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Table of Contents
Table of Contents of Volume 52 - 2004 相似文献5.
SALLOW W 《Public Health Reports》1953,68(12):1239-1242
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《American journal of primatology》1998,45(2):184-192
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BARG L 《Polski tygodnik lekarski (Warsaw, Poland : 1960)》1954,9(5):suppl, 38-suppl, 40
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Cai DY Yu F Jiang W Jiang HF Pan CS Qi YF Chang L Zhao J Yang JH Zhu MJ Jia YX Geng B Ma TM Pang YZ Tang CS 《Regulatory peptides》2005,129(1-3):125-132
Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52). The rat vascular calcific model was replicated with vitamin D3 and nicotine. ADM or/and ADM(27-52) were systemically administrated with mini-osmotic pump beginning at seventh day after the model replication for 25 days. Vascular calcific nodules histomorphometry, vascular calcium content, vascular calcium uptake, alkaline phosphatase activity, and osteopontin-mRNA quantification in aorta were assessed. ADM limited 40.2% vascular calcific nodules (P<0.01), did not effect on calcium content (P>0.05), reduced 44.4% calcium uptake (P<0.01), lowered 21.1% alkaline phosphatase activity (P<0.01), and regulated 40.9% downwards osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. ADM(27-52) receded 32.0% vascular calcific nodules (P<0.01), taken from 55.5% calcium content (P<0.01), did not affect calcium uptake (P>0.05), inhibited 22.5% alkaline phosphatase activity (P<0.01), and restrained 21.9% osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. Both of ADM and ADM(27-52) did interact on vascular calcification each other. ADM could partially antagonize the effects of ADM(27-52) in taking from calcium content (17.5%, P<0.01) and in receding vascular calcific nodules (18.6%, P<0.01). ADM could obviously enhance the action of ADM(27-52) in inhibiting alkaline phosphatase activity (14.4%, P<0.01) and in reducing calcium uptake (11.4%, P<0.01). ADM(27-52) could partially antagonize the effects of ADM on regulating downwards osteopontin-mRNA expression (17.0%, P<0.01). It is concluded that ADM(27-52) derived from ADM acts as an inhibitory agent on vascular calcification, with special mechanisms different from ADM derived from ADM progenitor molecule. 相似文献
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The recently reported structural connectivity in F-actin between the DNase I binding loop on actin (residues 38-52) and the C-terminus region was investigated by fluorescence and proteolytic digestion methods. The binding of copper to Cys-374 on F- but not G-actin quenched the fluorescence of dansyl ethylenediamine (DED) attached to Gin-41 by more than 50%. The blocking of copper binding to DED-actin by N-ethylmaleimide labeling of Cys-374 on actin abolished the fluorescence quenching. The quenching of DED-actin fluorescence was restored in copolymers (1:9) of N-ethylmaleimide-DED-actin with unlabeled actin. The quenching of DED-actin fluorescence by copper was also abolished in copolymers (1:4) of DED-actin and N-ethylmaleimide-actin. These results show intermolecular coupling between loop 38-52 and the C-terminus in F-actin. Consistent with this, the rate of subtilisin cleavage of actin at loop 38-52 was increased by the bound copper by more than 10-fold in F-actin but not in G-actin. Neither acto-myosin subfragment-1 (S1) ATPase activity nor the tryptic digestion of G-actin and F-actin at the Lys-61 and Lys-69 sites were affected by the bound copper. These observations suggest that copper binding to Cys-374 does not induce extensive changes in actin structure and that the perturbation of loop 38-52 environment results from changes in the intermolecular contacts in F-actin. 相似文献
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肾上腺髓质素(13-52)降压机制的探讨 总被引:2,自引:0,他引:2
本工作在整体和离体大鼠模型上观察研究了肾上腺髓质素(13-52)[AdM(13-52)]的降压机制,发现AdM(13-52)的降压作用可被一氧化氮合酶(NOS)的竟争性桔抗剂L-NG-硝基-精氨酸(LNNA)部分抑制;AdM(13-52)的舒血管作用依赖于血管内皮并可被LNNA抑制,且具有剂量效应关系,LNNA的这种效应可被L-精氨酸(L-Arg)逆转;用亚甲蓝(MB)阻断血管内的环-磷酸鸟苷酸(cGMP),则导致AdM(13-52)的舒血管作用消失;放免测定显示LNNA可以降低血管内cGMP含量,而AdM(13-52)则使后者含量增加,这一现象在AdM(13-52)与LNNA合用时消失。实验结果提示,AdM(13-52)的舒血管降血压效应与NO有关,可能是通过NO介导的。 相似文献