Objective To explore the relation between serum nesfatin-1 ,tumor necrosis factor (TNF)-αand insulin resistance. Methods A total of 105 subjects were enrolled in this study and divided into two groups:patients with newly diagnosed type 2 diabetes mellitus (T2DM group,n= 64)and normal controls (NC group,n= 41). The fasting serum nesfatin-1 and TNF-αlevels were measured by enzyme-linked immuno sorbent assay (ELISA). FPG,HbA1 c,TG,TC,and FIns were also tested. BMI, HOMA-IR,HOMA-β,and ISI were calculated. Results Serum nesfatin-1 and TNF-αlevels were significantly higher in T2DM group than in NC group. Multiple linear regression analysis showed that the most significant influencing factors for nesfatin-1 were TNF-αand ISI(β= 0. 005、-6. 847,P<0. 05). The most significant influencing factors for TNF-αwas HbA1 c (β= 26. 652,P<0. 01). Conclusion Serum nesfatin-1 and TNF-αare significantly elevated in patients with newly diagnosed T2DM,which may influence the glucolipid metabolism through the signal pathway of insulin and play a role in the pathogenesis of T2DM and IR.

Objective:To prepare and identify the monoclonal antibody against hPPAR?2.Methods:cDNA of hPPAR?2 was obtained from pMD18-T/hPPAR?2.hPPAR?2 was expressed in prokaryocyte and purified successfully.The anti-hPPAR?2 monoclonal antibodies (mAbs) 1B4,3H2,3H10,10D6 and 10D8 were produced by immunization with purified hPPAR?2.The specificity of the antibodies was identified by ELISA,Western blot assay and immunocytochemistry.Results:Five novel murine monoclonal antibodies only against hPPAR?2 were harvested,and they were all specific to hPPAR?2.Conclusion:The antibodies obtained provide more useful tools for following research and settling the basis for screening new drugs and mechanism.

BACKGROUND: The primary pathophysiology of Alzheimer disease (AD) is linked to β-amyloid (Aβ)protein. Neural progenitor cells (NPCs), which have the ability of multipotency, self-renewal and repair,have been detected in the central nerve system (CNS) of adult rat recently. But effective function of these neural progenitor cells are not seen in the AD brain ,which mechanism is unclear.It is unclear if Aβ1-40protein is compromised by the signal pathway of c-Jun N-termial kinase associated with the neurotoxicity to the progenitor cells on the cortex of embryonic rats.OBJECTIVE: To investigate the mechanism of c-Jun N-terminal kinase signal transduction pathway of Aβ1-40 protein, which has neuronal toxicity to progenitor cells(CPC)on the cortex of embryonic rats . To detect the neuroprotective effects of c-Jun N-termial kinase inhibitor (SP600125) against Aβ1-40-induced neuronal toxicity to the cortical progenitor cells on the cortex of embryonic rats.DESIGN: A randomized and controlled trial with cells as objects.SETTING: Department of Neurology, First Hospital Affiliated to China Medical UniversityMATERIALS: This experiment was carried out at the Central Laboratory,China Medical University from May to October 2005. Embryos at age of 14 days from Wistar rats were used in this experiment.METHODS: Cortical progenitor cells harvested from Wistar embryonic rats were cultured in vitro, passaged and identified. Embryonic rat cortical progenitor cells of rats with good growth state were randomly divided into 4groups:Aβ1-40 group (10 nmol/L Aβ1-40 in each well);SP600125+Aβ1-40group (10 μmol/L SP600125 for 30 minutes and then with 10 nmol/L Aβ1-40 in each well); SP600125 group ( 10 μmol/L SP600125 in each well); Normal saline group (same volume of normal saline). The incubated durations were 0,2 hours, 4 hours, 6 hours, 12 hours, 24 hours respectively,8 wells for each time point. The cell survival rate was measured by MTF assay (The concentration of cortical progenitor cells on the cortex was 1×10s L-1 in each group), the apoptosis rate was detected by flow cytometer (The concentration of cortical progenitor cells on the cortex was 1 ×1010 L-1in each group) and the expression of c-Jun N-termial kinase and p-c-Jun N-termial kinase, c-Jun,p-c-Jun were measured by Western Blot(The concentration of cortical progenitor cells on the cortex was 1×1013 L-1 in each group). t test was adopted for the comparison of difference in measurement data.sion of c-Jun N-terminal kinase, p-c-Jun N-termial kinase ,c-Jun and p-c-Jun of embryonic rat CPC .ture time in Aβ group and SP600125 +Aβ group, decreased obviously at 4hours; cellular survival rate in Aβ1-40 group was lower obviously than that in the other 3 groups at 0,2,4,6,12,24 hours (P ＜ 0.01); Cellular survival rate in SP60025 +Aβ1-40 group was lower obviously than that in SP600125 group and normal saline group at 2,4,6,12,24 hours (P ＜ 0.01);Compared with normal saline group, the difference of cell survival rate was not significant without time-dependent manner in SP600125 group (P＞ 0.05).amyloid protein group and SP600125 +Aβ group, increased obviously at 4hours; cell apoptosis rate in Aβ1-40 group was higher obviously than that of the other 3 groups at 0,2,4,6,12,24 hours(P ＜ 0.01); Cellular apoptosis rate in SP60025+Aβ1-40 group was higher obviously than that in the SP600125 group and normal saline group at 2,4,6,12,24 hours (P ＜ 0.01);Compared with normal saline group, the difference of cellular apoptosis rate was not significant without time-dependent manner in SP600125 group 12,24 hours without changes in Aβ1-40 group; the expression of p-c-Jun N-terminal kinase and p-c-Jun in Aβ1-40 group were seen at 0hour ,increased gradually, reached to the peak at hour 4 and decreased gradually.CONCLUSION: Aβ1-40 could inhibit the cell activity of CPC , reduce cellular survival rate and induce cellular apoptosis. c-Jun N-terminal kinase signal transduction pathway may mediate the Aβ1-40 inducd neurnal apoptosis in AD which may be one reason for unseen rescue mechanism in AD. SP600125 (c-Jun N-terminal kinase inhibitor) could inhibit the activation of c-Jun N-terminal kinase and c-Jun and protect the embryonic rats CPC from the Aβ1-40-induced neurotoxicity.

Objective To observe the effects of Tangshenjiaonang (TSJN) on biochemistry, renal function and hemorheology of alloxan and achromycin induced diabetic nephropathy rats. Methods The diabetic nephropathy rats induced by alloxan and achromycin were divided into 5 experimental groups. compared with control group, to observe the changes of the indicators shown about. Results TSJN can significantly decrease the level of SCr, BUN, CCr, FIB, plasma viscosity and UAER (P

0.05). After treating, the accumulating points of syndrome of the treatment group dropped more, the treatment group was superior to the control group. Conclusions The curative effects of Huoxin capsule on angina of coronary arheroselerosis heart disease is exact. It can take effect quickly and improve the whole symptom of the patients noticeably.

Diabetes Mellitus, Type 2 ; complications ; Diagnosis, Differential ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Myelinolysis, Central Pontine ; complications ; diagnosis ; Prognosis

Hypoxia occurs in chronic and acute vascular diseases and tumor formation. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducible factor 1 (HIF-1). Tumor hypoxia mediated by HIF-1 would facilitate the likelihood of resistance to chemotherapy and radiotherapy, proliferation, metastasis and the invasive potential; all of which culminate in a decrease in patient survival. And HIF-1 alpha subunit decides the activity of HIF-1, which is regulated by oxygen. So understanding the role of HIF in signal pathway, drug resistance mechanism and its feature is crucial for developing novel anticancer therapies. In recent years, more attentions have focused on HIF-1 alpha inhibitors. It is expected that development of more potent and selective HIF inhibitors will provide an effective treatment of cancer and other HIF-related diseases. So we will focus on the biological characteristics and mechanism of HIF-1 to review currently studied HIF-1 inhibitors.

This paper reviewed the classification of hemp,distinction between industrial hemp and marijuana hemp,and the use value of industrial hemp.Some research problems and future research trends were also discussed.

Objective To explore the cause of repeated offline of files in the database of No.1 Military Project and find the method to solve the problem. Methods The abnormal offline of files in database is not by chance,and its document in oracle is not very clear. Using the knowledge from internet,the fault was repeatedly simulated on test machine and the source of the fault was found. Results Solving plans and countermeasures were put forward. Conclusion The database of the No.1 Military Medical Project is the core of military hospital work,so its importance is self-evident. The technical support of No. 1 Military Project is strengthened,the right maintenance direction of the database is pointed out as well as the right solution to deal with the problem.

Objective To detect patients with cancer of the stomach cancer tissue and serum Periostin protein expression of the situation,the preliminary explore its clinical significance.Methods Selected 60 cases of our hospital diagnosed as gastric carcinoma patients with carcinoma tissue samples,tissue adjacent to carcinoma specimens and serum,and choose 60 cases of healthy check-up serum specimens at the same time.Classified all patients according to clinical classification factors,inclu-ding age,sex,TNM stage,degree of infiltration,lymph node metastasis and pathological grading,immunohistochemical meth-od determination of Periostin in gastric cancer and adjacent tissue protein expression,enzyme-linked immunoassay detection in patients with gastric cancer patients and normal serum Periostin protein content.Results The method of ELISA to detect gastric cancer patients serum Periostin protein level was 46.76.4 ng/ml,and healthy crowd Periostin protein levels was 23.1 ±4.5 ng/ml,statistically significant difference (t= 7.34,P<0.05).Immunohistochemical methods showed that Periostin in patients with cancer of the stomach cancer tissue protein positive rate was (73.2±5.4)%,positive rate of (33.4±6.5)%in the tissue adjacent to carcinoma,statistically significant difference (t=8.52,P<0.05).Ⅲ~Ⅳ period patients serum Periostin protein level was 64.9±6.3 ng/ml,Ⅰ~Ⅱ period patients serum Periostin protein level was 41.6±4.1 ng/ml, statistically significant difference (t=9.17,P< 0.05).Periostin protein inⅢ~Ⅳ positive rate was 67.8% in patients with carcinoma tissue,Ⅰ~ phase Ⅱ positive rate was 52.9%,statistically significant difference (t=9.64,P<0.05).According to infiltrate the classification:T3,T4 patients serum Periostin protein level was 61.9±6.6 ng/ml,T1 and T2 patients serum Periostin protein level was 44.6±3.7 ng/ml,statistically significant difference (t=8.24,P<0.05).Periostin protein in T3 and T4 positive rate was 6 6.2% in patients with carcinoma tissue,T1 and T2 positive rate was 5 1.4%,statistically signifi-cant difference (t=7.58,P<0.05).Lymph node metastasis patients serum Periostin protein level was 65.2±4.3 ng/ml, without metastasis in patients with serum Periostin protein level was 42.6±3.2 ng/ml,statistically significant difference (t=7.63,P<0.05).Periostin protein in the tissue of carcinoma patients with lymph node metastasis group positive rate was 60.8%,no transfer of positive rate was 37.5%,statistically significant difference (t=8.56,P<0.05).Conclusion Periostin protein expression in patients with gastric cancer tissue and serum was significantly higher than that of healthy people,and to a certain extent is proportional to the illness,Periostin protein is a predictable stomach occurrence,lesion degree of poten-tial biological indicators.