Objective To investigate the causes and features of fever of unknown origin(FUO).Methods This study enrolled 89 patients who fullfilled the criteria of FUO and were admitted in China-Japan Friendship hospital from October 2005 to May 2008.Results The final diagnosis were made in 80 cases(89.9%).Etiologies of FUO were as follows:infections,41 cases(46.1%);rheumatic disease,15 cases(16.9%);neoplasm,18 cases(20.2%)(hematological malignancy,17 cases),miscellaneous diseases 6 cases(6.7%),unknown etiology,9 cases(10.1%).Conclusion Infection is the main cause of FUO;rheumatic disease and neoplasm are also important causes of FUO.Hematological malignancy is the most common neoplasm related to FUO.Detailed history contributes greatly to FUO diagnosis.

Objective To investigate the long-term efficacy of transendocardial injection of vascular endothelial growth factor (VEGF) into ischemic porcine myocardium.Methods Thirty pigs were divided into two groups:control group and treatment group (15 each).A angioplasty balloon was used to occlude the left anterior descending coronary arteries of the animals to reproduce a porcine myocardial ischemic model.Blank plasmid (control group) or constructed pIRES2-EGFP-hVEGF165 eukaryotic expression plasmid (treatment group) was directly injected into the ischemic myocardium through an transendocardial injection catheter of NOGA system,respectively.Before and one year after injection,left ventricular electromechanical mapping (LVEMM) was used to detect local linear shortening (LLS) and unipolar potential (UpV);M-mode local wall motion,cycle variation of integrated backscatter (CVIB) and left ventricular ejection fraction (LVEF) were detected by ultrasonagraphy.One year later,the animals were sacrificed for the observation of the capillary formation in myocardial tissue with immunohistochemical staining.Results One year after injection,as compared with that of control group,local linear shortening (LLS) showed a significant increase (P0.05),and ultrasonagraphy showed better heart function in the treatment group (P

Objective: To explore the effects of Vitamin K2 (VK2) on theaortic artery calciifcation and oxidative stress injury in experimental rats.
Methods: A total of 24 rats were divided into 4 groups:①Control group,②6-week calciifcation group,③12-week calciifcation group and④6-week calciifcation + 6-week VK2 group;n=6 in each group. The arterial calciifcation was induced by warfarin (WFN) treatment. The calcium nodule and deposition in rat’s theaortic artery were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) were measured by DHE probe staining and the morphological changes of mitochondria in smooth muscle cells were detected by transmission electron microscopy.
Results: Calciifcation nodule formed in both 6-week and 12-week calciifcation groups, the calciifcation deposition and ROS were higher than Control group,P<0.01. Compared with both calcification groups, the above indexes were decreased in 6-week calciifcation + 6-week VK2 group,P<0.01. Both calciifcation groups showed mitochondria swelling with unclear structure and cytoplasm vacuoles degeneration in vascular smooth muscle cells. The vascular smooth muscle cell volumes were similar between Control group and 6-week calcification + 6-week VK2 group, and no cytoplasm vacuoles degeneration was observed.
Conclusion: Warfarin induced aortic calciifcation is related to oxidative stress injury which may cause the ultra-micro structural damage in smooth muscle cells; VK2 may reduce the oxidative stress injury and improve the condition of vessel calciifcation in experimental rats.

Objective: To explore the effect of oxidative stress injury on the mechanism of vascular smooth muscle cell (VSMC) calciifcation induced by calcium and phosphorus in experimental rats.
Methods: The VSMC calcification was induced by incubating the cells with calcium chloride (CaCl2) andβ-sodium glycerophosphate (β-GP) for 8 days, and the cells were divided into 4 groups: ① Control group, ② Calcification group,③ Calciifcation+H2O2 group, ④ Calciifcation+catalase group. The calcium nodule formation and calcium deposition in VSMC were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) was detected by DCFH-DA probe staining and the protein expression of Runx2 was examined by Western blot analysis.
Results: Compared with Control group, Calciifcation group showed the higher ROS production, more calcium nodule and calcium deposition, higher Runx2 protein expression;while compared with Calciifcation group, the above indexes were even higher in Calciifcation+H2O2 group, P<0.05. The ROS production, calcium nodule, calcium deposition and Runx2 protein expression were lower in Calciifcation+catalase group than those in Calciifcation group and Calciifcation+H2O2 group, but still higher than that in Control group. The protein expression of Runx2 was similar between Calciifcation+catalase group and Control group, P>0.05.
Conclusion: CaCl2 andβ-GP treatment may induce VSMC calciifcation via activating ROS-Runx2 signal pathway in experimental rats.

Objective We aimed to investigate whether magnetic stent has preventive effect on in-stent restenosis by observing expressions of matrix metalioproteinase (MMP)2,MMP9,tissue inhibitor of matrix metalloproteinase (TIMP)1 and TIMP2 after balloon angioplasty,bare and magnetic stent implantation in rabbits.Methods Rabbits underwent balloon angioplasty,bare and magnetic stent implantation in the left iliac arteries.The changes of MMPs and TIMPs were examined at various time points in the injured arteries using the methods of zymography,Western blot analysis,reverse transcription-polymerase chain reaction (RT-PCR) and morphometric analysis.Results Balloon angioplasty group (BA) and magnetic stent group (MS) showed lower intrinsic gelatinolytic activity and higher expression of TIMPs with less intimae hyperplasia;Whereas bare stent (BS) group exhibited higher intrinsic gelatinolytic activity and lower expression of TIMPs with significant intimae hyperplasia.Conclusion Magnetic stent probably has preventive effect on in-stent restenosis by changing intrinsic matrix metalloproteinases activity and expression of TIMPs.

Objective To investigate the preventive effect of magnetic stent on coronary restenosis after percutaneous arterial stenting.Methods Twenty rabbits were divided randomly into 2 groups.Bare stent(BS group,n=10)or magnetic stent(MS group,n=10)wasimplanted in the left iliac artery of the rabbits of the 2 groups,respectively.Aspirin (25mg,qd )was administered orally to the rabbitsof both groups from 3 days before stenting until the rabbits were executed.Unfractionated heparin (2500u,qd) was delivered subcuta-neously after stenting for 7days.Five rabbits of each group were randomly selected to be executed at 7 or 30 days.Stmctural changesin the iniured arteries were studied by optical microscopey,transmissive electronic microscopey and immunohistochemistry.ResultsAt 7 days.more myofibroblasts were found migrating from adventitia to tunica media and intima in BS group than in MS group.insidethe media and intima,large amount of smooth muscle cells of synthetic type were observed.At 30 days after stenting,in magnetic group,most uascular smooth musele cells(SMCs)under the intima had transformed to contractile type and only little extracellular matrix(ECM)was observed around the SMCs;whereas,in BS group,the SMCs remained to be synthetic type and large amount of ECM wasobserved around the SMCs.which was composed mainly of proteoglycans and glycoproteins. Conclusions Magnetic stent caninhibit proliferation and migration of SMCs and reducing the production of ECM.and therefore,may prevent restenosis after coronarystenting.

Objective:To investigate the effects of moxibustion on the serum metabolism in healthy human body based on the 1H nuclear magnetic resonance (1H NMR) metabolomics technology, and to find the differences in metabolites, as well as to elucidate the effects of moxibustion on healthy human body from the viewpoint of global metabolism. Methods:Sixty subjects of healthy young men from the enrolled students were randomly divided into a moxibustion group and a control group using random number table, with 30 cases in each group. Subjects in the moxibustion group accepted mild moxibustion on the right Zusanli (ST 36), once a day, 15 min for each time, and continuous treatment for 10 d; those in the control group did not receive any intervention. There were 28 cases in the moxibustion group and 23 cases in the control group after interventions. On the 1st day, 5th day and 10th day of the intervention, serum samples were collected from subjects of the two groups, and metabolic spectra were obtained by the1H NMR technology. Results: Before and after the intervention, serum1H NMR of the moxibustion group was significantly different, while the difference was insignificant in the control group. Metabolite changes in the moxibustion group were mainly in low density lipoprotein (LDL)/very low density lipoprotein (VLDL), valine, isoleucine, leucine, lactic acid, glutamine, citric acid, polyunsaturated fatty acids, creatine, glycine, glycerol, glucose, tyrosine, histidine, formic acid, alanine, lysine, acetic acid, and glutamic acid. Conclusion:Moxibustion can cause changes of serum metabolic patterns in healthy human by influencing the concentrations of branched-chain amino acids, polyunsaturated fatty acids, and other metabolites to strengthen body's metabolisms of amino acids and fatty acid.

Based on the understanding of TCM and western medicine on diabetes mellitus (DM) and diabetic peripheral neuropathy (DPN), the relationship between DPN pathogenesis and blood stasis of TCM is discussed from the perspective of modern medicine. It is indicated blood stasis is the key pathogenesis to DPN, and a two-step acupuncture treatment of DPN from the theory of blood stasis is proposed. The first step is to analyze the pathogenesis of blood stasis, which could block the progress of the disease and diminish the symptoms. The second step is to apply acupuncture for pathological result of blood stasis by following the principle of, as a result, the purpose of treating both symptoms and root cause is achieved.

Objective: To explore the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection who received entecavir alone or in combination with anluohuaxianwan for 78 weeks. Methods: Patients with chronic HBV infection were randomly treated with entecavir alone or in combination with anluohuaxian for 78 weeks. Ishak fibrosis score was used for blind interpretation of liver biopsy specimens. The improvement in liver fibrosis condition before and after the treatment was compared. Student's t test and non-parametric test (Mann-Whitney U-Test and Kruskal-Wallis test) were used to analyze the measurement data. The categorical variables were analyzed by Chi-square test method and Spearman’s rank correlation coefficient was used to test bivariate associations. Results: Liver fibrosis improvement rate after 78 weeks of treatment was 36.53% (80/219) and the progression rate was 23.29% (51/219). The improvement of liver fibrosis was associated to the degree of baseline fibrosis and treatment methods (P < 0.05). The improvement rate of hepatic fibrosis in patients treated with anluohuaxianwan combined with entecavir at baseline F < 3 (54.74%, 52/95) was significantly higher than that in patients treated only with entecavir (33.33%, 16/48), P = 0.016 and the progression rate of hepatic fibrosis (13.68%, 13/95) was lower than that in patients treated alone (18.75%, 9/48), P = 0.466. In patients with baseline F < 3, the proportion of patients with improved and stable liver fibrosis in the combined treatment group (68.1%, 32/47) was higher than that in the treatment group alone (51.7%, 15/29). Conclusion Combined anluohuaxianwan and entecavir treatment can significantly improve the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection. Furthermore, it has the tendency to improve the stability rate and reduce the rate of progression of liver fibrosis.