Objective:To reconstruct pcDNA3.1/VEGF165 and combine it with deproteinized bone(DPB) to repair avascular necrosis of the femoral head (AVNFH).Methods:Clone plasmid pUC18/VEGF165 containing the whole cDNA sequence of VEGF165 was combined with pcDNA3.1(+) to reconstruct pcDNA3.1/VEGF165.Sixty-nine AVNFH model New Zealand adult rabbits with a mean weight of 2.8 kg were randomly divided into three groups.In group 1,DPB combined with the reconstructed plasmid pcDNA3.1/VEGF165 was implanted in the drilled channel of the necrotic femoral head.In group 2,only DPB was implanted.In group 3,only channel was drilled without DPB or plasmid implanted.Femoral head specimens were obtained 3 days,1,2,4,and 8 weeks after operation.The expression of vascular endothelial growth factor (VEGF) was examined by RT-PCR,Western blotting techniques.Angiogenesis and repair of the femoral head were observed by histological and histomorphometric analysis.Results:pcDNA3.1/VEGF165 was reconstructed successfully.In group 1,the expression of VEGF was detected in the femoral head implanted by DPB-VEGF compound.VEGF165 mRNA and protein detected went up to apex 1 week postoperatively and lasted more than 3 weeks.The femoral head implanted by DPB-VEGF compound showed a significant difference in vascularization 2 and 4 weeks after operation and a significant difference in bone formation 2,4 and 8 weeks after operation from those in other groups on histomorphometric analysis (P

Quantum dots (QD),a kind of nanocrystal,are made from Ⅱ-Ⅵ or Ⅲ-Ⅴ group elements.It has been reported that compared with current conventional fluorescent markers,QD have excellent optical properties such as strong fluorescence,photochemical stability and can be used for simultaneous multi-channel imaging.Meanwhile,as nanoparticle,QD can be easily surface modified with a variety of biological molecular and can reach cancer cells easily by penetrating the tumor angiogenesis.Therefore,QD have unique advantages in targeted real-time visual imaging of in vivo tumor and have great prospects in the individual diagnosis and treatment of tumor.However,the long-term biosafety after QD into the body still needs further study.

OBJECTIVE: To review the outcomes of experiments about vascular endothelial growth factor(VEGF) and the effect of it on bone formation, and to make sure whether VEGF can promote bone formation or not.DATA SOURCES: Electronic data searches were performed to obtain data from the databases of http://www.ncbi. nlm. nih. gov/pubmed and http://www. zglckf.com. DATA SELECZION: Nearly 30 articles about VEGF and the role of VEGF affecting bone formation were selected, regardless of the randomized design,blind method involved in or not.DATA EXTRACTION: These researches proved the structures, biologic properties and expression of VEGF and vascular endothelial growth factor receptor(VEGFR), and showed that VEGF plays an important role in endochondral ossification by promoting angiogenesis, bone turnover and preventing apoptosis of chondrocyte. In intramembranous ossification, absence of cartilage, osteoblasts are likely producing, and responding to, VEGF. VEGF also acts to recruit and activate osteoclasts as well as stimulate osteoblast chemotaxis, differentiation and matrix mineralization. It is debatable whether local application of exogenous VEGF can promote bone repair or not. However, in certain situation such as ischemia, the increase of VEGF locally may promote bone repair.DATA SYNTHESIS: Compared with the control group, VEGF can promote osteogenesis, bone formation and remodeling through the effect of VEGF on endochondral ossification and intramembranous ossification.CONCLUSION: One possible advantage of local VEGF therapy may be its ability to couple angiogenesis with bone formation and remodeling. If we can ultimately apply VEGF to treat osteonecrosis, bone defect and nonunion, we will find a new therapy for these diseases.

BACKGROUND: The invasion of highly metastatic carcinoma cells on reconstituted basement membrane component is considered as a common model for in vitro experimental studies of invasion and metastasis of malignant tumors. It has been reported that synthetic peptide influences some tumor cells. However, the effect of synthetic peptide on highly metastatic human lung giant-cell carcinoma cell(PG) has been rarely studied.OBJECTIVE: To study the effects of synthetic peptide RGD, YIGSR and their derivatives on invasive ability of PG in vitro.DESIGN: A completely randomized controlled trial was conducted.SETTING and MATERIALS: The human lung highly metastatic tumor and NIH3T3 cell line were both supplied by the Department of Pathology of Beijing Medical University. The synthetic peptides were provided by the Synthetic Laboratory of the Institute of Materia Medica of the Chinese Academy of Medical Sciences and Chengde Medical College. Transwell invasion chamber was purchased from Costor Company. The whole experiment was conducted at the Department of Biochemistry of Chengde Medical College.INTERVENTIONS: NIH3T3 cell line was used to prepare chemotactic factor. PG cells were seeded in Transwell invasion chamber. Under the effect of chemotactic factor, the effects of synthetic peptides on PG invasive ability were examined.MAIN OUTCOME MEASURES: PG cell number of passing through the reconstituted basement membrane was used as an index to evaluate the invasive ability of tumor cells.RESULTS: An appropriate number of PG cells were cultured for 10 hours with chemotactic factor, and the number ofinvasive cells reached a number range that can be applied to statistical analysis(50 to 100 invasive cells). After 100 mg/L of synthetic peptides RGD, YIGSR were incubated for 48 hours with PG cells,the rate of inhibition on invasive ability was 53.63% and 36.86% respectively, and 0% and 6.48% respectively after incubation for 10 hours.CONCLUSION: The PG cells were the proper cells for in vitro experimental studies of invasive ability of cancer cells for the purpose of screening of anti-tumor medicine. RGD and Juncha/Zacha-peptide YIGSR showed a strong activity in inhibiting tumor invasion and a potential value in prevention and treatment of malignant tumor development.

Objective To investigate the effect of Ginkgolide B (BN52021) on lipopolysaccharide (LPS) induced pancreas microvascular endothelialv (MS1) cells, and to explore its molecular mechanism.Methods The optimal concentration and best time point of LPS inhibing MS1 cell survival and the optimal concentration of BN52021 increasing survival of LPS induced MS1 cells were determined by MTT.The mRNA and protein expression of adenylate cyclase (AC), phospholipase A2 (PLA2), phospholipase Cβ (PLCβ),protein tyrosine kinase (PTK) and G protein coupled receptor kinase (GRK) in platelet activating factor receptor(PAFR) signal pathway in MS1 cells were determined by real-time PCR and Western blot.Results It was showed that 10 μg/ml LPS for 24 h was the optimal concentration and best time point to induce the decrease of MS1 cells.50 mmol/L of BN52021 was the optimal concentration of increacing survival of LPS induced MS1 cells.After LPS induction, AC, GRK, PLA2, PLCβ, PTK mRNA expressions of MS1 cells were 4.02 ±0.14, 2.63 ± 0.03, 3.31 ± 0.12, 2.09 ± 0.08, 1.85 ± 0.07, which were significantly higher than those in control group (P ＜ 0.01).After BN52021 treatment, AC, GRK, PLA2, PLCβ mRNA expressions of LPS induced MS1 cells were 2.35 ±0.13, 1.17 ±0.14, 1.87 ±0.11, 1.65 ±0.10, which were significantly lower than those in LPS induction group (P ＜ 0.01).The expression of PTK mRNA was 1.83 ± 0.13, which was not significantly different from that in LPS induction group.Western blot showed that the levels of protein expression were consistent with those of mRNA expression.Conclusions BN52021 can down-regulate the up-regulated genes expression of AC, GRK, PLA2 and PLCβ in the PAFR signal pathway in LPS induced MS1 cells.

Objective Pancreatic neuroendocrine tumor( PNET) is a rare kind of tumor with slow growth for which surgery is the main treatment.The histological grading of PNET was closely related to the choice of operation mode and the comprehensive treat-ment after operation.Imaging examinations such as enhanced CT and MRI are of great value in the preoperative diagnosis of PNET. The aim of this study was to investigate the characteristic features of CT and MRI in the PNET. Methods Preoperative imaging data of 80 patients with PNET confirmed by pathology were reviewed, including CT and MRI, and the image features of each PNET were an-alyzed and the statistical analysis was performed. Results There were significant differences in the lesion morphology between the G1 and G2 levels of PNET.The majority of forms of the G1 stage PNET lesions presented round-like regular shape, but the G2 stage did not show regular shape.CT examination showed that regular morphological lesions accounted for 91.30%(21/23) in the G1 level, and 52.00%(13/25)in the G2 level,χ2 =8.857,P=0.003.MRI examination showed that regular morphological lesions accounted for 88.48%(22/27)in the G1 level, and 55%(11/20) in the G2 level, χ2 =3.862,P=0.050.The difference of scan density in PNET lesions was statistically significant.Low density lesions accounted for 73.91%(17/23)in the G1 level, and 32%(8/25)in the G2 level.Equidensity lesions accounted for 26.09%(6/23)in the G1 level, and 68.00%(17/25)in the G2 level,χ2 =8.842,P=0.004.The difference of bile pancreatic duct expansion in the G1 and G2 level lesions was statistically significant by MRI examination. Lesions with expanded pancreatic duct accounted for 7.41%(2/27)in the G1 level,and 40%(8/20) in the G2 level, χ2 =7.287, P =0.007.There was significant difference in the peak time after en-hanced scanning between the G1 and G2 levels.Lesion enhancement peak at the arterial phase by CT examination of accounted for 21.74%(5/23) in the G1 level,and 64%(16/25) in the G2 level,χ2 =8.694,P=0.003.Lesion enhancement peak at the arterial phase by MRI examination accounted for 29.63% (8/27) in the G1 level, and 70% (14/20) in the G2 level, χ2 =7.521,P=0.006. Conclusion The lesion morphology, density of CT plain scan, CT or MRI enhancement peak time, and expansion of the bile duct and pancreatic duct can provide reliable information to distinguish the G1 and G2 stage in PNET.

Adult ; Aged ; Axilla ; innervation ; surgery ; Brachial Plexus ; surgery ; Breast Neoplasms ; physiopathology ; surgery ; Female ; Follow-Up Studies ; Humans ; Lymph Node Excision ; methods ; Mastectomy, Radical ; adverse effects ; methods ; Middle Aged ; Pain, Postoperative ; etiology ; Somatosensory Disorders ; etiology

ObjectiveTo investigate the effect of SalB on bone marrow-derived mesenchymal stem cells (BMSCs) apoptosis induced by hypoxia and serum deprivation (hypoxia/SD) in the vitro. Methods BMSCs were cultured in the vitro and randomly divided into control group, hypoxia/SD group and SalB group.SalB group was composed by four groups and were pretreated by complete medium with 0.1、 1、 10、 100 mg/L SalB for 1 hour. And after that they were washed with phosphate buffer for 2 times, added by IMDM with 0.1、1、 10、 100 mg/L SalB and cultured with hypoxia/SD group together in the same condition of hypoxia/SD for 6hours. The control group was cultured for 6 hours in the condition of aerobic and enough serum. Apoptosis was detected by Hoechst33342 staining with inverted phase contrast, fluorescence microscope and Annexin V/PI dual-color flow cytometry. Results Significant apoptosis of BMSCs was induced by hypoxia/SD in the vitro.The early apoptosis of BMSCs induced by hypoxia/SD was significantly decreased by SalB of 0.1、 1、 10 mg/L(P＜0.05) . Conclusion0.1、 1、 10 mg/L SalB can decrease the early apoptosis of BMSCs induced by hypoxia/SD.

OBJECTIVETo investigate protective effect of paeonol (Pae) on human umbilical vein endothelial cells (HUVECs)injured by hyperlipidemic serum and explore its possible mechanism.METHODS The injury model was induced by 20％ hyperlipidemic serum incubating HUVECs for 24 h.Pae 124,247 and 495.μmol· L-1 were given followed by administration of hyperlipidemic serum for 24 h.The morphological changes were observed under inverted microscope,cell survival rate was evaluated by MTT method,the nitric oxide (NO) content was measured by nitric acid reductase method and the endothelial nitric oxide synthase (eNOS) mRNA expression was determined by RT-PCR.RESULTSCompared with normal contorl group,most cells in model group split and exfoliated.However,the morphology was tending to normal level after intervention with Pae.Pae significantly improved cell viability(P ＜0.01).Compared with model group,the survival rate increased from (53.0 ±10.1 ) ％ to ( 68.4 ± 9.1 ) ％,( 84.5 ± 6.7 ) ％ and (98.1 ± 7.5 ) ％,respectively.The NO content and eNOS mRNA expression both increased greatly in Pae groups(P ＜ 0.01 ).Compared with model group,content of NO increased from 54 ± 4 to 79 ± 6,115 ± 5 and ( 136 ± 6) μmol · L- 1,respectively.The expression level of eNOSmRNA improved from 0.215 ± 0.060 to 0.451 ± 0.045,0.563 ± 0.013,0.704 ± 0.068,respectively.CONCLUSIONPae exerts protective effect on HUVECs injured by hyperlipidemic serum by increasing eNOS mRNA expression,which might therefore improve the content of NO.

Dental Materials ; Dental Porcelain ; Humans