Objective: To evaluate the inhibition of human endostatin on tumor growth and metastasis of lung adenocarcinoma LA795 in mice. Methods: Recombinant human endostatin was purified from pCX expressed endostatin clones. Plasminogen was purified from outdated human plasma by affinity chromatography, and human angiostatin was produced from human plasminogen digested by elastase and purified by affinity chromatography. LA795 cells were inoculated subcutaneously into the dorsa of T739 mice, and the mice were randomized into 3 groups. From the 1Oth day, the first group was given 20 mg/kg of recombinant human endostatin s.c. qd, the second was treated daily s. c. of 7.5 mg/kg of human angiostatin, and the third group received daily s.c. with equal volumes of PBS for 14 days. Volumes of the subcutaneous tumors, lung weights, the number of lung surface metastases and mice life span were observed. The results were analyzed by q-test. Results: The tumor volumes of both the 1 st and the 2nd groups increased slowly. From the 8th day after being treated, the tumor volumes were decreasing. However, in the 3rd group, the tumor volumes increased continuously. The lung weight and the number of lung surface metastases of the 1st and 2nd groups were less than that of the 3rd group. The average survival periods of the 1st and 2nd groups were longer than that of the 3rd group. Conclusion: Human endostatin and angiostatin have strong inhibitory effects both on growth of primary tumor and metastasis of lung adenocarcinoma LA795, and prolongs the survival period of the tumor-bearing mice.

Objective: To investigate the combined inhibitive effect of TNP-470 and rhES on the growth of lung adenocarcinoma LA795 in T739 mice. Methods: The purified rhES was acquired by using methanol to induce the recombinant pichia pastoris. GS115 and heparin affinity chromatography. The T739 mice inoculated with LA795 cells were randomized into three groups, 10 mice per group, one group was injected with PBS for 14 days, the other two groups were respectively treated with rhES and TNP-470+rhES. To observe the tumor growth in different groups, and the tumor volume was measured with caliper. The microvessel density(MVD) of tumors were measured by using immunohistochemistry. Results: The purified rhES was acquired. In compared with PBS group, the tumor growth of other two groups was inhibited significantly. And the tumor volume of TNP-470+rhES group are smaller than the rhES group (P

AIM: To determine differentially expressed genes associated with cell adhesion and immune regulation in peripheral blood eosinophils from asthmatic patients. METHODS: Peripheral blood eosinophils were isolated from the asthmatic patients at the time of exacerbation and after improvement. Total RNA was extracted. Super SMART PCR cDNA was synthesized, suppression subtractive hybridization (SSH) and PCR-select differential screening technology were used to detect expressed genes. The differentially expressed genes were sequenced. RESULTS: High efficiency subtractive cDNA library was constructed successfully. Differential screening identified 15 differentially expressed genes, which were Charcot-Leyden crystal protein (CLC protein; galectin-10), putative pre-mRNA splicing regulator female-lethal (2D), aquaporin 9 (AQP9), IL-8, slingshot 2L (SSH-2L), PP1 catalytic subunit, beta isoform, helicase with zinc finger domain (HELZ), ?2-microglobin (?2-MG) and a gene associated with mitochondrion. CONCLUSION: Increased expression of these genes might be associated with eosinophil migration, adhesion and immune regulation. Intervention of these pathways may provide a theoretical base for future new targeting treatment for asthma.