The professional care by multi-disciplinary team and priority of prevention should be carried out in the treatment of diabetic foot disease to reduce diabetic amputation.This article describes the professional experience in the treatment of four complicated cases with diabetic foot disease and emphasizes the importance of the co-operation among different specialists,including diabetologists and wound,vascular,orthopedic surgeons,etc.as well as of varied therapies applied in staged management of the diabetic foot care,by treating these patients with diabetic foot disease as early as possible.

Objective To investigate the relationship between heart rate variability ( HRV) and chronic complications in pa-tients with type 2 diabetes mellitus (T2DM).Methods A total of 96 patients with T2DM was given chronic complication assessment . Demographic data were obtained .Diabetic retinopathy , diabetic kidney disease , diabetic peripheral neuropathy ( DPN) , and peripher-al artery disease ( PAD) were diagnosed according to international clinical classification .The parameters of HRV in the patients with diabetes and non-diabetes were examined with24 h Holter recorder .Results The HRV parameters of type 2 diabetic patients were significantly lower than those of non-diabetes ( P <0.05 ) .HRV time domain parameters [ standard deviation of normal RR intervals (SDNN), standard deviation of 5-minute mean RR intervals (SDANN), root mean square difference among successive RR normal in-tervals ( RMSSD) ] were especially impaired in diabetic patients with retinopathy compared to those without retinopathy .HRV parame-ters except low-to-high frequency ratio ( LF/HF) and MNN were lower in diabetic patients with kidney disease than those without kid-ney disease .HRV parameters were no significant difference between patients with or without PAD .Conclusions HRV of diabetic pa-tient is lower.Diabetic retinopathy and kidney disease impact on the HRV .

Objective:To investigate the role of microRNA (miR)-155 in hydrogen peroxide (H 2O 2)-induced oxidative stress injury in lens epithelial cells (LECs) and its mechanism regulating silent information regulator factor related enzymes 1 (SIRT1). Methods:The HLE-B3 at the logarithmic growth phase was taken and cultured for 24 hours under different concentrations of H 2O 2 (0, 50, 100, 200, 400, 800 μmol/L), and the cell viability was detected by MTT assay to determine the optimal concentration of H 2O 2 for establishing an oxidative stress injury model.HLE-B3 cells were divided into 6 groups, untreated blank control group, model control group cultured with 100 μmol/L H 2O 2, miR-155 mimics group transfected with miR-155 mimics, miR-155 mimics negative control group transfected with miR-155 mimics negative control, miR-155 inhibitor group transfected with miR-155 inhibitor, and miR-155 inhibitor negative control group transfected with miR-155 inhibitor negative control.Transfected cells were cultured with 100 μmol/L H 2O 2.Cells in various groups were cultured for 24 hours, and cell morphology was observed under an inverted microscope.The relative expression of miR-155 and SIRT1 mRNA in cells was assayed by fluorescent quantitative PCR.Cell apoptosis rates were detected by flow cytometry.Reactive oxygen species (ROS) content was identified by 2', 7'-dichlorofluorescein diacetate (DCFH-DA) fluorescent probe method.Superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration were measured by ELISA method.The targeting of SIRT1 by miR-155 was tested by dual luciferase reporter gene system.Expressions of SIRT1, B-cell lymphoma/leukemia-2 gene (bcl-2), bcl-2 associated X protein (bax), cleaved-cysteine aspartase 3 (cleaved-Caspase-3) proteins were determined by Western blot. Results:With the increase of H 2O 2 concentration, the cell viability gradually decreased, and the differences in cell viability among different concentrations were statistically significant (all at P<0.05), and 100 μmol/L was selected as the experimental concentration.Cells in blank control group grew well adherently.The number of cells in model control group decreased, and the morphology of some surviving cells changed, and their boundaries were blurred.There were fewer cells in miR-155 mimics group than model control group, and the cell morphology changed.There were more cells in miR-155 inhibitor group than model control group, and the cells grew well.Compared with model control group, the relative expression level of miR-155, the apoptosis rate, ROS content, MDA concentration, as well as the relative expression levels of bax and cleaved-Caspase-3 proteins were increased, and the relative expression level of SIRT1 mRNA, the SOD activity, the relative expression of SIRT1 and bcl-2 proteins, as well as bcl-2/bax were decreased in miR-155 mimics group, and the differences were statistically significant (all at P<0.05). Compared with model control group, the relative expression of miR-155, the apoptosis rate, ROS content, MDA concentration, as well as the relative expression levels of bax and cleaved-Caspase-3 proteins were decreased, and the relative expression level of SIRT1 mRNA, SOD activity, the relative expression levels of SIRT1 and bcl-2 protein, as well as bcl-2/bax were significantly increased in miR-155 inhibitor group, and the differences were statistically significant (all at P<0.05). The relative luciferase activity of wild-type SIRT1 in cells transfected with miR-155 mimics was 0.41±0.07, which was significantly weaker than 1.00±0.11 in cells transfected with miR-155 mimics negative control, and the relative luciferase activity of wild-type SIRT1 in cells transfected with miR-155 inhibitor was 1.98±0.17, which was significantly higher than 1.00±0.12 in cells transfected with miR-155 inhibitor negative control, showing statistically significant differences ( t=7.838, 8.157; both at P<0.05). No obvious effect on the relative luciferase activity of mutant SIRT1 was found in transfected cells. Conclusions:miR-155 is involved in H 2O 2-induced oxidative damage of LECs, and its overexpression can target the expression of SIRT1 and play a role in cell injury.

According to the alanine aminotransferase (ALT)level, 4 509 patients were assigned into group A (n=449, with raised ALT)and group B (n=4 060, normal ALT). Between the patients of group A and B, differences existed in age [(48.5 ± 11.3 vs 55.7 ± 11.4) years, P＜0.01], duration of diabetes [( 36.8 ±45.0 vs 56.2±58.8 ) months, P＜0. 01], body mass index[BMI, (27.7±3.9 vs 25.8±3.4) kg/m2, P＜0.01], waist-tohip ratio (0.95±0.06 vs 0. 93±0.07, P＜0. 01 ), diastolic blood pressure [( 78± 10 vs 75± 10) mm Hg, 1 mm Hg=0. 133 kPa, P＜0. 01], fasting blood glucose [(9.04±2.91 vs 8.63 ±3.05 ) mmol/L, P = 0. 008], 2 h blood glucose after meal[( 13.85±4.67 vs 13.07 ± 4. 92 ) mmol/L, P=0. 002], HbA1c(8. 11% ± 1.82% vs 7.74% ±1.96%, P＜0. 01 ), fasting serum insulin[( 10.59±7.31 vs 7.97±7.18) mU/L, P＜0. 01], postprandial insulin [(48.96±43.80 vs 35.25 ±32.37 ) mU/L, P＜0. 01], homeostasis model assessment for insulin resistance ( HOMA-IR, 4.11±-2.85 vs 3.00 ± 2.92, P＜ 0. 01 )、 triglycerides [( 2.77 ± 2.50 vs 2. 19 ± 2.99 ) mmol/L, P＜0. 01], and high-density lipoprotein-cholesterol [HDL-C, ( 1.20 ± 0. 30 vs 1.29 ± 0. 83 ) mmol/L, P = 0. 01].Logistic regression analysis showed that HbA1C, postprandial insulin, and HOMA-IR, uric acid and urinary albumin were positively, and HDL-C negatively related with the ALT level. It suggests that raised ALT seems to be an index related to the clustering of cardiovascular risk factors, insulin resistance, and earlier onset of type 2 diabetes.