[Efficacy Observation of Yiguanjian Decoction Combined Adefovir Dipivoxil Tablet in Treating HBeAg Negative Chronic Viral Hepatitis B Active Compensated Liver Cirrhosis Patients].

Objective: To explore clinical efficacy of Yiguanjian Decoction (YD) combined Adefovir Dipivoxil Tablet (ADT) in treating HBeAg negative chronic viral hepatitis B (CVHB) active compensated liver cirrhosis (LC) patients.

Methods: Totally 68 HBeAg negative CVHB active compensated LC patients initially treated were assigned to the treatment group and the control group using random digit table, 34 in each group. Patients in the control group took ADT alone, 10 mg each time, once per day.

Suppression of tumor growth and metastasis by a VEGFR-1 antagonizing peptide identified from a phage display library.

Although the VEGF-Flk-1-pathway has been known as the major driving force of angiogenesis, new evidence has shown that VEGFR-1/Flt-1 plays important roles during the neovascularization under pathological conditions including tumor, atherosclerosis and arthritis. In search of Flt-1 receptor antagonizing peptides, we screened a phage display 12-mer-peptide library with recombinant Flt-1 protein. Seven candidate peptides were identified that specifically bound to VEGF receptor Flt-1, of which peptide F56 (WHSDMEWWYLLG) almost abolished VEGF binding to receptor Flt-1 in vitro.

[Inhibition of tumor growth by a peptide fusion protein binding to vascular endothelial growth factor receptor Flt-1].

Objective: Investigating the bio-activities of peptides selected from phage display peptide library with vascular endothelial growth factor receptor Flt-1.

Methods: Activities of DHFR-F56/F90 binding to human ubilial vein endothelial cells were detected by immunocytochemistry, and the activity of antiangiogenesis was determined with chick embryo chorioallantoric membrane (CAM) assay. Balb/c nude mice were used as model to detect the activity of DHFR-F56/F90 on inhibiting tumor growth, and immunohistochemistry was employed to determine the localization of the DHFR-F56/F90 in tumor.

A novel peptide isolated from a phage display library inhibits tumor growth and metastasis by blocking the binding of vascular endothelial growth factor to its kinase domain receptor.

Vascular endothelial growth factor (VEGF), one of the most important angiogenic factors, plays an essential role in both physiological and pathological angiogenesis. The VEGF receptor KDR/Flk-1 (a kinase domain receptor) mediates various biological activities of VEGF related to proliferation, differentiation, and migration of endothelial cells. Here we present a novel peptide designated K237-(HTMYYHHYQHHL), which was isolated from a phage-displayed peptide library, binding to KDR with high affinity and specificity.