摘要：
Material WC-12Co has good characters of wear resisting, anticorrosion and high temperature resisting. High performance material can be made by surface technology that adds WC-12Co on the surface of common material. With the flame spraying and laser cladding technique, the surface of 45＃ steel is covered firstly with a layer of WC-12Co cermets powder, and then cladded with laser. The laser cladding microstructure and micro-appearance is analyzed with SEM; interface element distributing with EDS; and micro penetration hardness distributing with HXD-IOOOB Vickers hardness tester. After laser-cladding, the original slice-like structure of flame spraying layer changes into a denser clad coat, which is metallurgic with the base. The coating micro organization presents as polygon, dendrite arm and granularity from the surface into depth. The hardness of coat is highest on the surface, decreases with the increase of the depth, and has an abrupt change on the interface between coat and metallic base.
作者：
Yang, S. H.;Brindley, P. J.;Zeng, Q. R.*;Zeng, T. B.;Li, Y. S.;...
作者机构：
[Li, Y. S.; Liu, Y.; Cai, L. T.; Liu, B. Y.; Zeng, T. B.; Lan, L. M.; Yang, S. H.; Zeng, Q. R.] Cent S Univ, Xiangya Sch Med, Ctr Cell & Mol Biol Expt, Changsha, Peoples R China.;[Wu, C. R.; Tan, Z. J.; Lu, F. G.; Yang, S. H.] Hunan Univ Chinese Med, Dept Pathogen Biol & Immunol, Changsha, Peoples R China.;[Brindley, P. J.] George Washington Univ, Med Ctr, Dept Microbiol Immunol & Trop Med, Washington, DC 20037 USA.;[Liu, Y.; Liu, B. Y.; Zeng, T. B.] Univ South China, Sch Med, Hengyang, Peoples R China.;[Li, Y. S.; McManus, D. P.] Queensland Inst Med Res, Mol Parasitol Lab, Brisbane, Qld, Australia.
会议名称：
12th International Congress of Parasitology (ICOPA)/6th Novel Approaches to the Control of Helminth Parasites of Liverstock Conference
会议时间：
AUG 15-20, 2010
会议地点：
Melbourne, AUSTRALIA
会议主办单位：
[Yang, S. H.;Zeng, Q. R.;Zeng, T. B.;Li, Y. S.;Liu, Y.;Liu, B. Y.;Cai, L. T.;Lan, L. M.] Cent S Univ, Xiangya Sch Med, Ctr Cell & Mol Biol Expt, Changsha, Peoples R China.^[Yang, S. H.;Wu, C. R.;Lu, F. G.;Tan, Z. J.] Hunan Univ Chinese Med, Dept Pathogen Biol & Immunol, Changsha, Peoples R China.^[Brindley, P. J.] George Washington Univ, Med Ctr, Dept Microbiol Immunol & Trop Med, Washington, DC 20037 USA.^[Zeng, T. B.;Liu, Y.;Liu, B. Y.] Univ South China, Sch Med, Hengyang, Peoples R China.^[Li, Y. S.;McManus, D. P.] Queensland Inst Med Res, Mol Parasitol Lab, Brisbane, Qld, Australia.^[Zhou, J.] Cent S Univ, Expt Ctr Xiangya Third Hosp, Changsha, Hunan, Peoples R China.
摘要：
Retroviral transduction of cultured schistosomes was explored in our study. The vesicular stomatitis virus glycoprotein (VSVG)-pseudotyped pantropic retroviral vector pBABE-puro was modified to incorporate the human telomerase reverse transcriptase gene (hTERT) as a reporter gene under the control of retroviral long terminal repeat (LTR). Pseudotyped virions were employed to transduce Schistosoma japonicum (Sj) to investigate the utility of retrovirus mediated Sj transgenesis and to investigate the activity as human telomerase as a reporter transgene in schistosomes. The presence of transgene hTERT was detected by PCR. Furthermore, analysis of RNAs from transduced parasites, immunohistochemistry of thin sections and immunoblot analysis revealed expression of hTERT transgene in the transduced worms. These findings indicated that Sj could be effectively transduced by VSVG pseudotyped retrovirus carrying the hTERT gene.
摘要：
Resistant starch (RS) films were designed to target a protein to the colon by exploiting the colonic microbiota fermentative capacity. The RS films were coated to pellets and their mechanical resistance to the shear forces and the hydrostatic pressure within the pellets were investigated after contact with the gastrointestinal tract (GIT). In vitro tests showed that desired colon-targeted drug release can easily be obtained through controlling the proper relationship between enzymatic resistance and mechanical properties of RS film.
作者机构：
[ShiPing Wang; DongMei Gao] Department of Parasitology, Xiangya School of Medicine, Central South University, Changsha, China;[QiuGui Zhang] The First Affiliated Hospital, University of South China, Hengyan, China;[YiMou Wu; FeiJun Zhao; TieBing Zeng; YueJun Zhang] Department of Microbiology and Immunology, University of South China, Hengyan, China;[ShuangQuan Liu] Department of Parasitology, Xiangya School of Medicine, Central South University, Changsha, China<&wdkj&>The First Affiliated Hospital, University of South China, Hengyan, China
通讯机构：
[ShiPing Wang] D;Department of Parasitology, Xiangya School of Medicine, Central South University, Changsha, China
摘要：
The tissue destruction characteristic of syphilis infection may be caused by inflammation due to Treponema pallidum and the ensuing immune responses to the pathogen. T. pallidum membrane proteins are thought to be potent inducers of inflammation during the early stages of infection. However, the actual membrane proteins that induce inflammatory cytokine production are not known, nor are the molecular mechanisms responsible for triggering and sustaining the inflammatory cascades. In the present study, Tp0751 recombinant protein from T. pallidum was found to induce the production of proinflammatory cytokines, including TNF-α, IL-1βand IL-6, in a THP-1 human monocyte cell line. The signal transduction pathways involved in the production of these cytokines were then further investigated. No inhibition of TNF-a, IL-1β, or IL-6 production was observed following treatment with the SAPK/JNK specific inhibitor SP600125 or with an ERK inhibitor PD98059. By contrast, anti-TLR2 mAb, anti-CD14 mAb, and the p38 inhibitor SB203580 significantly inhibited the production of all three cytokines. In addition, pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of NF-κB, profoundly inhibited the production of these cytokines. Tp0751 treatment strongly activated NF-κB, as revealed by Western blotting. However, NF-κB translocation was significantly inhibited by treatment with PDTC. These results indicated that TLR2, CD14, MAPKs/p38, and NF-κB might be implicated in the inflammatory reaction caused by T. pallidum infection.
