Objective To study the correlation between chronic infection of three microorganism and coronary artery lesion by detecting their antibodies and high-sensitivity C-reactive protein(hs-CRP) .Methods According to their severity of coronary artery lesion ,patients enrolled in the study were divided into 4 groups ,including normal control group(n=37) ,single-branch lesion group (n=36) ,double-branch lesion group(n= 30) and multi-branch lesion group(n= 29) .Serum Chlamydia pneumonia IgG(CPN-IgG) ,Helicobacter pylori IgG(HP-IgG) ,human cytomegalo virus IgG (HCMV-IgG) and hs-CRP tests were performed .Results CPN-IgG ,HP-IgG ,HCMV-IgG positive rates and the mixed infection positive rates increased sequentially from normal group to multi-branch group .There were significant differences of CPN-IgG ,HP-IgG ,HCMV-IgG and hs-CRP contents among the 4 groups (P<0 .05) .Logistic analysis showed that CPN-IgG ,HP-IgG and HCMV-IgG were dangerous factors to coronary artery lesion . Conclusion Chronic infections of three microorganism might affect the development of coronary artery lesion .

Objective: To observe the efficacy of azithromycin in treating the bacterial infectious diseases.　Methods: Intravenous administration of azithromycin was carried out in 40 cases.　Results: The clinical cure rate and eradication rate were 85.0% and 84.8%, respectively. Drug sensitivity tests showed that more isolates were sensitive to azithromycin (87.9%) than to erythromycin (42.4%). The MIC of azithromycin was lower than that of erythromycin. In addition, the adverse effects occurred with low frequency and were usually mild.　Conclusion: Azithromycin is effective and safe in treating bacterial infectious diseases.

Carcinoma, Hepatocellular ; Humans ; Lipase ; Liver Neoplasms ; Membrane Proteins ; Polymorphism, Genetic

Objective To evaluate the clinical value of MR spectroscopy in intracranial neoplasm. Methods 52 cases with brain neoplasm or recurrent neoplasm or non-tumor lesion confirmed by pathology were undergone proton MRS before stereotactic biopsy, or operation. Results Of 52 cases, 38 were neoplasm and 14 were nonneoplastic lesion, 34 of 38 brain tumor, 11 of 14 nonneoplastic lesion were diagnosed correctly. The characteristics on MRS of glioma were remarkable Cho increase and NAA decrease, Lac in the tumors and the central necrotic area was elevated. Metastasis: Cho increased,NAA disappeared or obviously decreased and Lac increased, but the peritumoral region was normal. Lymphoma: Cho increased, NAA decreased moderately, Lip presented, but the peritumoral region was normal. Demyelination lesion: slight or median decreased NAA and normal Cr, Lac increased slightly. All metabolism decreased or disappeared in radiation necrosis, Cho was relative high compared with NAA. Brain abscess: Lac increased in the centre of abscess and perilesion was normal.Conclusion MRS has significant value in detecting and differentiating brain lesions.

Objective To study the correlation between coronary lesion and Cystatin C (CyC),Nitric Oxide (NO)and Super oxide dismutase,accumulate the clinical experience in prevention and diagnose of Coronary Heart Disease (CHD)by analy-zing the contents of serum Cystatin C (CyC),Nitric Oxide and Superoxide Dismutase in patients with coronary lesion.Meth-ods According to their severity of coronary artery lesion,all cases were divided into four groups:Normal compared group (40 cases);Simple branch pathological group (44 cases);Double branch pathological group (43 cases):Multi-branch patho-logical group (35 cases).All cases were tested CyC,NO,SOD and hs-CRP in serum.Results The level of CyC and hs-CRP were increased gradually from normal group to multi-branch group.The level of NO and SOD were decreased gradually from normal group to multi-branch group.There were significant differences the levels of CyC,NO,SOD and hs-CRP among the four groups.Coronary lesion Gensini in the CHD patients had significant positive relationship to the level of CyC or hs-CRP respectively (r=0.473,0.429),had significant negative relationship to the level of NO or SOD respectively (r=-0.356, 0.384)(P<0.05).CyC in the CHD patients had significant positive relationship to the level of hs-CRP (r=0.458),had sig-nificant negative relationship to the level of NO or SOD respectively (r=-0.426,0.484,P<0.05).Conclusion By aggra-vation of coronary artery lesion,the level of CyC increased,reduced the contents of NO,SOD,aroused endothelial dysfunc-tion,induced occurrence and aggravation of coronary artery lesion.CyC,NO and SOD play important mark in the assistant diagnosis of the disease.

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.

This study is to explore whether the Wnt/beta-catenin signaling pathway is involved in the process of tripchlorolide (T4) protecting against oligomeric Abeta(1-42)-induced neuronal apoptosis. Primary cultured cortical neurons were used for the experiments on day 6 or 7. The oligomeric Abeta(1-42) (5 micromol x L(-1) for 24 h) was applied to induce neuronal apoptosis. Prior to treatment with Abeta(1-42) for 24 h, the cultured neurons were pre-incubated with T4 (2.5, 10, and 40 nmol x L(-1)), Wnt3a (Wnt signaling agonists) and Dkk1 (inhibitors) for indicated time. Then the cell viability, neuronal apoptosis, and protein levels of Wnt, glycogen synthase kinase 3beta (GSK3beta), beta-catenin and phospho-beta-catenin were measured by MTT assay, TUNEL staining and Western blotting, respectively. The result demonstrated that oligomeric Abeta(1-42) induced apoptotic neuronal cell death in a time- and dose-dependent manner. Pretreatment with T4 significantly increased the neuronal cell survival and attenuated neuronal apoptosis. Moreover, oligomeric Abeta(1-42)-induced phosphorylation of beta-catenin and GSK3beta was markedly inhibited by T4. Additionally, T4 stabilized cytoplasmic beta-catenin. These results indicate that tripchlorolide protects against the neurotoxicity of Abeta by regulating Wnt/beta-catenin signaling pathway. This may provide insight into the clinical application of tripchlorolide to Alzheimer's disease.

Objective To observe the effects of histone deacetylases inhibitor (HDACi) on cognitive performance and cerebral tau phosphorylation in transgenic mice coexpressed five familial Alzheimer' s disease mutations (5XFAD).Method The total 12 5XFAD-CC and 12 wild type (WT) mice were administrated with suberoylanilide hydroxamic acid ( SAHA,n =7) and vehicle ( n =5 ),respectively.The cognitive performance was assessed by Y-maze and Morris water maze.The protein levels of acetylated α-tubulin,total tau and phosphorylated tau and phosphorylated glycogen synthase kinase-3β (GSK3β) were determined by Western blotting.Results SAHA ameliorated learning and memory deficits in 5XFAD-CC mice (39.10％ ±2.25％,t =2.688,P =0.0312 for total numbers of entrance in novel arm; 26.81％ ±0.78％,t =3.271,P =0.017 for time spending in novel arm; F =5.936,P =0.045 for hidden platform;31.70％ ±4.21％,t =2.317,P =0.049 for probe trial).Administration of SAHA significantly increased acetylated α-tubulin in hippocampus of WT and 5XFAD-CC mice (26.42％ and 29.64％,respectively).Additionally,SAHA attenuated tau-pSer396,tau-pSer404 and tau-pThrThr231 in hippocampus of 5XFAD-CC mice (24.22％,48.98％ and 26.95％,respectively). Moreover,hippocampal phosphorylated GSK3β was markedly reduced in SAHA-treated 5XFAD-CC mice (31.29％). Conclusion SAHA may improve cognitive performance in 5XFAD-CC mice, which is associated with its significant effects on the phosphorylation of tau and GSK3β.

Objective To investigate the relationship between the neuroprotective effect of epigallocatechin gallate ( EGCG ) for PC12 cells induced by 1-methyl-4-phenyl-pyridinium ( MPP+ ) and activating nuclear factor-related factor 2 ( NRF2 ).Methods Well differentiated PC12 cells treated with MPP+ were used as the in vitro cell models,and PC12 cells were pretreated with different concentrations of EGCG.MTT assay was used to investigate the cell viability.Western blot was used to observe the expression of NRF2 in cells and distribution in the nucleus and the cytoplasm.Real-time PCR was used to observe the antioxidant enzymes,HO-1 and NQO1 mRNA expression.Results Pretreatment of PC12 cells with different concentrations of EG CG for an hour could restore cell viability.Western blot showed that expression of NRF2 in cells treated with MPP+ for 24 hours was increased 148％ +5％ compared with the control group (t =6.102,P ＜0.01 ).The level of NRF2 in EGCG pretreated group was 188％ + 6％ compared with the control group(t =11.172,P ＜0.01 ).Moreover the NRF2 protein level in the nuclear was also increased.Western blot showed that the NRF2 protein level in the nuclear was 258％ +2％ compared with the control group (t =21.995,P ＜ 0.01 ).Further research found U 120,an inhibitor of ERK,could inhibit the effect of EGCG.The levels of NRF2 in both samples were 148％ ± 15％ and 158％ ± 1％ compared with their respective control groups(t =6.118,8.058,both P ＜0.01 ).In accordance with the NRF2 data,real-time PCR indicated that the levels of HO-1 and NQO1 mRNA expression increased obviously in the group pretreated with EGCG.Likewise,U120 could also inhibit HO-1 and NQO1 mRNA expression induced by EGCG.Conclusions EGCG can repair oxidative damage to PC12 cells induced by MPP+.The protective effect may be related through the ways to activate ERK-NRF2 and induce downstream of antioxidant enzyme expression,such as HO-1 and NQO1.

BACKGROUND:Currently, there is no effective treatment for keloids that often recur. Its pathogenesis is stil entirely unclear, and fibroblast proliferation and apoptosis have become a research hotspot.
OBJECTIVE:To investigate the expression of Livin, Smac and Caspase-3 in keloids and to analyze their relationship so as to preliminarily explore the significance of Livin, Smac and Caspase-3 in the pathogenesis of keloids.
METHODS:RT-PCR and immunohistochemical methods were used to detect the mRNA and protein expressions of Livin, Smac and Caspase-3 in keloids (n=20) and normal skin tissues (n=20).
RESULTS AND CONCLUSION:Compared with the normal skin tissue, the mRNA and protein positive expressions of Livin were significantly higher in keloids (P < 0.05), while the mRNA and protein positive expressions of Smac and Caspase-3 were lower in keloids (P < 0.05). There was a negative association between Livin and Smac, Caspase-3 protein expression in keloids. These findings indicate that the high mRNA expression of Livin may cause the imbalance between proliferation and apoptosis of fibroblasts by inhibiting the mRNA expression of Smac and Caspase-3, and eventualy lead to the formation of keloid.