Objective To explore the relationship of hardiness,stress and psychological symptoms.Methods 622 college students participated the present study.Hardiness Scale,Chinese College Student Psychochological symptoms(r=-0.240,P＜0.01).Stress had significantly positive correlation with psychological sympefficient of interaction between stress and hardiness had significant predictability on psychological symptoms(△R2=0.041,P＜0.01).Conclusion Stress had a significant predictability on psychological symptoms.Hardiness was a moderator on stress and psychological symptoms,which can relieve adverse effects induced by stress.

In order to improve works of helping this special group,medical students' current ideological and political situation and characteristics are analyzed.Then applying the Satir family therapy into the medical students' ideological and political education process and analyzing the applicability of Satir into the ideological and political work from the three views of system,family values and humanity.Family tree technology,home remodeling,empty chair technique and iceberg metaphor technology of Satir family therapy are analyzed in details in ideological and political education of medical students with learning difficulties through some helping cases.the three views of system,family values and humanity of Satir family therapy have some value in helping students,building positive value instead of their negative mind towards learning.With the promotion of Satir family's concept and technology,it also helps the ideological and political educators have deep thoughts about the education methods.

Objective To investigate the ABO blood type and sepsis complicated with acute kidney injury,to provide the basis for prevention and treatment.Methods A total of 130 patients with sepsis from renmin hospital of Wuhan University intensive care unit from january 2015 to december 2015 were enrolled in this study,divided into complicated AKI group (64 patients in the observation group) and non-complicated AKI group (66 patients in the control group),analyzed two groups of general data,laboratory indicators,multivariate logistic regression analysis was used to screen out the risk factors for AKI in patients with sepsis.Results A total of 64 patients with AKI were collected from the observation group and 66 patients with non-AKI in the control group,the age of the observation group was higher than that of the control group (65.7 ± 13.1 years old vs 58.5 ± 15.4 years old,P =0.005),male proportion was higher than control group (76.6％ vs 56.1％,P =0.014),drop calcium pigment original quantitative was higher than control group (28.1 ± 21.0pg/L vs 21.1 ± 13.61μg/L,P =0.026),positive blood culture rate was higher than in the control group (30.2％ vs 15.3％,P =0.006).There was no significant difference in ABO blood group distribution between the two groups (P =0.825).The levels of white blood cell count,C-reactive protein and partially activated thrombin were higher in the observation group than in the control group,the platelet count and albumin level were lower than those in the control group,the difference was not statistically significant.The risk factors associated with the incidence of sepsis with AKI were analyzed by multivariate analysis of the logistic regression model:age(P =0.021,OR =0.965),gender (P =0.003,OR =5.321),calcitonin-original(P =0.047,OR =0.975),positive blood culture (P =0.002,OR =1.009),comparison of type A blood and type O blood (P =0.037,OR =5.409) were associated with sepsis complicated with AKI.Conlusion Type A blood and sepsis with AKI associated with the existence of independent correlation,type A blood may increase the risk of sepsis with AKI.

ObjectiveTo investigate the effect of Simvastatin on LOX-1 and ROS in NRK52E induced by ox-LDL.MethodsNRK-52E cells were divided into three groups: Control group,ox-LDL group (50 μg/ml ox-LDL) and Simvastatin group (10 μmol/L Simvastatin +50 μg/ml ox-LDL).After incubation for 24 h,the expression of LOX-I was analyzed by Western blotting,and production of reactive oxygen species (ROS) was analyzed with confocal laser scanning microscopy.ResultsNRK-52E expressed LOX-1 at low level,50 μg/ml ox-LDL increased the expression of LOX-1 by 6.80 times.Pre - treatment with Simvastatin decreased LOX-1 expression by 65％.There was little ROS generation in NRK52E cells,50μg/ml ox-LDL promoted the expression of LOX-1 by 4.86.times.Pre - treatment with Simvastatin decreased ROS generation by 60％.ConclusionsSimvastatin upregulate LOX-1 expression and ROS generation induced by Ox-LDL in NRK52E cells.

Objective To evaluate the effect of aldosterone (Ald) on glomerular mesangial cells apoptosis and to explore the possible mechanisms.Methods Twenty-four Sprngue-Dawley rats were subcutaneously embedded with osmotic mini-pumps and randomly divided into 3 groups.Aldosterone (1.5 μg/h) was administrated subcutaneouly by osmotic mini-pumps in Ald group,eplerenone (Epl,100 mg·kg-1·d-1) and Ald (1.5 μg/h) was given to Epl group.And normal saline was used in control group (Con group).Systolic blood pressure and urinary albumin excretion rate (UAER) were detected on day 0,7,14,21,28.Blood and kidney samples were harvested on day 28.Plasma creatinine,potassium and aldosterone were measured.Renal paraffin sections were stained by PAS and the morphological changes were evaluated by light microscopy.Apoptosis index of mesangial cells were detected by TUNEL assay.The glomerular mesangial cells (MCs) were cultured in a DMEM-F12 media.MCs apoptosis was evaluated by staining cells with Annexin V and propidium iodide (PI) using flow cytometer.Expression of Bcl-2 and Bax mRNA was examined by RT-PCR.The protein level of Bad or phospho-Bad was measured by Western blotting.Results Ald-infused rats developed hyperaldosteronemia and hypokalemia.Rats in Ald group exhibited significant hypertension and marked albuminuria.Ald group rats showed increased number of TUNEL-positive mesangial cells when compared with control rats (P＜0.05).Aldosterone induced mesangial cells apoptosis in a time-dependent manner.Expression of Bcl-2 mRNA was decreased but Bax mRNA was increased in aldosterone treated MCs compared to that in Con group (P＜0.05).Aldosterone promoted dephosphorylation of cytosolic phospho-Bad compared with vehicle treated cells (P＜ 0.05).However,eplerenone attenuated these effects of aldosterone.Conclusion Aldosterone directly promotes mesangial cells apoptosis,and eplerenone can attenuate this effect of aldosterone.Dephosphorylation of cytosolic phospho-Bad may be the key role in the progression of mesangial cells apoptosis induced by aldosterone.

Objective To investigate the effect of angiotensin 1-7(Ang 1-7) on renal proximal tubular epithelial cell(HK-2) transdifferentiation induced by high glucose.Methods All the raised HK-2 cells were divided into 5 groups: normal control group,high glucose group,high glucose with Ang1-7 group,high glucose with Ang1-7 and A779 group,high glucose with pioglitazone group.Expression of peroxisome proliferator activated receptor-γ(PPAR-γ) and α-smooth muscle actin(α-SMA) was detected by Western blotting,real-time PCR and immunofluorescence.Results The levels of PPAR-γ protein and mRNA in HK-2 cells were significantly increased after treatment with high glucose and Ang 1-7.Expression of α-SMA protein and mRNA was inhibited remarkably after treatment with high glucose and Ang 1-7.These effects of Ang 1-7 on HK-2 cells could be reversed by Mas receptor antagonist A779.Conclusion Ang 1-7 inhibits high glucose-induced expression of o-SMA in HK-2 cells,which is in part through the Mas.

Objective To investigate the effects of angiotensin1-7 (Ang1-7) on renal tubulointerstitial fibrosis of diabetic rats.Methods Thirty-two male Wistar rats were randomly divided into four groups: normal control group,diabetic group,telmisartan group,Ang1-7-treated group.For 9 weeks after diabetes mellitus model established,24 h proteinuria,urine NAG/Cr,glucose,insulin,TG,TC,BUN,Scr,Na+ and K+ were assessed.Renal pathological changes were evaluated by PAS staining; Expression of TGF-β1,PPARγ and α-SMA mRNA was deteeted by real-time PCR; Protein levels of PPARγ,α-SMA and TGF-β1 were detected by Western blotting.Results (1)At the end of the ninth week,the blood pressure,proteinuria,renal weight/body weight in group DM were significantly higher than those in group NC (P＜0.05).(2)Renal interstitial fibrosis in group DM was obviously severe as compared to group NC (P＜0.05),but was improved in group TM and group T(P＜0.05).(3)TGF-β1 and α-SMA mRNA in group DM were significantly increased,and PPARγ mRNA was significantly decreased.Compared with group DM,TGF-β1 and α-SMA mRNA were significantly decreased,and PPARγ mRNA was significantly increased in group TM and group T,especially in group T.(4)TGF-β1 and α-SMA in group DM were significantly increased,and PPARγ decreased significantly.Compared with group DM,TGF-β1 and α-SMA decreased significantly,PPARγ increased significantly in group TM and group T,especially in group T.Conclusion Ang1-7 inhibits high glucose-induced α-SMA expression in vivo through up-regulating the PPAR expression and may inhibit renal tubulointerstitial fibrosis of diabetic rats.

Objective To investigate the effect of surfactant protein D(SP-D)overexpression on lipopolysaccharide(LPS)-induced monocyte chemoattractant protein-1(MCP-1)expression in human renal proximal tubular epithelial cells(HK-2)and its mechanism. Methods HK-2 cells were treated with LPS at various concentrations (0, 0.1, 1, 2, 5, 10 mg/L)for 8 h and at 5 mg/L for various time points(0, 2, 4, 8, 16, 24 h). Expression of SP-D was detected by Western blotting and real-time PCR. Expression of MCP-1 was determined by ELISA and real-time PCR. Human SP-D cDNA eukaryotic expression vector pEE14-hSP-D was transfected to HK-2 cells. The changes in transfected cells of SP-D protein were observed by Western blotting. Expression of MCP-1 was detected by ELJSA and real-time PCR. Results SP-D was expressed in HK-2 cells. The levels of SP-D protein and mRNA in HK-2 cells were significantly decreased after treatment with LPS(P<0.05). Expression of MCP-1 protein and mRNA was increased remarkably after treatment with LPS(P<0.05). HK-2 cells transfected with pEE14-hSP-D showed up-regulated expression of SP-D. The overexpression of SP-D inhibited the LPS-inducedexpression of MCP-1(P<0.01). Conclusions SP-D inhibits LPS-induced expression of MCP-1 in HK-2 cells. SP-D may play an important role in the modulation of renal inflammation.

Objective To investigate the effect of surfactant protein A (SP-A) on the production of MIP-2 and binding activity of NF-?B in rat tubular epithelial cells, and evaluate its possible role in renal inflammation. Methods Confluent cultures of NRK-52E cells (a renal tubular epithelial cell line of rat origin) were pretreated with various concentrations of SP-A(0 to 80 ?g/ml) and stimulated by lipopolysaccharide (LPS) (10 ?g/ml) with 2% serum. MIP-2 expression was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The effect of SP-A on NF-?B binding activity was assessed by electrophoretic mobility shift assay (EMSA). Results MIP-2 mRNA and protein was expressed and up-regulated in NRK-52E cells stimulated by LPS. The expression of MIP-2 was down-regulated by SP-A. NF-?B binding activity was inhibited by SP-A in a concentration-dependent manner. Conclusion SP-A binding activity and down-regulates the expression of MIP-2 in renal tubular epithelial cells, which may play an important role in the modulation of renal tissue inflammation.

Objective To evaluate the effect of ALD on podocyte apoptosis and the possible roles of Akt in ALD-induced apoptosis. Methods The cultured rat podocytes were incubated with increasing concentrations of ALD (10-9~10-5 mol/L) for variable time periods. Apoptosis was evaluated by cell nucleus staining and flow cytometry. RT-PCR was used to examine the expression of mineralocorticoid receptor (MR)and 11 Beta-hydroxysteroid dehydrogenase type 2 (11?-HSD2) mRNA in podocyte. Activation of Akt/PKB was evaluated by performing Akt kinase assay. Results ALD induced podocyte apoptosis in a dose- and time-dependent manner. The proapoptotic effect was attenuated by the presence of spironolactone (10-7mol/L). The expression of MR and 11P-HSD2 mRNA was demonstrated in the podocytes by RT-PCR. ALD also inhibited the activity of Akt in a dose-dependent manner, but the inhibitory effect was significantly ameliorated by the presence of spironolactone. The activity of Akt was negatively correlated with podocyte apoptosis. Conclusion ALD induces apoptosis in rat podocytes through the signaling mechanism by which Akt is inhibited.