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1.
Journal of International Oncology ; (12): 645-647, 2014.
Artigo em Chinês | WPRIM | ID: wpr-459897

RESUMO

Increases of platelet amount and activation are associated with tumor metastasis.Current studies reveal that platelets participate in the process of tumor metastasis via promoting immune escape,adhe-sion and angiogenesis.The direct interactions between platelets and tumor cells are also founded as an important determinant in metastasis.The functions of platelets in tumor progression and metastasis suggest that platelets could be served as new potential targets for cancer treatment.

2.
Chinese Journal of Medical Education Research ; (12): 1012-1014,1015, 2013.
Artigo em Chinês | WPRIM | ID: wpr-573607

RESUMO

To improve the quality of postgraduate students,school of medicine of Shanghai Jiao Tong University have offered medical molecular genetics course to postgraduates and obtained good teaching efficiency. More than ten professors gave lectures on the academic foreland,leading students to find and solve academic problems and training practical and innovative ability of students. Accord-ing to the questionnaires of evaluation of the course and suggestions from postgraduates in the recent two years,some recommendations for the further teaching reform were proposed,such as using multi-plex teaching models,strengthening communication for teaching information with the students,em-ploying comprehensive evaluation methods and strengthening coordination and management of the course.

3.
Progress in Biochemistry and Biophysics ; (12)2006.
Artigo em Chinês | WPRIM | ID: wpr-587463

RESUMO

Adiponectin is an adipocyte-derived secretory protein. It was found to be associated with insulin resistance, inflammation and arteriosclerosis. To further study the biological function and expression of adiponection in vivo, adipoenctin gene knock-out and LacZ gene knock-in mouse model was constructed. Gene targeting strategy was designed to replace part of exon 2 and exon 3 of adiponectin gene with full length LacZ gene in frame with remaining upstream ATG and signal peptide sequence of exon 2. The targeting vector (Adipo-LacZ-XpPNT) was constructed and verified by restriction enzyme digestion and sequencing. CJ7 ES cells were transfected with targeting vector linearized by NotⅠ digestion, selected in the medium containing both G418 and ganciclovoir. Resistant clones were screened by PCR and further confirmed by Southern blot for correct homologous recombinants. Chimera mice were obtained by routing microinjection of homologous recombined ES cells into blastocysts. After mating, mice heterozygous and further homozygous for adiponectin knockout and LacZ gene knock-in were established. Expression of both endogenous adiponectin and exogenous LacZ gene in mouse tissues and sera were detected by RT-PCR, Northern-blot, Western blot and ELISA. The results show that adiponectin was disrupted at both mRNA and protein levels. LacZ gene is expressed exclusively in adipose tissue of mutant mice. Its expression profile is identical to endogenous adiponection. Unexpectedly, LacZ activity could not be detected in both adipose tissue and serum although LacZ protein can be detected in adipose tissue but not in serum of mutant mice. In conclusion, mice homozygous for adiponectin knockout and LacZ gene knock-in have been successfully constructed. Mutant mice display LacZ expression profile identical to endogenous adiponectin albeit neither LacZ activity nor protein can be detected in serum of mutant mice.

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