Objective Analysis the bacteria distribution and drug resistance change in our hospital from 2011 to 2013 ,and pro‐vide evidence for clinical rational use of antimicrobial drugs .Methods Isolate all kinds of pathogens from outpatient ,inpatient from 2011 to 2013 in statistics and the analysis of drug resistance .Results The top four highest separation rates were Escherichia coli , Pseudomonas aeruginosa ,Acinetobacter baumannii and Staphylococcus aureus .Methicillin‐resistant staphylococcus aureus (MRSA) separation rate of 3 years were 52 .17% ,57 .9% ,55 .52% respectively .Conclusion Production extended spectrum β‐lactamases (ELBLs) of Escherichia coli has a tendency to increase;the third generation cephalosporins and aztreonam resistance rates also show an upward trend ,Carbapenems Enterobacteriaceae is still the most active drugs;Glycopeptides ,linezolid ,moxifloxacin ,and rif‐ampicin always maintain a high activity against MRSA ;the resistant rates of non‐fermenting bacteria is higher ,we need to concerned about the emergence of multi‐drug resistant .Recommend giving antibiotics under the guidance of susceptibility results .

Objective: To study effect of small ubiquitin related modifier protein 1 (SUMO1) in inflammatory reactions mediated by tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB in myocardial damage of rats with type 2 diabetes mellitus (T2DM). Methods: A total of 20 Goto-Kakizaki (GK) rats with spontaneous diabetes mellitus (DM) were randomly divided into group DM1 (pure DM group, n=10) and group DM2 (DM+high-fat diet group, n=10), and another 10 normal Wistar rats were regard as healthy control group. Expressions of SUMO1, TNF-α and NF-κB were measured by immunohistochemical method. Results: 1. Levels of blood glucose and TG in group DM1 and group DM2 were significantly higher than those of healthy control group, and those of DM2 group were higher than of DM1 group ,P<0.05 all; 2. Myocardial cells lined up in order and there was no hypertrophy in group DM1; but those in group DM2 showed cells loosely lined up and hypertrophy under light microscope; 3 Immunohistochemical assay indicated that expression of SUMO1 in group DM2 and DM1 group were significantly higher than those of healthy control group [(44.5±1.1) vs. (27.2±2.2) vs. (21.7±3.0)], and of group DM2 was significantly higher than that of DM1 group (P<0.01 all); expression of TNF-α in group DM2 and group DM1 were significantly higher than that of healthy control group [(27.5±1.5) vs. (20.2±2.7) vs. (13.1±1.6)], and of DM2 group was significantly higher than that of group DM1 (P<0.01 all)；expression of NF-κB in group DM2 and group DM1 were significantly higher than that of healthy control group [（30.1±1.7）vs.40.7±1.5）vs.（16.0±2.6）], but of group DM1 was significantly higher than that of group DM2 (P<0.01 all). Conclusion: There are obvious metabolic disorders of glucose and lipid in T2DM rats, and complicated morphological changes of myocardial tissues similar to myocardial lesions in DM humans; the expressions of SUMO1, NF-κB and TNF-α significantly increase, suggest SUMO1 takes part in inflammatory reaction mediated by NF-κB, TNF-α in myocardial lesion of rat with T2DM，and may inhibit NF-κB, possesses effect of protect myocardium.

Objective: To study influence of overweight and obesity on blood coagulation and metabolic disorders in patients with type 2 diabetes mellitus (T2DM). Methods: A total of 248 preliminary diagnosed T2DM patients were selected. According to body mass index (BMI), they were divided into normal BMI control group (n=95), overweight group (n=87) and obesity group (n=66). Blood lipids, blood glucose and fasting insulin (FINS) were measured in all patients and homeostasis model-insulin resistance index (HOMA-IR) was calculated then. Statistical analysis was performed. Results: Compared with normal BMI control group, there were significant increase in fibrinogen [(3.37±0.55) g/L vs. (4.04±0.70) g/L vs. (5.20±0.69) g/L], urine microalbumin [(14.46±8.90) mg/g vs. (47.33±42.54) mg/g vs. (104.45±60.78) mg/g], fasting blood glucose [ (7.15±0.97) mmol/L vs. (8.84±1.81) mmol/L vs. (10.06±2.28) mmol/L], FINS [(10.09±8.21) IU/ml vs. (14.33±15.55) IU/ml vs. (19.69±10.86) IU/ml], HOMA-IR[(3.19±2.59) vs. (5.51±5.38) vs. (8.48±4.62)], TG, TC and LDL-C levels in overweight group and obesity group, and the more BMI patients were, the higher these indicators were; There were significant decrease in plasma prothrombin time [(13.33±0.69)s vs. (12.74±0.69)s vs. (11.43±0.53)s], activated partial thromboplastin time [ (37.32±2.31)s vs. (36.55±2.41)s vs. (34.61±1.53)s] and HDL-C [(1.54±1.12) mmol/L vs. (1.27±0.41) mmol/L vs. (1.09±0.28) mmol/L] in overweight group and obesity group（P<0.05 all）. Conclusions: Overweight and obesity aggravate coagulation and metabolic disorders in patients with type 2 diabetes mellitus. It also aggravates degree of insulin resistance, the more BMI patients are, the more serious they are.

AIM: To find out whether different dosage of rare earth element-lanthanum can influence the expression of aquaporin 7(AQP 7) in the testis of rats. METHODS:Rats were fed with lanthanum nitrate [La(NO 3) 3] and killed 6 months later. Testes were then removed immediately to extract total RNA. Northern blot analysis is performed finally. RESULTS:0.1 mg/kg La(NO 3) 3 depressed the expression of AQP 7 in rat testis, while 20 mg/kg La(NO 3) 3 had no significant effect on it. CONCLUSION: AQP 7 expession is found in the rat testis; La(NO 3) 3 can depress the expression of AQP 7 in the rat testis.

AIM: To find out whether different dosage of rare earth element-lanthanum can influence the expression of aquaporin 7(AQP 7) in the testis of rats. METHODS:Rats were fed with lanthanum nitrate ［La(NO3)3］ and killed 6 months later. Testes were then removed immediately to extract total RNA. Northern blot analysis is performed finally. RESULTS:0.1 mg/kg La(NO3)3 depressed the expression of AQP 7 in rat testis, while 20 mg/kg La(NO3)3 had no significant effect on it. CONCLUSION: AQP 7 expession is found in the rat testis; La(NO3)3 can depress the expression of AQP 7 in the rat testis.

Objective: To study expressions of small ubiquitin-related modifier protein（SUMO）4 (SUMO4), nuclear factor (NF)- κB and inhibitory factor of NF-κB (IκB) in kidneys of rats with type 2 diabetes mellitus (T2DM). Methods: A total of ten 40-week-old male Goto-Kakizaki (GK) rats （with spontaneous diabetes mellitus）of specific-pathogen free (SPF) grade, and ten 40-week-old male Wistar rats of SPF grade were selected. The lesion of renal tissue was observed by hematoxylin eosin (HE) staining. Expressions of SUMO4, NF-κB and IκB in renal tissue were observed by immunohistochemistry methods. Results: In the GK rats, glomerular capillary ball hypertrophy, basilar membrane slightly thickening; glomerular mesangial cells hyperplasia, hypertrophy and renal tubular epithelial cells hypertrophy were observed. Compared with normal Wistar rats, expression levels of NF-κB [(0.232±0.034) vs. (0.634±0.058)], IκB [(0.242±0.027) vs. (0.712±0.078)] and SUMO4 [(0.160±0.031) vs. (0.545±0.045)] significantly increased in renal tissue of GK rats (P<0.01 all). Conclusion: Compared with Wistar rats, expressions of NF-κB, IκB and SUMO4 significantly increase in renal tissue of GK rats, suggesting that SUMO inhibiting transcriptional activity of NF-κB may exist in kidneys of T2DM rats. Therefore, sumoylation may be a new therapeutic target for inhibit renal microvascular lesion of diabetic disease.

BACKGROUND:Dapagliflozin,an inhibitor of sodium-glucose cotransporter 2,can delay the progression of atherosclerosis by regulating glucose metabolism,inhibiting inflammation and improving endothelial cell function. OBJECTIVE:To study the effect of dapagliflozin on cell pyroptosis and endothelial dysfunction induced by oxidized low-density lipoprotein. METHODS:Human umbilical vein endothelial cells were divided into a control group(no intervention),a model group(treated with oxidized low-density lipoprotein for 24 hours),and a dapagliflozin group(treated with oxidized low-density lipoprotein + dapagliflozin for 24 hours).Endothelial cell proliferation activity was measured by cell counting kit-8 assay.The levels of intercellular adhesion molecule 1,vascular cell adhesion molecule 1,and monocyte chemotactic protein-1 in cell supernatant were detected using ELISA.Nitric oxide level in the cells was detected by nitrate reductase assay.The pyroptosis rate and characteristics of endothelial cells were detected by Hoechst 33342/PI fluorescence co-staining and lactate dehydrogenase release assay.The protein expression levels of NLRP3,caspase-1,GSDMD,interleukin-1β,and interleukin-18 were detected by western blot assay. RESULTS AND CONCLUSION:(1)Oxidized low-density lipoprotein could cause pyroptosis and dysfunction of endothelial cells.(2)Compared with the control group,the level of nitric oxide and cell activity were decreased(P<0.05),while lactate dehydrogenase,intercellular adhesion molecule 1,vascular cell adhesion molecule 1,and monocyte chemotactic protein-1 levels were significantly increased in the model group(P<0.05).Compared with the model group,cell activity and nitric oxide levels significantly increased(P<0.05),but lactate dehydrogenase,intercellular adhesion molecule 1,vascular cell adhesion molecule 1,and monocyte chemotactic protein-1 levels were significantly diminished in the dapagliflozin group(P<0.05).(3)Compared with the model group,cell pyroptosis rate and the protein expression of pyroptosis factor NLRP3,caspase-1,GSDMD,interleukin-18 and interleukin-1β significantly reduced in the dapagliflozin group(P<0.05).(4)The results indicate that dapagliflozin inhibits oxidized low-density lipoprotein-induced endothelial pyroptosis and ameliorates endothelial cell dysfunction.