kin treatment. We found that Kin repolarized M1 macrophages to the M2 phenotype. Mechanistically, Kin inhibited the phosphorylation of IB, which further reduced the downstream phosphorylation of P65 in nuclear factor-B (NF-B) signaling. Moreover, Kin inhibited mitogen-activated protein kinases (MAPK) signaling molecules p-JNK, p-ERK and p-P38. Additionally, Kin attenuated macrophage CM and IL-1-induced chondrocyte damage. , Kin reduced the infiltration of M1 macrophages, promoted M2 macrophages in the synovium, inhibited subchondral bone destruction and reduced articular cartilage damage induced by ACLT. All the results indicated that Kin is an effective therapeutic candidate for OA treatment.