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.

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

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.

Objective To study the effect of implanted stent or selected operation in patients with acute occlusion of right coronary artery during the emergency coronary arteriongraphy. Methods Forty-three patients with acute occlusion of right coronary artery who underwent the emergency coronary arteriongraphy were divided into two groups: the implanted stent group ( n = 23) during the emergency coronary arteriongraphy and the selected operation group (n =20) during the emergency coronary arteriongraphy . Then we observed the general data, the coronary artery pathological changes, preoperative and postoperative thrombus, the blood flow, remained stenosis and the prognosis. Results The implanted stent group was similar to the control group in general condition, but implanted stent group was significantly different from the control group in the near, intermediate and distal coronary artery pathological changes ( <0.05) . The control group was significantly different from the implanted stent group in the thrombus and slowly blood flow ( <0.05) . After three months, we reviewed coronary arteriongraphy and selected operation, The implanted stent group was significantly different from the control in the remained stenosis and slowly blood flow (<0.05) . But the implanted stent group was similar to the control groug in the thrombus and new proceeding cardiovascular events. Conclusion When thrombus appears in acute occlusion of right coronary artery, we can implant stent during the emergency coronary arteriongraphy if the thrombus is little, or we can select operation after PTCA on the contrary.

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.

To establish the identification method for Physalis angulatae fructus Seu calyx and Physalis calyx Seu fruc-tus. Methods:Four methods including macroscopy,microscopy,TLC and HPLC were used. Results: There were some differences in macroscopic and microscopic characteristics and physicochemical identification between Physalis angulatae Fructus Seu Calyx and Phys-alis Calyx Seu Fructus. Conclusion:The established method is simple and easy,which can objectively and accurately distinguish Phys-alis angulatae Fructus Seu Calyx from Physalis Calyx Seu Fructus.

Objective To compare the changes in TLR4-NF-κB signaling pathway in infant and adult mice infected with influenza virus, and to provide experimental evidence for the study of immunopathological mechanism in pediatric respiratory virus susceptibility. Methods Immunohistochemistry and RT-PCR were applied to detect the expressions of lung TLR4 and NF-κB P65 mRNA and proteins in the infant and adult mice, and to compare the changes in TLR4-NF-κB P65 signaling pathway after infection with influenza virus.Results (1) The infant model group showed the strongest expression of TLR4 protein in the lung tissue, compared with that in the normal group and adult model group showing significant differences (P<0.05).(2) The expression of NF-κB P65 protein in the lung tissue was strongest in the infant model group, and it was gradually increased over time, showing a significant difference between each time point and the next time point (P<0.05).(3) The infant model group showed the strongest expression of TLR4 mRNA in lung tissue, significantly higher than that in the normal and adult model groups (P<0.05).(4) The expression of NF-κB P65 mRNA in the lung tissue was highest in the infant model group, and significantly higher than that in the normal and the adult model groups ( P<0.05) , and it was gradually increased with the time.Conclusions The over-activation of TLR4-NF-κB P65 signaling pathway may be one of the immunopathological mechanisms of serious injury in the lung tissue in infant rats.

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: 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.

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.