ObjectiveTo develop an emotion regulation competence scale for Chinese edolescents.MethodsOn the basis of literature review and experimental analysis,703 edolescents were administrated.Item analysis,exploratory factor analysis,confirmatory analysis and correlation analysis were conducted.ResultsFinal scale consisted of three dimensions which were emotion controlling competence,emotion recovering competence and strategies application competence.The Cronbach's α coefficient of the total-scale was 0.874,the test-retest coefficients of total-scale was 0.851.Confirmative factor analysis revealed that the three-dimension model was proper( x2/df =3.06,NNFI =0.95,CFI =0.96,RMSEA =0.079 ).ConclusionThe emotion regulation competence scale has satisfactory psychometric characteristics.

ObjectiveTo explore the effect of adolescents'personality on emotion regulation.Methods 1073 adolescents were surveyed by adolescents' personality scale and emotion regulation scale.Resultspositive emotion regulation strategies were positively correlated with openness,agreeable,extraversion and conscientiousness ( r =0.359 ～ 0.455,P ＜ 0.01 ),and were negatively correlated with neuroticism ( r =- 0.266,P＜ 0.01 ) ; negative emotion regulation strategies were negatively correlated with openness,agreeable,extraversion and conscientiousness ( r =- 0.117 ～ - 0.318,P ＜ 0.01 ),and were positively correlated with neuroticism ( r =0.621,P＜ 0.01 ) ;emotion regulation competence were positively correlated with openness,agreeable,extraversion and conscientiousness ( r =0.402 ～ 0.498,P ＜ 0.01 ),and were negatively correlated with neuroticism ( r =- 0.466,P ＜ 0.01 ).Hierarchical regression analysis showed that cognitive reappraisal,positive refocusing,behavior diverting,rumination,self-suppressing and attacking others had an indirect effect between personality and emotion regulation competence (P ＜ 0.01 ).ConclusionAdolescents' personality and emotion regulation strategies have effect on emotion regulation competence.

Objective To investigate the prevalence of Helicobacter pylori infection and the incidence of gastric mucosal lesions in type 2 diabetes mellitus(DM)and diabetic kidney disease(DKD)patients with dyspepsia symptoms.Methods A total of 241 type 2 diabetic patients and 69 non -diabetic subjects with dyspeptic symptoms were enrolled in the study.Gastroduodenal lesions were observed by gastrointestinal endoscopy and the presence of Helicobacter pylori infection was identified by rapid urease test and serum IgG antibodies to Helicobacter pylori.Urine albumin excretion rate(UAE)at 24 hours was measured in all subjects.According to the urinary albumin excretion rate,patients were classified into diabetes mellitus group(DMgroup,with UAE <30mg/24h),diabetic kidney disease group 1(DKD group 1,with UAE 30mg/24h to <300mg/24h)and diabetic kidney disease group 2(DKD group 2 >300mg/24h).Estimated glomerular filtration rate were above 60mL·min -1 ·(1.73m2 )-1 in the three groups of patients.The 69 cases of non -diabetic subjects were used as the control group.Results The prevalence of H pylori infection in the DKD group[145 /72(62.5%)]and the DKD group 2[34 /53(64.15%)]were significantly higher than those in the control group[28 /65(43.1%)](χ2 =3.901,P =0.04;χ2 =4.223,P =0.03)and the DM group [27 /63 (42.9%)](χ2 =4.104,P =0.04;χ2 =5.116,P =0.03).No significant differences of H.pylori prevalence were detected between the DKD groups(χ2 =1.304,P =0.29)as well as the DMgroup and the control group (χ2 =0.723,P =0.40).Gastroscopy results showed that the incidence of normal endoscopic performance in the DMgroup was higher than that of the control group(57.1% vs.38.5%,χ2 =4.612,P =0.03).There were no significant differences between the control group and DM group,DKD1 group and DKD2 group in the incidence of gastric mucosal lesions (Superficial gastritis:χ2 =1.206,0.912,0.707;erosive gastritis:χ2 =1.422,1.836 0.870;duodenal ulcer:χ2 =243.1, 1.716,2.233;gastric ulcer:χ2 =1.440,0.971,1.322 and esophagitis:χ2 =2.116,2.318,2.488,all P >0.05). Conclusion Diabetic nephropathy patients are more susceptible to Helicobacter pylori infection.There is no significant difference in the infection rate of Helicobacter pylori between type 2 diabetic nephropathy with microalbuminuria and with macroalbuminuria.There are no significant differences in the type of gastric mucosal lesion between Type 2 diabetes mellitus,diabetic nephropathy patients and non diabetic patients.

Objective To analyze the clinical features and prognostic factors of patients with malignant tumor complicated by acute kidney injury (AKI),and provide the basis for preventing AKI and improving the prognosis.Methods Malignant tumor patients complicated by AKI were screened with the electronic medical records system from January 2001 to December 2012 at the Affiliated Hospital of Qingdao University.The clinical characteristics in the 12 years were analyzed by statistical analysis and compared.The risk factors of the hospital mortality in malignancies tumor complicated by AKI were analyzed by Logistic regression analysis.Results A total of 100 patients with malignant tumor complicated by AKI were collected,accounting for 24.94％ of AKI patients and 1.66‰ of malignant tumor patients at the same period.Malignancies were consist of hematologic malignancies (11％),non-metastatic solid tumor (47％),metastatic solid tumor (42％).The most common factor leading to AKI for malignancies was post-renal obstruction (64％),followed by nephrotoxic drugs or contrast agents (24％),hypovolemia (18％).There was no significant change of the etiologies for AKI between the first six-year and the second six-year (P ＞ 0.05).The hospital mortality of patients with malignant tumor complicated by AKI was 25％,and multivariate Logistic regression analysis showed that multiple etiologies (OR=13.356),multiple organ failure (OR=222.256),and metastatic solid tumors (OR=8.497) were the independent risk factors for hospital mortality.Conclusions AKI is a common complication in patients with malignant tumors,and the most common factor leading to AKI is postrenal obstruction.The hospital mortality in malignancies with AKI is high,which should get the attention of clinicians.

Objective To evaluate the effects of renin-angiotensin system (RAS) blockades [angiotensin-converting enzyme inhibitors (ACEI) and angiotensin Ⅱ type 1 receptor blockers (ARB)]on contrast-induced nephropathy (CIN) in patients undergoing angiography.Methods Pubmed,Embase,Cochrane library,Wanfang database and CNKI were searched.The literature limited range was from their start year to July 2015.Randomized controlled trials (RCTs) and non-randomized controlled trials of renin-angiotensin system blockades in influencing CIN were assessed.Two investigators extracted data and performed quality analysis independently from all trims included.Rev man 5.3 software was used.Results 16 trials with a total of 15 897 patients were identified.There were 7490 patients who received renin-angiotensin system blockades and 8407 patients in control group.The meta analysis revealed a higher CIN incidence in ACEI/ARB group than that in control group (14.35％ vs 12.13％,P=0.04,OR=1.44,95％CI 1.01-2.04).For patients with renal insufficiency,ACEI/ARB group had a higher CIN incidence than control group (12.23％ vs 7.32％,P=0.02,OR=1.80,95％CI 1.10-2.94),and the serum creatinine changes in ACEI/ARB group were higher than those in control group.There was statistical difference in serum creatinine changes between groups (P=0.02,MD=0.08,95％CI 0.02-0.15).Conclusions Renin-angiotensin system blockades can increase theincidence of CIN in patients undergoing angiography.Renin-angiotensin system blockades can contribute to CIN for patients with renal insufficiency.

Objective To investigate the renal expression of stem cell factor (SCF) in lupus nephritis (LN) and its correlation with disease activity and renal injury parameters. Methods Histochemical stain was used to examine all renal specimens (LN group n=34, chronic glomerulonephritis n=16, control group n=8). Hyhridization in situ and immunohistochemistry were used to detect the expression of SCF and infiltration of mast cells, macrophages , α-SMA (+) cells in renal tissues of the two groups. SPS software was used for tissue of the control group. However, they increased markedly in lupus nephritis and CGN (t=6.03～14.25, P< 0.01). But there was no significant difference between LN and CGN in SCF and mast cells in renal interstitium. Positive correlation was observed among the expression of SCF and α-SMA and the number of mast cells and macrophages (r=0.47～0.84, P<0.01) at their corresponding locations. The expression of SCF and ot-SMA and the number of macruphages were positively correlated with renal pathological active index, chronic index, albuminuria and the injury of renal interstitium (r=0.34～0.93, P<0.05 or 0.01); meanwhile, it was negatively correlated with Ccr(r=-0.39～0.61, P<0.01). There was significant correlation between SCF, macrophages and anti-dsDNA antibody, complement C3 level, SLE disease activity index (SLEDAI). The number of mast cells in renal interstitium was positively correlated with chronic indexes and the injury of renal interstitium (r=-0.86, r=0.93, P<0.01) and negatively correlated with Ccr (r=-0.56, P<0.01), but not correlated with active index and albuminuria (r=0.27, r=0.23, P>0.05). Conclusion The expression of SCF is widespread in kidney, and it is markedly eorrelated with various kinds of inflammatory cells, renal inherent cells, renal function, and urine protein levels. SCF may be an critical participant in the initiation and progression of renal injuries in human lupus nephritis.

Objective To investigate the expression of 4-hydroxynonenal (4-HNE) in the kidney of diabetic rats and the effect of probucol.Methods The rats were being intraperitoneal injected with STZ (60 mg/kg) to establish diabetic models.Then diabetic rats were randomly divided into diabetic group (group D,n =24),probucol treated group (group P,n =24).Normal rats were taken as control group (group C,n =24).Rats in group P were treated by probucol (110 mg·kg-1·d-1); rats in group D and group C were given equal volume water instead.Scr,BUN,triglyceride (TG),total cholesterol (TC) and 24-hour urinary proteinin were measured at the 4th,8th and 12th week.PAS staining and HE staining were used to evaluate the pathological changes of the kidney.The immunohistochemistry and Western blotting were used to detect the expression of 4-HNE in renal tissue.Results Levels of Scr,BUN,TG,TC and 24-hour urinary protein in group D were higher than those in group C at the 4th,8th and 12th week(all P ＜ 0.05); Levels of Scr,BUN,TG,TC and 24-huor urinary protein in group P were lower than those in group D at 4th,8th and 12th week (all P ＜ 0.05).The pathological changes of the kidney in group D were more serious than that in group P.The expression of 4-HNE in group D were higher than group C at the 4th,8th and 12th week (all P ＜ 0.05);The expression of 4-HNE in the kidneys of group P decreased significantly compared to that of group D at the same time (P ＜ 0.05).Conclusions As an indicator of lipid peroxidation,the expression of 4-HNE significantly increases in the kidney of diabetic rat.Probucol may protect the diabetic kidney through decreasing the expression of 4-HNE and the level of lipid peroxidation.

ObjectiveTo investigate the protective effect of combination of triptolide and irbesartan on the podocytes in a type 2 diabetic(T2DM) rat model,and evaluate its mechanism.Methods T2DM rats were induced by fed with high-sucrose-high-fat diet combined with a low dose of streptozocin.The rats were randomly divided into 5 groups:normal control group ( NC,n =10),diabetes group ( DM,n =11),triptolide treatment group (DT,n =12),irbesartan treatment group (DI,n =12) and triptolide combined with irbesartan treatment group (DTI,n =13). Ultrastructure of podocytes was observed by electronic microscopy and urinary albumin (UAL) excretion by ELISA was determined after 8 weeks.The expression of nephrin and bone morphogenetic protein-7(BMP-7), connective tissue growth factor (CTGF),transforming growth factor (TGF)β1 mRNA and proteins were detected by immunohistochemistry,real-time PCR and Western blot. Results Increased UAL was significantly attenuated in all treatment groups.Compared to NC group,UAL in DM group was increased significantly (0.45 ± 0.09 vs 6.36 ± 0.87,P ＜ 0.01 ),while decreased in triptolide or irbesartan alone treatment group (2.48 ± 0.37 and 2.68 ±0.42,both P ＜ 0.01 ).Compared with those in control groups,kidney expression of nephrin,BMP-7 mRNA and proteins were downregulated while CTGF, TGFβ1 mRNA and proteins were significantly upregulated in T2DM rats. Triptolide or irbesartan each alone moderately ameliorated albuminuria and podocyte damage.However,their combined usage showed a dramatic therapeutic synergism,manifested by prevention of progressive albuminuria,restoration of the glomerular filtration barrier,reversal of the decline in slit diaphragm proteins,reduction expression of CTGF,TGFβ1,and upregulation of BMP-7.Conclusion Our findings show that triptolide can increase the efficacy of irbesartan,leading to a more effective prevention of kidney disease in T2DM rat model,which may through upregulation of BMP-7 and inhibition the overexpression of CTGF and TGFβ1.

To reveal the involvement of oxidative stress in hypertension and insulin resistance. Angiotensin Ⅱ was given to adrenomedullin-knockout mice for 4 weeks. 4-Hydroxy-TEMPOL, a superoxide scavenger mimetic was also employed. The results suggested that adrenomedullin may exert a protective effect against insulin resistance via its intrinsic antioxidant effect.

AIM: To examine Nucleostemin (NS) expression in tumor cells, and observe the effect of NS specific RNA interference on the cell proliferation in Hela cells. METHODS: Total RNA was extracted from 6 kinds of cultured tumor lines, the NS expression level was measured by RT-PCR and Northern blot. An NS-specific siRNA expression vector was constructed to transfect HeLa cell (NS-siRNA-HeLa), and the proliferation of the cell was observed. RESULTS: NS was highly expressed in 6 kinds of tumor cells. NS expression level in the NS-siRNA-HeLa cells was remarkably reduced, and the percentage of G_0/G_1 cells increased. The neoplasm forming ability in nude mice by the NS-siRNA-HeLa cells was decreased. CONCLUSION: NS is highly expressed among tumor cells. NS-specific siRNA inhibits the entry of the cell cycle into the S phase, and remarkably reduces the proliferation ability of HeLa cells in vitro and in vivo.