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.

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 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.

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.

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

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

Objective To evaluate the role of SPECT cerebral perfusion imaging in assessing the stent implantation for cerebral artery stenosis.Methods A total of 35 patients (31 males,4 females,average age (63.9±10.8)years) with cerebral artery stenosis confirmed by DSA for cerebral artery stent implantation were retrospectively analyzed.99Tcm-ECD cerebral perfusion imaging was performed for all patients before and after stent implantation.The images were realigned and normalized by SPM 2.0 and then analyzed by Brain Search software for quantitative analysis.The brain was automatically separated to 210 functional areas according to Talarich map.The normalized averaged counts (NAC) of each area were calculated and compared with the data of 28 health controls (8 males,20 females,average age (35.8± 9.4) years).Less than 1.96s was defined as low perfusion lesions.The NAC values before and after stent implantation were compared for classifying improved from non-improved group.The mean number of lesions and Essen stroke risk score (ESRS) were analyzed between the two groups.The mean number of lesions and postoperative improvement rate of the internal carotid artery (ICA) occlusion and stenosis were compared.Paired rank sum test,two-sample t test,two-sample rank sum test and x2 test were used for statistical analysis.Results In 35 patients with low perfusion areas,20 were significantly improved after stent implantation.The mean number of lesions in the improved group (34.05± 14.41)was significantly higher than that in the non-improved group (22.93±17.24; t=2.067,P＜0.05).The mean ESRS of the improved patients (14.8)was significantly lower than that of the non-improved patients (22.3,Z=2.24,P＜0.05).The improvement rate of 28 cases with ICA stent implantation was (60.7％,17/28)higher than that of 7 cases with middle cerebral artery (MCA) stent implantation (3/7; P＞0.05).The mean number of the ICA occlusion lesions (34.36± 14.31)was higher than that of the ICA stenosis lesions(31.35± 16.37),but the difference was not statistically significant(t=0.498,P＞0.05).The improvement rate of the ICA occlusion was higher than that of the ICA stenosis (7/11 vs 10/17),but the difference was not statistically significant (P＞0.05).Conclusion SPECT cerebral perfusion imaging and its quantitative analysis can evaluate the low perfusion lesions before stent implantation and predict the perfusion improvement after stent implantation.

Atherosclerosis is the most important cause of ischemic stroke. microRNAs can play an important role in the lipid metabolism, vascular inflammatory response, angiogenesis, as wel as smooth muscle cel proliferation and phenotypic conversion, etc. by regulating the functions of vascular endothelial cel s, vascular smooth muscle cel s, and mononuclear macrophages. It is closely associated with the occurrence and development of atherosclerosis. This article mainly reviews the regulatory effect of microRNAs on lipid metabolism and vascular inflammatory response in pathogenesis of atherosclerosis.

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.

DNA methylation is closely related to the genesis and development of glioma.The CpG islands hypermethylation in promoter region of DNA repair genes,cell cycle controlling genes,apoptosis related genes,tumor suppressor genes and invasion related genes are found in glioma.Finding the specific methylation profile and molecular marker of glioma is helpful for the pathology class,early diagnosis and prognostic evalua-tion.Meanwhile,DNA methylation has the characteristic of reversibility,which may provide new ways for the treatment of glioma.