Nowadays,aging is the general trend of population development in the world.Type 2 diabetes is one of the most common chronic diseases in the elderly.Because of the atypical symptoms and signs,accompaniment of chronic cardiovascular disease and vulnerability to low blood glucose in the elder patients with diabetes,we should to make safe,effective,and individualized therapeutic programs for them.This paper will review the current prevalence,characteristics,and oral drug selection among elderly individuals with T2DM.

Autoimmune disease is a condition arisen from an abnormal immune response to the tissue cells itself, its precise mechanism remains unknown, and the failure to distinguish self from non-self is often termed a breach of tolerance and is the basis for autoimmune illness. The tumor necrosis factor-α (TNF-α) induced protein 8 like-2 (TIPE2) is a newly discovered member of TNF-α induced protein 8 (TNFAIP8) family which is an essential negative controller of both innate and adaptive immunity. It has been documented that marked expressions of TIPE2 are evident in various autoimmune diseases, including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), myasthenia gravis (MG) and systemic lupus erythematosus (SLE), which appear to be closely related to the severity, progression as well as prognosis of the illness, thereby contribute to the pathogenesis of autoimmune diseases. Deficient expression of TIPE2 might contribute to the hyper-reactivity of auto-reactive lymphocytes and macrophages, or aggregate inflammatory reaction by prompting high concentration of pro-inflammatory cytokines in peripheral blood, thus, trigger the development and progression of autoimmune diseases. In addition, dysregulation of immune homeostasis could be another latent target involved into the mechanism of autoimmune diseases. The present paper summarized the potential role and its mechanism of TIPE2 in the development of autoimmune diseases.

11? Hydroxysterold dehydrogenases (11?-HSDs )catalyse the interconversion of active glucocorticoids(cortisol,corticosterone )and their inert 11?-keto derivatives(cortisone,11-dehydrocorticosterone)They play an important role in regulating the local glucocorticoids activities.Glucoeorticoids can induce insulin resistance.The alteration of 11?-HSD activities in tissues such as liver ,adipose tissue, is closely relevant to some common disorders,including obesity and type 2diabetes mellitus.

hydroxysteroid dehydrogenase (11? HSD) catalyzes the interconversion of cortisol with its inactive metabolite cortisone. The congenital deficiency of 11? HSD2 induce hypertension and hypokalemia. This disorder is called "Apparent Mineralocorticoid Excess(AME)". Glycyrrhizic acid and other endo and xenobiotics have been found to inhibit the activity of 11? HSD and cause excess mineralocorticoid effects that is similar to AME. The decrease in 11? HSD activity is related with the acquired and congenital hypertention.

Peroxiredoxins(Prxs) are a family of antioxidant protein that have been identified in prokaryotes and eukaryotes. As antioxidants, Prxs protein contains an active site cysteine that is sensitive to oxidation by H 2 O2, eliminate active oxygen that exist in normal tissues and cells, protect cells from oxidative damage induced by reactive oxygen species ( ROS). Prxs protein is a known free radical scavenger, and has been shown to play a role in several diseases. In this review, recent advances on the study of Prxs protein family and tumor related diseases are reviewed, which is expected to provide new ideas for the diagnosis and treatment of the related clinical diseases.

Infectious diseases are resulted from the invasion of an organism's body tissues by multiple disease-causing agents. It has been demonstrated that the occurrence and development of infectious diseases are closely associated with the functional status of immune system. Cytokines play significant roles in modulating the host immune response to the clearance of pathogenic microorganisms and maintaining immune homeostasis. Interleukin-35 (IL-35), as a newly identified member of IL-12 family, exerts suppressive effect on immune response by means of a specific pattern. With the progress of research in recent years, IL-35 might serve as an essential contributor in the immunopathogensis of vast infectious diseases, including hepatitis B, sepsis, tuberculosis and parasite infection, which simultaneously appear to be closely related to the severity, progression as well as prognosis of the illness. Apparently, IL-35 is regarded as a potent and promising anti-inflammatory cytokine in clinical application; its potential value may shed light on the therapeutic strategies for infectious diseases. Herein, we mainly review the potential role and its mechanism of IL-35 in the pathogenesis of infectious diseases.

Objective Up to now, the role of Brucea in early embryonic development of mice and its mechanism is still unclear.This paper aims to explore the role of Brusatol in mouse early embryonic development and its possible mechanism.Methods 100 kunming rats of clean grade(80 female rats and 20 male rats) were divided into 6 group: negative control group(no DMSO)、blank control group(culture in fresh CM with equal DMSO)、20nmol/L brusatol treated group、50nmol/L brusatol treated group、100nmol/L brusatol treated group、200nmol/L brusatol treated group(A solution of Brusatol was diluted in CM to concentrations of 20, 50, 100 or 200nmol/L.).Each group used an average of 20 embryos each time, repeated 4 times.Fertilized eggs after cultured 24h, 48h,72h, 96h were respectively 2-cell stage, 4-cell stage,morula and blastocyst stage..The embryo development rate was observed in the culture medium and the optimal concentration was selected, the embryos were collected to analysis the subcellular localization of the Nrf2 by immunofluorescence.The mRNA expression level of Cyclin B, CDK1 and the protein expression of Nrf2 were detected by Q-PCR and western blot respectively.Results In 4-cell stage, the embryo development rates of 20、50、100nmol/L brusatol treated groups[(75.0±2.8)%、(30.4±7.5)%、(4.2±5.9)%] significantly reduced compared with the negative control group[(93.0±2.8)%]、blank control group[(90.9±1.2)%].In morula stage, compared with blastocyst rates of negative control group、blank control group [(83.5±2.1)%、(84.2±1.2)%], 50nmol/L brusatol treated group[(19.3±13.1)%] decreased obviously [(79.00±0.06)% vs 100%, P<0.05].In the cellular immunofluorescence assay, the expression of Nrf2 protein in 50nmol/L brusatol treated group was lower than blank control group(P<0.05).We further found that 50nmol/L brusatol treated group decreased more mRNA levels of Cyclin B[(59.5±9.2)%] and CDK1[(56.0±1.4)%] than blank control group(100%) in G2/M phase(P<0.05).Conclusion In this study, Brusatol mainly affects the cell cycle transformation from G2 to M phase dependent on Cyclin B-CDK1, further inhibiting the development of the embryo through down-regulating Nrf2.

Objective To evaluate the efficacy of telbivudine in HBeAg-positive chronic hepatitis B (CHB) patients by comparing the efficacy of initial telbivudine therapy in treatment-naive patients with sequential telbivudine therapy in patients with poor response to adefovir.Methods A total of 90 HBeAg-positive CHB patients were assigned to receive sequential telbivudine therapy following poor response to adefovir dipivoxil (n=45),or initial telbivudine therapy in antiviral treatment-naive patients (n=45).All patients were treated with telbivudine 600 mg daily for 104 weeks.The efficacy was evaluated in terms of liver function tests,serum HBV markers,HBV DNA and antiviral drug resistance.Results Telbivudine showed good overall efficacy after treatment for 104 weeks in terms of alanine aminotransferase normalization rate (91.1％),HBV DNA negative conversion rate (80.0％),HBeAg loss rate (57.8％),and HBeAg/HBeAb seroconversion rate (30.0％).The HBV DNA negative conversion rate in initial treatment group was significantly higher than that in sequential treatment group (P＜0.05).However,among the patients with early response,the efficacy did not show significant difference between groups (P＞0.05).The patients with early response showed significantly better efficacy than those without early response,in terms of higher HBV DNA negative conversion rate,higher HBeAg loss rate and HBeAg/ HBeAb seroconversion rate (P＜0.000 1 or P＜0.05),but lower virological breakthrough rate (P＜0.05).Conclusions Telbivudine has shown reliable efficacy in CHB patients.Initial telbivudine therapy is better than sequential therapy in CHB patients with poor response to adefovir.However,for patients with early response to telbivudine,no statistical difference is found between initial and sequential therapy in long-term treatment efficacy (104 weeks).The patients receiving sequential telbivudine therapy should be monitored closely for early antiviral response to optimize treatment.

Objective To investigate the effect of stress induced by fear on germ cells apoptosis in rat's testis. Methods 36 SD rats were randomly assigned to acute stress group, subacute stress group, chronic stress group and control group, respectively. The model of the stress rat induced by fear was reproduced. The levels of caspase-3 mRNA and bax /bcl-2 mRNA expression in rats' testis were determined by fluorescent quantitative RT-PCR. The apoptosis of spermatogonic cell, primary spermatocyte, secondary spermatocyte and spermatid was identified by TUNEL. Results Caspase-3 mRNA, compared with that in control group, was expressed highly in the subacute stress group (5.34?1.13 vs 3.67?0.34, P0.05). The ratio of bax /bcl-2 mRNA, compared with that in the control group, was increased significantly in the subacute stress group (2.68?0.86 vs 1.60?0.42, P0.05). Compared with that in control group (1.50?0.58), the apoptotic index of germ cells was higher in the subacute stress group (10.50?1.29, P0.05). Conclusion Stress induced by fear plays an important role in inducing germ cells apoptosis, and caspase-3, bax and bcl-2 were involved in this process.

Objective To summarize the modified clinical technique and experience of simultaneous kidney-pancreatic transplantation (SKPT) with enteric drainage(ED). Methods Two patients with insulin-dependent diabetes mellitus and end-stage renal disease underwent SKPT with enteric drainage of exocrine secretions.The patients were treated with quadruple therapy including antithymocyte globulin (ATG) induction therapy,prednisone,FK506,and Mycophenolate-Mofetil(MMF), as maintenance immunosuppression. Results The two patients became insulin-independent after treated by small dose insulin for 5～10 days and Scr,BUN became normal 3～5 days after the operation.Until now all the grafts of the patients functioned well. Conclusions ED-SKPT is more effective than simultaneous kidney-pancreatic transplantation with bladder drainage (BD-SKPT).ED-SKPT is an effective method for treating type Ⅰdiabetes mellitus with uremia.Finer allograft and nicer HLA-typing can decrease complications.