Computer-based online research was performed in Pubmed Database from January 1995 to January 2008, China National Knowledge Infrastructure (CNKI) and Vip Database from January 2001 to January 2008. Forty-four publications referred to the seeding cell sources of tissue engineering heart valve demonstrated some disadvantages of clinically used mechanical prosthetic valve and biological valve. Tissue-engineered heart valve had advantages, such as no anticoagulant therapy, infection resistance, cellular viability and the potential to grow and to repair. Seeding cells have different sources, such as blood vessels, bone marrow, blood, umbilical cord, chorionic vesicle and embryonic stem cells, with particular regard to cell phenotypes and their suitability for extracellular matrix production for tissue engineering purposes. Despite an exciting potential for tissue-engineered heart valves, significant technical barriers and clinical problems must be solved and overcome. Further studies should be conducted before widespread clinical application can be envisioned, such as biodegradable polymers, stem cell differentiation, understanding how to harvest the potential of endogenous recruitment of cells and techniques to non-invasively assess the speed and quality of tissue healing and remodeling. This needs to engender a host of novel testing strategies and methods, which will include in vivo safety studies and preclinical studies.

TLR4 mediates I/R injury involving endogenous ligands.Interaction of TLR4 with endogenous ligands provides a critical link between tissue damage and activation of the innate immune response.In the early phase of liver,kidney,heart,or lung I/R injury,endogenous ligands are secreted from several kinds of cells,they are recognized by TLR4.Interaction of TLR4 with endogenous ligands,such as HMGB1,seems to be the most important trigger of inflammation and initiates signaling cascades leading to inflammatory and immune responses.Blocking the interaction of TLR4 with endogenous ligands may be useful in clinical management of inflammation and cellular necrosis caused by ischemic insults.

ObjectiveTo assess the value of endoscopic retrograde cholangiography(ERC) before laparoscopic cholecystectomy(LC) for gallstone disease complicated by suspected cholelithiasis. MethodsIndications for ERC included history of jundice, pancreatitis,abnormal liver function, suspected or BUS proven cholelithiasis. ResultsA history of jaundice( P

Objective To investigate the role of PDR1 gene in azole-resistant Candida glabrata (C.glabrata).Methods Thirty-eight clinical isolates of C.glabrata were collected from five different hospitals.The minimal inhibitory concentrations (MIC) of azole antifungals including fluconazole,itraconazole and voriconazole against C.glabrata were determined by broth microdilution.Sequencing and amplification of PDR1 gene was achieved by real-time quantitative polymerase chain reaction (PCR).The mutation was cloned into an expression plasmid and then transferred into C.glabrata.The efflux of rhodamine 6G and drug sensitivity test were performed,and expressions of CDR1 and CDR2 were examined to verify function of mutation.Results Among these 38 isolates of C.glabrata,17 were resistant to at least one of azole antifungals.Moreover,mutations of PDR1 gene existed in every resistant isolates.Results of phenotyping test showed that in the isolate that expressed PDR1P927S,the expression of CDR1 and CDR2 were increased by 20.53 and 4.03 fold,respectively.And the fluorescence intensity of rhodamine 6G was decreased to 0.62 in efflux experiment.Conclusion P927S mutation of PDR1 gene could induce azole resistance of C.glabrata by increasing the expressions of CDR1 and CDR2,which results in drug resistance due to enhanced effect of efflux pump.

Objective To investigate the mechanisms of fluconazole resistance in clinical and experimental induced isolates of C.glabrata.Methods Efflux of rhodamine 6G was performed to evaluate the effects of efflux pumps.The expression levels of transporter genes CDR1,CDR2,SNQ2 and ERG11 were examined by real-time RT-PCR.Meanwhile,sequence of PDR1 was determined by PCR based DNA sequencing.Results Efflux pumps of all fluconazole-resistant isolates had stronger effects than that of susceptible isolates,consistently with significant upregulation of CDR1,but no obvious difference was found in CDR2 or SNQ2.Also,no notable change in the expression level of ERG11 between susceptible and resistant isolates.PDR1 mutations existed in both clinical and experimental induced isolates of C.glabrata,among which P927S,L543P and S947L haven't been reported previously.Conclusion Mutations of PDR1 were induced by fluconazole both in vivo andin vitro,which will result in overexpression of CDR1 and strengthen the effect of efflux pump.

Background and purpose:Recently, it was reported that tanshinoneⅡA (TanⅡA) could inhibit proliferation, induce differentiation and apoptosis of human cancer cells. Previous studies also indicated that TanⅡA could inhibit the migration and invasion of osteosarcoma. However, the effects of TanⅡA on the migration and invasion of gastric cancer and the mechanism remains unclear. The aim of this study was to investigate the effect of TanⅡA on gastric cancer cell SGC7901 migration and invasion of in vitro. Methods:After different concentrations (0.5, 1, 2, and 4μg/mL) of TanⅡA treatment for 24, 48, and 72 h respectively, MTT assay were developed to detect the cell proliferation of SGC7901. The wound healing assay and 3D-transwell assay were used to observe the migration and invasion of SGC7901 cells, respectively. Expression of intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase 2 (TIMP-2) mRNA and protein were measured with real-time PCR and Western blot. Results: 1, 2, and 4 μg/mL Tan ⅡA showed a dose-and time-dependent growth inhibition on SGC7901 cells. 2μg/mL TanⅡA showed a time-dependent migration inhibition of SGC7901 cells. 1, 2, and 4μg/mL TanⅡA could inhibit the invasion of SGC7901 cells. Real-time PCR and Western blot showed a reduction in expression of ICAM-1, MMP-2, and MMP-9, as well as an increase in expression of TIMP-2 (P<0.05).Conclusion:TanⅡA inhibits human gastric cancer SGC7901 cell migration and invasion in vitro. TIMP-2 upregulation and, ICAM-1, MMP-2, MMP-9 downregulation might be one of the mechanisms of anti-tumor of TanⅡA.

The aim of the study is to evaluate the feasibility and safety of Bispectral index (BIS) monitoring in pediatric radio frequency catheter ablation. One hundred and six children aged 0. 6-12 years, scheduled for radio frequency catheter ablation, were randomly divided into two groups. In group A patients received BIS monitoring during the operation (n = 50), and the group B received modified Observer's Assessment of Alertness/Sedation (OAA/S) scaling (n = 56). The anesthesia was maintained with propofol target-controlled infusion. The intraoperative propefol target concentration was adjusted to maintain the BIS values between 55-65 in group A and OAA/S scale about 1 in group B respectively, The heart rate (HR), mean arterial pressure (MAP) and pulse oximetric saturation (SpO2) were measured before anesthetic induction, 1 min after induction, catheter puncturing and the end of operation respectively. The requirements of propofol, the times of supporting ventilation and recovery, the respiratory depression, nausea and vomiting postoperatively were also recorded. The intraoperative HR, MAP and SpO2 showed no differences between two groups, but the requirements of pmpofol, the times of supporting ventilation and recovery were less in group A than that of group B (P<0.05). All children didn't have nausea, vomiting and respiratory depression. The results suggest that in pediatric radio frequency catheter ablation, BIS monitoring has the advantages of timely adjustment of anesthetic depth, reducing anesthetic requirements, shortening the time of recovery, so as the perioperative safety can be improved.

BACKGROUND: Previous studies demonstrated that smooth muscle injury or ischemia/reperfusion injury result in tissue factor (TF) increasing. However, few reports concern the expression and mechanism of TF in venous bypass grafting.OBJECTIVE: To examine changes in TF protein expression in response to venous bypass grafting.DESIGN, TIME AND SETTING: The animal observation experiment was performed at the Department of Cardiovascular Surgery, Affiliated Union Hospital of Tongji Medical College, Huazhong University of Science and Technology from May 2006 to May 2008.MATERIALS: A total of 30 Sprague-Dawley (SD) rats.METHODS: Rats were underwent interposition bypass grafting of the common carotid artery via the ipsilateral external jugular vein. Namely, the proximal end of external jugular vein was ligated at the joints of external jugular vein and internal jugular vein, and the distal end of external jugular vein was ligated before branches. The proximal and distal ends of common carotid artery were occluded by artery clamp, and a 5 mm artery was removed. The proximal end of artery was anastomosed with distal end of artery, and the frontal wall was sutured with posterior wall. After that, the proximal end of external jugular vein was cut down and coincided with the distal end of common carotid artery.MAIN OUTCOME MEASURES: The expression of TF and proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry. Meantime, TF activity in vessel protein extracts was determined with TF activity assay kit, and the thickness of intima, media were calculated by computer imaging analysis system. The contralateral external jugular veins were served as the control.RESULTS: The adventitia of all vessels showed abundant TF staining. In early vein grafts, TF staining was markedly increased in the intima and media. However, intimal and media TF staining was absent in the contralateral control jugular veins and late vein grafts. The number of PCNA positive cells was increased in the vein grafts at day 3 after grafting, obvious increased at day 7, and reached the peak at day 14. TF activity in whole-vessel protein extracts was similar in control veins and early and late vein grafts. The thickness of neointima of the vein graft increased significantly at days 7, 14, and 28, and the thickness of media increased significantly at days 14 and 28.CONCLUSION: The changes of TF expression at various time points may relate to hyperplasia of neointima.

Recent studies have found that peptide therapies tar-geting specific epitopes can avoid nonspecific immune suppres-sion induced by traditional medicines for the treatment of autoim-mune diseases, and have shown great therapeutic effect in ani-mal models of autoimmune diseases and clinical trials. The pa-per summaries the research progress and trends of peptide drugs for the treatment of autoimmune diseases from candidate peptide sources and their suppression mechanisms, which can provide a theoretical basis for the in-depth understanding of immune toler-ance and allow for discovery of new treatment for autoimmune diseases.

Objective To investigate the effect of intestinal lymphatic duct ligation and ω-3 polyun saturated fatty acids on intestinal and distant organ in intestinal ischemia-reperfusion injury. Methods Totally 40Sprague-Dawley (SD) male rats (SPF grade)after gastrostomy were equally randomized into sham group (Sham), enteral nutrition (EN) group, enteral nutrition and lymphatic duct ligation (EN + L) group, ω-3 polyunsaturated fatty acids (ω-3PUFA) group, and ω-3PUFA and lymphatic duct ligation (ω-3PUFA + L) group. After 7 days of nutritional intervention, rats were subjected to 60 minutes of intestinal ischemia, ischemia plus mesenteric lymph duct ligation, or sham procedures. After 3 days of continuous nutrition intervention using the original nutrient, lymph nodes, lung, intestine, liver, and blood specimens were harvested. Intestinal permeability and morphology, results of bacterial cultures, and serum cytokines were observed or detected. Result After 3 days of intestinal ischemia-reperfusion (I/R), the body weights of rats in EN group significantly decreased when com pared with the pre-I/R levels (P ＜ 0.05), while the body weights of rats in EN + L group were significantly lower than those in ω-PUFA group and ω-PUFA + L group (P ＜ 0. 05). After one day of intestinal ischemia-reperfusion (I/R), the L/M significantly increased in each group (P ＜0.05 or P ＜0. 01). After 3 days of intestinal ischemiareperfusion (I/R) , the L/M were significantly lower than the level one day after ischemia- reperfusion in EN + L group, ω-PUFA group, and ω-PUFA + L group (P ＜ 0.05). The L/M in EN group and EN + L group were significantly higher than that in ω-PUFA + L group (P ＜ 0. 05). The mucosa thickness and villus height of jejunum in ω-PUFA group and ω-PUFA + L group were significantly higher than those in Sham group, EN group, and EN + L group (P ＜ 0. 01 or P ＜ 0. 05). The mucosa thickness and villus height of ileum in ω-PUFA group and ω-PUFA +L group were also significantly higher than those in EN group (P ＜ 0.05). In ω-PUFA + L group, the serum endotoxin level and tumor necrosis factor-α level were significantly lower than those in EN group (P ＜ 0.05), interleukin (IL) -6 level was significantly lower than that in the ω-PUFA group (P ＜ 0.05), and IL-1 β level was significantly lower than those in other groups (P ＜ 0. 05). In EN group, the lung cell apoptosis index was significantly higher than those in other groups (P ＜ 0.05)and the levels of inducible nitric oxide synthase (iNOS)and myeloperoxidase (MPO) were significantly higher than those in ω-PUFA + L group (P ＜ 0. 05). The level of iNOS was also significantly higher in EN + L group than that in ω-PUFA + L group (P ＜ 0.05). Conclusions Sixty minutes of intestinal ischemia can cause intestinal injury, intestinal barrier dysfunction, and increased permeability of intestine. After 72 h of reperfusion, the intestinal injury can be partially recovered and the permeability can be lower than the post-ischemia level; however, bacterial endotoxin translocation and lung apoptotic cells still exist. Intestinal lymphatic ligation can alleviate the lung damage, promote repair of intestinal mucosa, reduce endotoxin translocation, and attenuate the systemic inflammatory response. EN added with ω-3PUFA is remarkably superior to conventional EN.