Objective To investigate the expression of tissue factor and explore its clinical significances in pulmonary artery after acute pulmonary thromboembolism.Methods Thirty-four Japanese white rabbits (Level Ⅱ animals) were randomly (random number) assigned into four groups:group A (specimen of pulmonary artery was taken 3 hours after pulmonary embolism,n =8),group B (specimen of pulmonary artery was taken 8 hours after pulmonary embolism,n =8),group C (specimen of pulmonary artery was taken 24 hours after pulmonary embolism,n =8) and control group (pseudo-operations were carried out without injecting autologous blood clots,n =10).The animal model of pulmonary thromboembolism was established by injecting autologous blood clots into jugular vein through a 5F catheter and confirmed by digital subtraction angiography.The mRNA expression of TF in different parts of pulmonary artery was assayed by RT-PCR.The q test was utilized if there was a significant difference in a given continuous variable among three groups analyzed by ANOVA.Results The TF expression in the specimen adjacentto emboli was stable at 3 h,8 h or 24 hours after embolism.The mRNA expression of TF at 3 h and 8 h after embolism was lower in specimen taken from distal-end of morbid pulmonary artery than those adjacent to emboli.While at 24 hours after embolism,there were similar mRNA expressions in specimen either adjacent or distal to emboli.Conclusions The high expression of tissue factor in pulmonary artery tissue adjacent to emboli could lead to locally increased coagulation activity,indicating the necessity of initiating anti-coagulation treatment as soon as possible after acute pulmonary embolism.

0.05). The time for fever reduced to normal level and for abscesses disappeared in Group A were significantly shorter than those in Group B(all P

OBJECTIVE:To study the implementation of Prescription Management Method (PMM) in our hospital and to promote rational drug use. METHODS: A total of 71 000 prescriptions were collected from Sept. 2006 to Dec. 2007 (before implementation) and from May to Dec. in 2007 (after implementation) for a statistical analysis and evaluation of the irrational prescriptions. RESULTS: The non-conformity rate of prescriptions was on the higher side before PMM implementation, accounting for 7.76% versus 3.38% after implementation (P

Objective: To explore the application value on combined examination of blood levels of growth differentiation factor-15 (GDF-15) and NT-pro B-type natriuretic peptide (NT-proBNP) in patients after successful cardiopulmonary resuscitation (CPR) for their recent prognosis.
Methods: A total of 102 patients with sudden cardiac arrest and successful CPR in our hospital were enrolled. Blood levels of GDF-15 were examined at immediately, 12 h and 24-48 h after CPR respectively. According to GDF-15 levels, the patients were divided into 3 groups: Group A, the patients with GDF-15<1200 ng/L at all-time points,n=31; Group B, GDF-15 level consistently increasing and GDF-15>1200 ng/L at all-time points,n=35; Group C, GDF-15 level consistently increasing at 12 h and 24-48 h after CPR, while it was lower at 24-48 h than 12 h after CPR,n=36. Blood levels of NT-proBNP and left ventricular ejection fraction (LVEF) were also examined. The patients were followed-up for 6 months for post-CPR death.
Results: Blood levels of GDF-15 and NT-proBNP were related, NT-proBNP level was changing with GDF-15 varying. GDF-15 and NT-proBNP level was negatively related to LVEF (r=-0.530,P<0.001), the patients with GDF-15>1800 ng/L and NT-proBNP>400 pg/ml had the higher mortality than those had the lower levels of GDF-15 and NT-proBNP,P<0.05. Survival analysis presented that 6 months survival rate in Group B was lower than Group A and Group C,P<0.05; survival rate was similar between Group A and Group C,P>0.05.
Conclusion: Combined examination for blood levels of GDF-15 and NT-proBNP may better predict the recent prognosis in patients who received CPR.

Objective To study the impact of hepatitis B virus (HBV) infection on the activity of cord hematopoietic stem cells. Methods CD34+ cells were isolated from healthy human cord blood by miniMACS. Cells were cultured in IMDM complete culture medium containing stem cell factor (SCF),fms-like tyrosine kinase 3 ligand (FL), thrombopoietin (TPO), interleukin-3 (IL-3) and 10% fetal bovine serum. High copies HBV were added to the culture system. The proliferation of stem ceils and virus replication were observed. Following the proliferation, dendritic cells (DCs) were induced by adding granulocyte-macrophage colony-stimulating factor and IL-4. Morphous of stem cells and DCs were observed by microscope and the cell surface molecules were detected. Results The proliferation of stem cells infected with HBV was significantly lower than that of healthy stem cells (P＜0.01),and enhanced after adding cytokines (P＜0.01). At the same time, HBV replication was increased after adding cytokines in the culture system (P＜0.01), but the proliferation was still lower than that of healthy stem cells with cytokines in the culture medium (P＜0.05). Dane particles were found in the cytoplasma of stem cells infected with HBV by electron microscope. The expression of CD80,CD86 ,CD1a and HLA-DR on DCs derived from HBV infected stem cells were all lower than those on DCs from non-infected stem cells (P＜0.01). Conclusions HBV could infect CD34+ stem cell and the proliferation of the stem cell could enhance the virus replication. HBV could not only inhibit the proliferation of stem cells,but also down-regulate the immuno-phenotype expression of DCs derived from CD34+stem cells.

To study the potential molecular mechanism of tumor angiogenesis in its microenvironment, we investigated the effects of HepG2 conditioned medium on the proliferation of vascular endothelial cell and vascular angiogenesis in our laboratory. Human umbilical vein endothelial EA. hy926 cells were co-cultured with HepG2 conditioned medium in vitro. The proliferation and the tubulogenesis of EA. hy926 cells were detected by teramethylazo salt azole (MTT) and tube formation assay, respectively. The results showed that the survival rate of the EA. hy926 cells was significantly increased under the co-culture condition. HepG2 conditioned medium also enhanced the angiogenesis ability of EA. hy926 cells. In addition, the expressions of intracellular VEGF and extracellular VEGFR (Flk-1) were regulated upward in a time-dependent manner. In conclusion, the proliferation of vascular endothelial cells and Vascula angiogenesis were improved under the condition of indirect co-culture.
Carcinoma, Hepatocellular ; pathology ; Cell Proliferation ; Coculture Techniques ; Culture Media, Conditioned ; Endothelial Cells ; cytology ; Hep G2 Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; Liver Neoplasms ; pathology ; Neovascularization, Pathologic ; Tumor Microenvironment ; Vascular Endothelial Growth Factor A ; metabolism ; Vascular Endothelial Growth Factor Receptor-2 ; metabolism

Due to the good tumor-targeting and excellent biocompatibility, the drug-loading nanoparticles (NPs) has been widely applied in the diagnosis and treatment of cancer. However, after the NPs are recognized and internalized by cancer cells, the effects of NPs on cell migration behavior were unclear. In the present study, the self-assembly techniques (SAMs) was used to modify gold (Au) nanoparticles (Au NPs) with different chemical functional groups (CH3, OH, COOH and NH2) as model NPs. The dispersion of these groups in solution and the distribution in cells were studied by transmission electron microscope (TEM), respectively, and the proliferation was examined by MTT assay in vitro. The wound-healing and the Transwell assay were used to examine the effect of internalized Au-NPs on HepG2 cells migration. The results showed that different Au-NPs mainly distributed at the edge of the vesicle membrane and the gap between cells. The Au-NPs resulted in decreased cell viability in a concentration-depended manner. In addition, the results of wound-healing and Transwells assay indicated that the internalization of the NH2-NPs and OH-NPs would inhibit cell migration compared with those in the control group.
Carcinoma, Hepatocellular ; metabolism ; Cell Movement ; Cell Proliferation ; Cell Survival ; Gold ; Hep G2 Cells ; Humans ; Liver Neoplasms ; metabolism ; Metal Nanoparticles ; chemistry

ObjectiveTo investigate the clinic and pathologic features of one patient diagnosed with neurocutaneous melanosis ( NCM ) by biopsy.MethodsA 21-year-old woman presented with a 2-month history of tinnitus,headache,vomiting and 1-month history of impaired vision.At birth,a massive nevus covering most of the posterior abdomen had been noted as well as the presence of multiple smaller lesions all over the body.Magnetic resonance imaging demonstrated a posterior fossa cyst compatible with the Dandy-Walker syndrome and extensive leptomeningeal enhancement. Surgery was performed to cystectomy and to obtain pathologic specimens from the leptomeninges. Biopsy and immunohistochemical study was performed.ResultsAt surgery,diffuse black pigmentation of the leptomeninges and the cyst was found.Under microscope,the cyst and leptomeninges were composed with melanocytes with variable pigmentation.Those cells positive for HMB45,MelanA,S100 and vimentin.Ki-67 positive cells ＜ 1％.The pathologic diagnosis wasleptomeningeal diffusemelanocytosis. Thepatientdied 2months after thesurgery.ConclusionsNCM is characterized by a focal or diffuse proliferation of melanin-producing cells in both the skin and the leptomeninges.NCM could be compatible with the Dandy-Walker syndrome.Definite diagnosis relies upon the histological data obtained by mean of biopsy.

Background Light-induced retinal damage results in the damage of retinl pigment epithelial (RPE) cells and therefore affects the pathogenesis and development of age-related macular degeneration (AMD).Studies showed that tissue factor (TF) is overexpressed in oxidative damaged RPE cells and the choroidal neovascularization (CNV) of AMD,speculating that the suppression of TF can prevent the damage of RPE cells and inhibit CNV.Objective This study was conducted to observe the protective effects of TF targeting peptide (TFTP),a new drug of autologous synthesis,on human RPE-cells induced by blue light.Methods Human RPE cells were isolated from donor eye and cultured.Cultured cells were divided into blank control group,model group and TFTP treated group.Light-induced RPE cell damage model was established by exposuring the cells in the blue light of (4.0±-0.5) mW/cm2 for 12 hours in the model group,and different concentrations (10,100,150,200,300 μmol/L) of TF-TP were added into the medium to pretreat the cells for 24 hours and then exposed the cells to the blue light for 12 hours in the TF-TP groups.The cell viability was determined by CCK-8 assay.The morphology and ultrastructure in the cells were observed under the inverted microscope and transmission electron microscope.The apoptosis of the cells was assayed by Hoechst staining.The expressions of TF and apoptosis-related protein bax,bcl-2 in the cells were determined by Western blot.Results CCK-8 assay showed that there was no significant difference in the cell viability among blank control group and different concentrations TF-TP groups (F=2.15,P =0.11).The cell survival rate of blank control group,model group and 150 μmol/L TF-TP group was (100.0±0.00) ％,(43.79±6.55) ％ and (63.45±3.57) ％,and the survial rate was increased in the 150 μmol/L TF-TP group compared with the model group (P =0.00),and 150 μmol/L was detemined as a optimal concentration of TF-TP.A lot of shrinkage,deformation,suspension cells were exhibited under the optical microscope,and decrease of microvilli structure,rupture of mitochondrial cristae and vacuolar degeneration of the cells were found in the model group,and the damage of the cells were evidently lightened in the 150 μ mol/L TF-TP group.The apoptosis rate of the cells were (0.98 ±0.19)％,(9.98 ±0.82) ％ and (5.73 ±0.88) ％ in the blank group,model group and 150 μmol/L TF-TP group,respectively,with a significant difference among the groups (F =206.18,P =0.00),and the apoptosis rate of the cells in the 150 μmol/L TF-TP group was significantly lower than that in the model group (P＜0.05).Compared with the blank control group,the relative expression of bax and TF was obviously increased and that of bcl-2 was decreased in the model group;while the expression of bax and TF was lower,and that of bcl-2 was higher in the 150 μmol/L TF-TP group compared with the model group (all at P ＜ 0.05).Conclusions Pretreation of TF-TP can lessen cell apoptosis and increase cell survival rate and therefore plays a protective role to blue light-induced human RPE cells possibly by inhibiting bax/bcl-2 apoptotic pathways mediated by TF.

Objective: To explore the neuroprotective effects of the Shaoyao Gancao decoction (SGD) against excitatory damage in PC12 cells and the role of the Src-NR2-nNOS pathway mediation by SGD in regulating γ-aminobutyric acid (GABA)-glutamate (Glu) homeostasis. Methods: N-Methyl-d-aspartic acid (NMDA) was used to establish a PC12 cell excitability injury model. To investigate the neuroprotective effect of SGD, a cell counting kit-8 (CCK-8) assay was used to determine PC12 cell viability, Annexin V/Propidium Iodide (Annexin V/PI) double staining was used to determine PC12 cell apoptosis, and Ca2+ concentration was observed using laser confocal microscopy. GABA receptor agonists and antagonists were used to analyze the neuroprotective interactions between γ-aminobutyric acid (GABA) and NMDA receptors. Additionally, molecular biology techniques were used to determine mRNA and protein expression in the Src-NR2-nNOS pathway. We analyzed the correlations between the regulatory sites of GABA and NMDA interactions, excitatory neurotoxicity, and brain damage at the molecular level. Results: NMDA excitotoxic injury manifested as a significant decrease in cell activity, increased apoptosis and caspase-3 protein expression, and a significant increase in intracellular Ca2+ concentration. Administration of SGD, a GABAA receptor agonist (muscimol), or a GABAB receptor agonist (baclofen) decreased intracellular Ca2+ concentrations, attenuated apoptosis, and reversed NMDA-induced upregulation of caspase-3, Src, NMDAR2A, NMDAR2B, and nNOS. Unexpectedly, a GABAA receptor antagonist (bicuculline) and a GABAB receptor antagonist (saclofen) failed to significantly increase excitatory neurotoxicity. Conclusions Taken together, these results not only provide an experimental basis for SGD administration in the clinical treatment of central nervous system injury diseases, but also suggest that the Src-NR2A-nNOS pathway may be a valuable target in excitotoxicity treatment.