Objective To investigate pulmonary capillary changes in patients with diabetes mellitus. Meth-otis Fifty-eight patients with diabetes mellitus were enrolled and forty-seven healthy subjects were taken as control. Diffusion capacity of carbonmonoxide (DLCO) and pulmonary ventilatory function were measured. DM and Vc were measured in twenty-one patients and twelve healthy subjects among them. Results FEV1/FVC was (81.02± 6.40) % in patients with diabetes mellitus and ( 81.20±6.96 ) % in controls, and FEV 1% was ( 102.03±14.40) in patients with diabetes mellitus and 103.94±11.42 in controls ,with no significant difference between patients with DLCO% was ( 72.79±19.85 ) % in patients with diabetes mellitus and ( 90.60±13.25 ) % in controls with a sig-patients whose course of disease was less than ten years,and DLCO% was (64.69±17.49)% in patients with dia-betes mellitus whose course of disease is equal or more than ten years and (80.90±18.98)% in patients whose course of disease is less than ten years,with significant difference between these two groups (t = 4.435, -3. 381, 13.88)% in patients with diabetes mellitas and (83.58±26.79)% in controls with a significant difference (t = 4. 612, P < 0.001 ). Vc was ( 61.40±52.84 ) ml in patients with diabetes mellitus and ( 66.99±19.63 ) ml in con-trols with no significant difference (P > 0.05 ), and Vc% was (78.05±64. 40)% in patients with diabetes mellitus and (79.33±23.32) % in controls, with no significant difference ( P > 0.05 ). Conclusions Diffusing capacity is decreased in patients with diabetes mellitus, which is related to the course of disease . DM decline is the main cause of DLCO decrease in patients with diabetes mellitus.

Objective To evaluate the efficacy of liraglutide in the treatment of Nonalcoholic Fatty Liver Disease(NAFLD).Methods Randomized controlled trials(RCTs)that evaluated the efficacy of liraglutide for NAFLD treatment were searched in multiple databases,including Pubmed,EMBASE,the Cochrane library,CNKI,Wanfang database and VIP.Literature identification and data extraction were based on the inclusion and exclusion criteria.RevMan 5.3 software was used for Meta-analysis.Results A total of 7 RCTs with 500 patients of NAFLD were included.Improved liver histology,or improved the level of alanine aminotransferase[WMD=-25.32,95％CI(-37.22,-13.41),P<0.01] and aspartate aminotransferase[WMD=-24.56,95％CI(-35.10,-14.03),P<0.01] were seen in 12-48 weeks liraglutide treatment.However,liraglutide could not decreased the level of serum cholesterol[WMD=-14.38,95％CI(-48.95,-20.20),P=0.42] and triglyceride[WMD=-15.55,95％CI(-36.20,-5.10),P=0.14].Conclusion liraglutide has the therapeutic effect of NAFLD.

Objective To verify that lncRNA-C21orF96 regulates the expression of miRNA-875-5p and USF2 genes and promotes the invasion and metastasis of gastric cancer.Methods RT-PCR was used to measure the expression of lncRNA-C21orF96 related miRNA in gastric cancer cells.pcDNA3.1 plasmid was used to over-express lncRNA-C21orF96 in KATO-Ⅲ and siRNA was used to knockdown the expression of lncRNA-C21orF96 in SGC-7901,and RT-PCR was used to measure the expression of miRNA-875-5p and USF2 genes;By overexpressing lncRNA-C21orF96 in MKN45,transwell was used to observe changes of cells invasion and migration.Results LncRNA-C21orF96 showed a significant inverse relationship with miR-875-5p,(SGC-7901:21.19 ±1.09 vs.3.28 ±0.06,P＜0.01;SNU-16:24.76 ±2.09 vs.8.16 ±0.07,P ＜ 0.01).In KATO-Ⅲ over-expressing lncRNA-C21 orF96,miR-875-5p expression decreased significantly while USF2 expression increased (P ＜0.01);In SGC-7901 with lncRNA-C21orF96 knockdown,miR-875-5p expression increased significantly while USF2 expression decreased (P ＜ 0.05).The number of cells passing through the artificial basement membrane in the experimental group was significantly different from that in the control group (migration:216.19 ± 2.30 vs.89.19 ± 4.60,P＜0.001;invasion:146.18 ±5.3 vs.59.18 ± 2.60,P ＜ 0.001).Conclusions The overexpression of lncRNA-C21orF96 significantly reduces the expression of miR-875-5p and promotes the expression of USF2,hence promoting the invasion and metastasis of gastric cancer.

Excessive N-acetyl-p-benzoquinone imine(NAPQI)formation is a starting event that triggers oxidative stress and subsequent hepatocyte necrosis in acetaminophen(APAP)overdose caused acute liver failure(ALF).S-glutathionylation is a reversible redox post-translational modification and a prospective mechanism of APAP hepatotoxicity.Glutaredoxin-1(Glrx1),a glutathione-specific thioltransferase,is a primary enzyme to catalyze deglutathionylation.The objective of this study was to explored whether and how Glrx1 is associated with the development of ALF induced by APAP.The Glrx1 knockout mice(Glrx1-/-)and liver-specific overexpression of Glrx1(AAV8-Glrx1)mice were produced and underwent APAP-induced ALF.Pirfenidone(PFD),a potential inducer of Glrx1,was administrated preceding APAP to assess its protective effects.Our results revealed that the hepatic total protein S-glutathionylation(PSSG)increased and the Glrx1 level reduced in mice after APAP toxicity.Glrx1-/- mice were more sensitive to APAP overdose,with higher oxidative stress and more toxic metabolites of APAP.This was attributed to Glrx1 deficiency increasing the total hepatic PSSG and the S-glutathionylation of cytochrome p450 3a 11(Cyp3a11),which likely increased the activity of Cyp3a11.Conversely,AAV8-Glrx1 mice were defended against liver damage caused by APAP overdose by inhibiting the S-glutathionylation and activity of Cyp3a11,which reduced the toxic metabolites of APAP and oxidative stress.PFD precede administration upregulated Glrx1 expression and alleviated APAP-induced ALF by decreasing oxidative stress.We have identified the function of Glrx1 mediated PSSG in liver injury caused by APAP overdose.Increasing Glrx1 expression may be investigated for the medical treatment of APAP-caused hepatic injury.