The effect of Sepia on the activity of tyrosine protein kinase (TPK) protein kinase C (PKC) and cAMP-dependent protein kinase (PKA) was studied in H 22 cancer cells by using the incorporation of ? 32 P ATP into exogenous substract.The results showed that membranous TPK activity of membrane,cytosol and mitochondria was elevated significantly,while the membranous TPK activity was increased obviously;while the cytosolic PKC activity was increased most.The cytosolic PKA activity was increased.These results suggested that Sepia can changeover the activity of TPK,PKC and PKA,which was abnormally changed by cancer cells,then caused that the up regulation was diminished and the down regulation was enhanced towards the Ras MAPK signal transduction pathways.This inhibited or interrupted the cascade transduction of the Ras MAPK pathway,thus produced the effect of anticancer and accelerated the differentiation by transforming cancer cells from undifferentiated proliferation to differentiated proliferation.

Objective To study the antitumor mechanism of DHA compound. Methods RT-PCR was used to investigate the effects of DHA compound on H-Ras and pl6 mRNA transcription in gastric adenocarcinoma. Results Compared with control, the content of H-Ras mRNA was decreased and the content of p16 mRNA was increased in gastric adenocarcinoma significantly after treated with DHA compound. Conclusion The transcription of H-Ras gene was decreased and the transcription of pl6 gene was increased in gastric adenocarcinoma after treated with DHA compound and thus the cancer cell growth was inhibited.

Objective To investigate the mechanism and epidemiological characteristics of carbap-enem-resistant Proteus mirabilis ( PM) strains deficient in swarming motility. Methods PM strains were isolated from Hangzhou General Hospital of CAPF ( Chinese People′s Armed Police Forces) during January 2013 to December 2014. Bacterial motility and flagella of the PM strains were observed through semi-solid agar culture and flagella staining. Pulsed-field gel electrophoresis ( PFGE) was performed for homology anal-ysis. Antimicrobial susceptibility test and phenotypic confirmatory test were also carried out. PCR analysis and DNA sequencing were performed to confirm the genotype of resistant genes. Plasmid electroporation and S1-PFGE in combination with Southern blot hybridization were used to determine the location of the carbap-enem-resistant genes. Genetic structure of the blaKPC-2 gene was obtained by PCR mapping. Results A total of 42 PM isolates deficient in swarming motility were screened out and the resistance rates to imipenem and meropenem were 57. 1% and 52. 4%, respectively. PCR analysis and DNA sequencing confirmed that 24 carbapenem-resistant PM isolates deficient in swarming motility carried blaKPC-2 gene and belonged to three clones as indicated by the results of PFGE. Southern blot hybridization indicated that the blaKPC-2 gene was located on plasmids varying in size (26 kb, 55 kb and 139 kb). In addition, some of the strains harbored several resistant genes, such as blaTEM-1 , blaCTX-M-65 and rmtB. The genetic structures of strains carrying blaKPC-2 gene were ISKpn8, blaKPC-2 and ISKpn6-like from upstream to downstream. Conclusion Compared with the PM strains with swarming motility, the carbapenem-resistance rate was significantly higher in these PM strains deficient in swarming motility. Carbapenemases KPC-2 played an important role in the carbapen-em-resistant PM strains deficient in swarming motility. There was a cloning spread trend for carbapenem-re-sistant PM strains in our hospital. Clinicians should pay more attention to the risk of spreading.