期刊：
Chemical Society Reviews,2012年41(2):797-828 ISSN：1460-4744
通讯作者：
Wang, Guoping
作者机构：
[Wang, Guoping] Univ S China, Coll Chem Engn, Hengyang 421001, Peoples R China.;[Zhang, Jiujun; Zhang, Lei; Wang, Guoping] Natl Res Council Canada, Inst Fuel Cell Innovat, Vancouver, BC V6T 1W5, Canada.
通讯机构：
[Wang, Guoping] Univ S China, Coll Chem Engn, Hengyang 421001, Peoples R China.
摘要：
In this critical review, metal oxides-based materials for electrochemical supercapacitor (ES) electrodes are reviewed in detail together with a brief review of carbon materials and conducting polymers. Their advantages, disadvantages, and performance in ES electrodes are discussed through extensive analysis of the literature, and new trends in material development are also reviewed. Two important future research directions are indicated and summarized, based on results published in the literature: the development of composite and nanostructured ES materials to overcome the major challenge posed by the low energy density of ES (476 references).
摘要：
The adsorption of chromium (VI) ions from aqueous solution by ethylenediamine-modified cross-linked magnetic chitosan resin (EMCMCR) was studied in a batch adsorption system. Chromium (VI) removal is pH dependent and the optimum adsorption was observed at pH 2.0. The adsorption rate was extremely fast and the equilibrium was established within 6-10 min. The adsorption data could be well interpreted by the Langmuir and Temkin model. The maximum adsorption capacities obtained from the Langmuir model are 51.813 mg g(-1), 48.780 mg g(-1) and 45.872 mg g(-1) at 293, 303 and 313 K, respectively. The adsorption process could be described by pseudo-second-order kinetic model. The intraparticle diffusion study revealed that film diffusion might be involved in the present case. Thermodynamic parameters revealed the feasibility, spontaneity and exothermic nature of adsorption. The sorbents were successfully regenerated using 0.1 N NaOH solutions. (C) 2010 Elsevier B.V. All rights reserved.
作者：
Ablikim, M.*;Achasov, M. N.;Ai, X. C.;Albayrak, O.;Ambrose, D. J.;An, F. F.;An, Q.;Bai, J. Z.;Ferroli, R. Baldini;Ban, Y.;Becker, J.;Bennett, J. V.;Bertani, M.;Bian, J. M.;Boger, E.;Bondarenko, O.;Boyko, I.;Briere, R. A.;Bytev, V.;Cai, H.
作者机构：
[Yu, B. X.; Mao, Z. P.; Zhao, Q.; Lu, J. G.; Liu, Zhiqiang; Chen, Y. B.; He, M.; Hu, T.; Wang, Z.; Liu, Fang; Sun, Z. J.; Xue, Z.; Ning, Z.; Zhang, C. C.; Wen, S. P.; Sun, G. X.; Zhang, D. H.; Li, C. H.; Yuan, C. Z.; Zhao, H. S.; Min, J.; Zhang, H. Y.; Zhao, Ling; Chen, M. L.; Ai, X. C.; Ma, T.; Zhu, Z. A.; Sun, D. H.; Xu, G. F.; Wang, K.; Heng, Y. K.; Ji, Q.; Zhang, J. W.; Hou, Z. L.; Rong, G.; Li, Lei; Sun, Y. Z.; Liu, B. J.; Min, T. J.; Wang, Y. F.; Zhu, K. J.; Liu, H. M.; Li, Q. J.; Ma, H. L.; Wang, L. L.; Jin, D. P.; Xiu, Q. L.; Ye, M.; Xie, Y. G.; Sheng, H. Y.; Ouyang, Q.; Song, X. Y.; Ma, S.; Li, S. L.; Zou, B. S.; Chen, H. S.; Ji, X. B.; Zhang, J. Q.; Qian, S.; Wang, P.; Deng, Z. Y.; Ma, Q. M.; Dong, M. Y.; Zhu, C.; Fang, S. S.; Chang, J. F.; Wang, Z. Y.; Zhao, T. C.; Liu, Z. A.; Cai, X.; Lv, M.; Wu, N.; Zhang, Y. H.; Wang, Q. J.; An, F. F.; Ye, H.; Sun, S. S.; Fu, C. D.; Zhang, Y.; Lou, X. C.; Zou, J. H.; Wang, Z. G.; Jiang, L. L.; Zhang, B. X.; Zhang, X. J.; Lai, W.; Li, W. G.; Cao, G. F.; Mo, X. H.; Zhou, L.; Wu, L. H.; Fang, J.; Zhao, Y. B.; Gao, Q.; Huang, L.; Shen, X. Y.; Zheng, J. P.; Zhu, Y. S.; Li, X. N.; Zhang, B. Y.; Jiang, X. S.; Gu, M. H.; Lu, Y. P.; Dong, L. Y.; Ma, X. Y.; Hu, H. M.; Gong, W. X.; Dai, J. P.; Wang, P. L.; Zhao, G.; Zhu, S. H.; Yuan, Y.; Wu, Z.; Chu, Y. P.; Luo, X. L.; Ji, X. L.; Li, H. B.; Zhuang, J.; Li, J. C.; Liu, Zhiqing; Liao, X. T.; Zhang, S. H.; Huang, Y. P.; Li, F.; Zhang, J. Y.; Wang, L. S.; Jin, S.; Liu, H. W.; Tang, X.; Song, W. M.; Yang, H. X.; Qin, Z. H.; Li, G.; Zhang, J. Z.; He, K. L.; Liu, H.; Chen, G.; Ping, R. G.; Qiu, J. F.; Zhao, J. W.; Chen, J. C.; Ablikim, M.; Han, Y. L.; Liu, C. X.; Zhu, K.; Qin, X. S.; Dai, H. L.; Li, W. D.; Bai, J. Z.] Inst High Energy Phys, Beijing 100049, Peoples R China.;[Leyhe, M.; Wiedner, U.; Becker, J.; Pelizaeus, M.; Kopf, B.; Friedel, P.; Held, T.] Ruhr Univ Bochum, D-44780 Bochum, Germany.;[Briere, R. A.; Liu, C. L.; Albayrak, O.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.;[Yang, Y.; Xue, F.; Liu, Feng; Huang, G. M.; Zhang, Zhenghao] Cent China Normal Univ, Wuhan 430079, Peoples R China.;[Ye, M. H.] China Ctr Adv Sci & Technol, Beijing 100190, Peoples R China.
通讯机构：
[Ablikim, M.] Inst High Energy Phys, Beijing 100049, Peoples R China.
作者：
Ablikim, M.*;Achasov, M. N.;Albayrak, O.;Ambrose, D. J.;An, F. F.;An, Q.;Bai, J. Z.;Ferroli, R. Baldini;Ban, Y.;Becker, J.;Bennett, J. V.;Bertani, M.;Bian, J. M.;Boger, E.;Bondarenko, O.;Boyko, I.;Braun, S.;Briere, R. A.;Bytev, V.;Cai, H.
作者机构：
[Yu, B. X.; Mao, Z. P.; Zhao, Q.; Lu, J. G.; Liu, Zhiqiang; Chen, Y. B.; He, M.; Hu, T.; Wang, Z.; Liu, Fang; Sun, Z. J.; Xue, Z.; Ning, Z.; Zhang, C. C.; Wen, S. P.; Sun, G. X.; Zhang, D. H.; Li, C. H.; Min, J.; Zhang, H. Y.; Zhao, Ling; Chen, M. L.; Ma, T.; Yang, Y. Z.; Zhu, Z. A.; Xu, G. F.; Wang, K.; Heng, Y. K.; Ji, Q.; Zhang, J. W.; Hou, Z. L.; Rong, G.; Li, Lei; Sun, Y. Z.; Liu, B. J.; Min, T. J.; Wang, Y. F.; Zhu, K. J.; Liu, H. M.; Li, Q. J.; Ma, H. L.; Wang, L. L.; Jin, D. P.; Xiu, Q. L.; Ye, M.; Xie, Y. G.; Ouyang, Q.; Ma, S.; Zou, B. S.; Ji, X. B.; Calcaterra, A.; Zhang, J. Q.; Qian, S.; Wang, P.; Deng, Z. Y.; Ma, Q. M.; Dong, M. Y.; Fang, S. S.; Chang, J. F.; Wang, Z. Y.; Zhao, T. C.; Liu, Z. A.; Cai, X.; Lv, M.; Wu, N.; Zhang, Y. H.; Wang, Q. J.; An, F. F.; Ye, H.; Sun, S. S.; Fu, C. D.; Zhang, Y.; Lou, X. C.; Zou, J. H.; Wang, Z. G.; Jiang, L. L.; Zhang, B. X.; Zhang, X. J.; Lai, W.; Li, W. G.; Cao, G. F.; Mo, X. H.; Zhou, L.; Wu, L. H.; Fang, J.; Zhao, Y. B.; Huang, L.; Shen, X. Y.; Zheng, J. P.; Zhu, Y. S.; Li, X. N.; Zhang, B. Y.; Jiang, X. S.; Gu, M. H.; Lu, Y. P.; Dong, L. Y.; Ma, X. Y.; Hu, H. M.; Gong, W. X.; Dai, J. P.; Wang, P. L.; Zhao, G.; Wang, B.; Wu, Z.; Chu, Y. P.; Luo, X. L.; Ji, X. L.; Li, H. B.; Zhuang, J.; Li, J. C.; Liu, Zhiqing; Zhang, S. H.; Li, F.; Zhang, J. Y.; Wang, L. S.; Jin, S.; Tang, X.; Yang, H. X.; Qin, Z. H.; Li, G.; Zhang, J. Z.; Chen, G.; Ping, R. G.; Qiu, J. F.; Zhao, J. W.; Chen, J. C.; Ablikim, M.; Han, Y. L.; Liu, C. X.; Zhu, K.; Qin, X. S.; Dai, H. L.; Li, W. D.; Bai, J. Z.] Inst High Energy Phys, Beijing 100049, Peoples R China.;[Shen, C. P.] Beihang Univ, Beijing 100191, Peoples R China.;[Leyhe, M.; Wiedner, U.; Becker, J.; Pelizaeus, M.; Kopf, B.; Friedel, P.; Held, T.] Ruhr Univ Bochum, D-44780 Bochum, Germany.;[Briere, R. A.; Liu, C. L.; Albayrak, O.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.;[Yang, Y.; Liu, Feng; Huang, G. M.; Zhang, Zhenghao] Cent China Normal Univ, Wuhan 430079, Peoples R China.
通讯机构：
[Ablikim, M.] Inst High Energy Phys, Beijing 100049, Peoples R China.
作者机构：
[Tang, Chao-Ke; Yu, Xiao-Hua] Univ South China, Life Sci Res Ctr, Hengyang 421001, Hunan, Peoples R China.;[Tang, Chao-Ke; Yin, Kai] Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Res, Hengyang 421001, Hunan, Peoples R China.;[Fu, Yu-Chang] Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.;[Zhang, Da-Wei] Univ Alberta, Dept Pediat, Edmonton, AB T6G 2S2, Canada.;[Zhang, Da-Wei] Univ Alberta, Grp Mol & Cell Biol Lipids, Edmonton, AB T6G 2S2, Canada.
通讯机构：
[Yin, Kai] Univ South China, Key Lab Atherosclerol Hunan Prov, Inst Cardiovasc Res, Hengyang 421001, Hunan, Peoples R China.
关键词：
ABCA1;ABCG1;ACAT1;AGE;ATP-binding cassette transporter A1;ATP-binding cassette transporter G1;Atherosclerosis;CD36;CE;ERK1/2;FC;Foam cells;HDL;LDLR;LXR;MAPK;PI3K;PKB;PKC;PPAR response elements;PPAR-gamma;PPREs;RCT;RXR;SR-A;SR-BI;TGF-beta;acyl coenzyme A:cholesterol acyltransferase-1;advanced glycation end products;apoA-I;apoE;apolipoprotein A-I;apolipoprotein E;cholesterol ester;extracellular signal-regulated kinases 1 and 2;free cholesterol;high-density lipoprotein;liver X receptor;low-density lipoprotein receptor;mitogen-activated protein kinase;nCEH;neutral cholesteryl ester hydrolase;ox-LDL;oxidized low-density lipoprotein;peroxisome proliferator-activated receptor-gamma;phosphatidylinositol 3-kinase;protein kinase B;protein kinase C;retinoid X receptor;reverse cholesterol transport;scavenger receptor BI;scavenger receptor class A;transforming growth factor-beta
摘要：
Atherosclerosis is a chronic disease characterized by the deposition of excessive cholesterol in the arterial intima. Macrophage foam cells play a critical role in the occurrence and development of atherosclerosis. The generation of these cells is associated with imbalance of cholesterol influx, esterification and efflux. CD36 and scavenger receptor class A (SR-A) are mainly responsible for uptake of lipoprotein-derived cholesterol by macrophages. Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification. ATP-binding cassette transporters A1 (ABCA1), ABCG1 and scavenger receptor BI (SR-BI) play crucial roles in macrophage cholesterol export When inflow and esterification of cholesterol increase and/or its outflow decrease, the macrophages are ultimately transformed into lipid-laden foam cells, the prototypical cells in the atherosclerotic plague. The aim of this review is to describe what is known about the mechanisms of cholesterol uptake, esterification and release in macrophages. An increased understanding of the process of macrophage foam cell formation will help to develop novel therapeutic interventions for atherosclerosis. (c) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience,2012年32(9):3044-3057 ISSN：1529-2401
通讯作者：
Liu, Wenlan
作者机构：
[Liu, Jie; Jin, Xinchun; Liu, Ke J.; Liu, Wenlan] Univ New Mexico, Coll Pharm, Hlth Sci Ctr, Albuquerque, NM 87131 USA.;[Liu, Ke J.] Univ New Mexico, Dept Neurol, Hlth Sci Ctr, Albuquerque, NM 87131 USA.;[Liu, Jie] Univ South China, Sch Med, Dept Med Microbiol & Immunol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Liu, Wenlan] Univ New Mexico, Coll Pharm, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
摘要：
Blood-brain barrier (BBB) disruption occurs early enough to be within the thrombolytic time window, and this early ischemic BBB damage is closely associated with hemorrhagic transformation and thus emerging as a promising target for reducing the hemorrhagic complications of thrombolytic stroke therapy. However, the mechanisms underlying early ischemic BBB damage remain poorly understood. Here, we investigated the early molecular events of ischemic BBB damage using in vitro oxygen-glucose deprivation (OGD) and in vivo rat middle cerebral artery occlusion (MCAO) models. Exposure of bEND3 monolayer to OGD for 2 h significantly increased its permeability to FITC-labeled dextran and promoted the secretion of metalloproteinase-2 and -9 (MMP-2/9) and cytosolic translocation of caveolin-1 (Cav-1). This same OGD treatment also led to rapid degradation of tight junction protein occludin and dissociation of claudin-5 from the cytoskeleton, which contributed to OGD-induced endothelial barrier disruption. Using selective MMP-2/9 inhibitor SB-3CT (2-[[(4-phenoxyphenyl)sulfonyl]methyl]-thiirane) or their neutralizing antibodies or Cav-1 siRNA, we found that MMP-2 was the major enzyme mediating OGD-induced occludin degradation, while Cav-1 was responsible for claudin-5 redistribution. The interaction between Cav-1 and claudin-5 was further confirmed by coimmunoprecipitation. Consistent with these in vitro findings, we observed fluorescence tracer extravasation, increased gelatinolytic activity, and elevated interstitial MMP-2 levels in ischemic subcortical tissue after 2 h MCAO. Moreover, occludin protein loss and claudin-5 redistribution were detected in ischemic cerebromicrovessels. These data indicate that cerebral ischemia initiates two rapid parallel processes, MMP-2-mediated occludin degradation and Cav-1-mediated claudin-5 redistribution, to cause BBB disruption at early stroke stages relevant to acute thrombolysis.
作者：
Ablikim, M.*;Achasov, M. N.;Albayrak, O.;Ambrose, D. J.;An, F. F.;An, Q.;Bai, J. Z.;Ferroli, R. Baldini;Ban, Y.;Becker, J.;Bennett, J. V.;Bertani, M.;Bian, J. M.;Boger, E.;Bondarenko, O.;Boyko, I.;Braun, S.;Briere, R. A.;Bytev, V.;Cai, H.
作者机构：
[Yu, B. X.; Mao, Z. P.; Zhao, Q.; Lu, J. G.; Liu, Zhiqiang; Chen, Y. B.; He, M.; Hu, T.; Wang, Z.; Liu, Fang; Sun, Z. J.; Xue, Z.; Ning, Z.; Zhang, C. C.; Wen, S. P.; Sun, G. X.; Zhang, D. H.; Li, C. H.; Yuan, C. Z.; Min, J.; Zhang, H. Y.; Zhao, Ling; Chen, M. L.; Ma, T.; Zhu, Z. A.; Xu, G. F.; Wang, K.; Heng, Y. K.; Ji, Q.; Zhang, J. W.; Hou, Z. L.; Rong, G.; Li, Lei; Sun, Y. Z.; Liu, B. J.; Min, T. J.; Wang, Y. F.; Zhu, K. J.; Liu, H. M.; Li, Q. J.; Ma, H. L.; Wang, L. L.; Jin, D. P.; Xiu, Q. L.; Ye, M.; Xie, Y. G.; Sheng, H. Y.; Ouyang, Q.; Song, X. Y.; Ma, S.; Zou, B. S.; Chen, H. S.; Ji, X. B.; Zhang, J. Q.; Qian, S.; Wang, P.; Deng, Z. Y.; Ma, Q. M.; Dong, M. Y.; Fang, S. S.; Chang, J. F.; Wang, Z. Y.; Zhao, T. C.; Liu, Z. A.; Cai, X.; Lv, M.; Wu, N.; Zhang, Y. H.; Wang, Q. J.; An, F. F.; Ye, H.; Sun, S. S.; Fu, C. D.; Zhang, Y.; Lou, X. C.; Zou, J. H.; Wang, Z. G.; Zhang, J. L.; Jiang, L. L.; Zhang, B. X.; Zhang, X. J.; Lai, W.; Li, W. G.; Cao, G. F.; Mo, X. H.; Zhou, L.; Wu, L. H.; Fang, J.; Zhao, Y. B.; Huang, L.; Shen, X. Y.; Zheng, J. P.; Zhu, Y. S.; Li, X. N.; Zhang, B. Y.; Jiang, X. S.; Gu, M. H.; Lu, Y. P.; Dong, L. Y.; Ma, X. Y.; Hu, H. M.; Li, K.; Gong, W. X.; Dai, J. P.; Wang, P. L.; Zhao, G.; Wang, B.; Yuan, Y.; Wu, Z.; Chu, Y. P.; Luo, X. L.; Ji, X. L.; Li, H. B.; Zhuang, J.; Li, J. C.; Liu, Zhiqing; Zhang, S. H.; Li, F.; Zhang, J. Y.; Wang, L. S.; Jin, S.; Tang, X.; Song, W. M.; Yang, H. X.; Qin, Z. H.; Li, G.; Zhang, J. Z.; He, K. L.; Chen, G.; Ping, R. G.; Qiu, J. F.; Zhao, J. W.; Chen, J. C.; Ablikim, M.; Han, Y. L.; Liu, C. X.; Zhu, K.; Qin, X. S.; Dai, H. L.; Li, W. D.; Bai, J. Z.] Inst High Energy Phys, Beijing 100049, Peoples R China.;[Shen, C. P.] Beihang Univ, Beijing 100191, Peoples R China.;[Leyhe, M.; Wiedner, U.; Becker, J.; Pelizaeus, M.; Kopf, B.; Friedel, P.; Held, T.] Ruhr Univ Bochum, D-44780 Bochum, Germany.;[Briere, R. A.; Liu, C. L.; Albayrak, O.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.;[Yang, Y.; Liu, Feng; Huang, G. M.; Zhang, Zhenghao] Cent China Normal Univ, Wuhan 430079, Peoples R China.
通讯机构：
[Ablikim, M.] Inst High Energy Phys, Beijing 100049, Peoples R China.
摘要：
We report on a study of the process e(+)e(-) -> pi(+/-) (D (D) over bar*)(-/+) at root s = 4.26 GeV using a 525 pb(-1) data sample collected with the BESIII detector at the BEPCII storage ring. A distinct charged structure is observed in the (D (D) over bar*)(-/+) invariant mass distribution. When fitted to a mass- dependent- width Breit- Wigner line shape, the pole mass and width are determined to be M-pole (3883: 9 +/- 1.5 (stat) +/- 4.2 dsyst__ MeV= c(2) and Gamma(pole) = (24: 8 +/- 3.3 (stat) +/- 11: 0 (syst)) MeV. The mass and width of the structure, which we refer to as Z(c)(3885), are 2 sigma and 1 sigma, respectively, below those of the Z(c)(3900) -> pi(+/-) J/psi peak observed by BESIII and Belle in pi(+)pi(-) J/psi final states produced at the same center- of- mass energy. The angular distribution of the pi Z(c)(3885) system favors a J(P) = J(P) = 1(+) quantum number assignment for the structure and disfavors 1(-) or 0(-). The Born cross section times the (D (D) over bar*) branching fraction of the Z(c)(3885) is measured to be sigma(e(+)e(-) -> pi(+/-)Z(c)(3885)(-/+)) x B(Z(c)(3885)-/+ -> (D (D) over bar*)(-/+) = (83.5 +/- 6.6 (stat) +/- 22.0 (syst)) pb. Assuming the Z(c)(3885) -> (D (D) over bar*)(-/+) signal reported here and the Z(c)(3900) -> pi J/psi signal are from the same source, the partial width ratio (Gamma(Z(c)(3885) -> D (D) over bar*)/Gamma(Z(c)(3900) -> pi J/psi)) = 6.2 +/- 1.1 (stat) +/- 2.7 (syst) is determined.
作者：
Ablikim, M.*;Achasov, M. N.;Albayrak, O.;Ambrose, D. J.;An, F. F.;An, Q.;Bai, J. Z.;Ferroli, R. Baldini;Ban, Y.;Becker, J.;Bennett, J. V.;Bertani, M.;Bian, J. M.;Boger, E.;Bondarenko, O.;Boyko, I.;Braun, S.;Briere, R. A.;Bytev, V.;Cai, H.
作者机构：
[Yu, B. X.; Mao, Z. P.; Zhao, Q.; Lu, J. G.; Liu, Zhiqiang; Chen, Y. B.; He, M.; Hu, T.; Wang, Z.; Liu, Fang; Sun, Z. J.; Xue, Z.; Ning, Z.; Zhang, C. C.; Wen, S. P.; Sun, G. X.; Zhang, D. H.; Li, C. H.; Yuan, C. Z.; Zhao, H. S.; Min, J.; Zhang, H. Y.; Zhao, Ling; Chen, M. L.; Ma, T.; Zhu, Z. A.; Sun, D. H.; Xu, G. F.; Wang, K.; Heng, Y. K.; Ji, Q.; Zhang, J. W.; Hou, Z. L.; Rong, G.; Li, Lei; Sun, Y. Z.; Liu, B. J.; Min, T. J.; Wang, Y. F.; Zhu, K. J.; Liu, H. M.; Li, Q. J.; Ma, H. L.; Wang, L. L.; Jin, D. P.; Xiu, Q. L.; Ye, M.; Xie, Y. G.; Sheng, H. Y.; Ouyang, Q.; Song, X. Y.; Ma, S.; Zou, B. S.; Chen, H. S.; Ji, X. B.; Zhang, J. Q.; Qian, S.; Wang, P.; Deng, Z. Y.; Ma, Q. M.; Dong, M. Y.; Zhu, C.; Fang, S. S.; Chang, J. F.; Wang, Z. Y.; Zhao, T. C.; Liu, Z. A.; Cai, X.; Lv, M.; Wu, N.; Zhang, Y. H.; Wang, Q. J.; An, F. F.; Ye, H.; Sun, S. S.; Fu, C. D.; Zhang, Y.; Lou, X. C.; Zou, J. H.; Wang, Z. G.; Jiang, L. L.; Zhang, B. X.; Zhang, X. J.; Lai, W.; Li, W. G.; Cao, G. F.; Mo, X. H.; Zhou, L.; Wu, L. H.; Fang, J.; Zhao, Y. B.; Huang, L.; Shen, X. Y.; Zheng, J. P.; Zhu, Y. S.; Li, X. N.; Zhang, B. Y.; Jiang, X. S.; Gu, M. H.; Lu, Y. P.; Dong, L. Y.; Ma, X. Y.; Hu, H. M.; Gong, W. X.; Dai, J. P.; Wang, P. L.; Zhao, G.; Zhu, S. H.; Wang, B.; Yuan, Y.; Wu, Z.; Chu, Y. P.; Luo, X. L.; Ji, X. L.; Li, H. B.; Zhuang, J.; Li, J. C.; Zhang, L.; Liu, Zhiqing; Liao, X. T.; Zhang, S. H.; Li, F.; Zhang, J. Y.; Wang, L. S.; Jin, S.; Liu, H. W.; Tang, X.; Song, W. M.; Yang, H. X.; Qin, Z. H.; Li, G.; Zhang, J. Z.; He, K. L.; Liu, H.; Chen, G.; Ping, R. G.; Qiu, J. F.; Zhao, J. W.; Chen, J. C.; Ablikim, M.; Han, Y. L.; Liu, C. X.; Zhu, K.; Qin, X. S.; Dai, H. L.; Li, W. D.; Bai, J. Z.] Inst High Energy Phys, Beijing 100049, Peoples R China.;[Shen, C. P.] Beihang Univ, Beijing 100191, Peoples R China.;[Leyhe, M.; Wiedner, U.; Becker, J.; Pelizaeus, M.; Kopf, B.; Friedel, P.; Held, T.] Ruhr Univ Bochum, D-44780 Bochum, Germany.;[Spataro, S.; Briere, R. A.; Liu, C. L.; Albayrak, O.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.;[Yang, Y.; Zhang, Z. H.; Liu, Feng; Huang, G. M.] Cent China Normal Univ, Wuhan 430079, Peoples R China.
通讯机构：
[Ablikim, M.] Inst High Energy Phys, Beijing 100049, Peoples R China.
作者：
Liu, L.;Yang, M.;Kang, R.;Wang, Z.;Zhao, Y.;Yu, Y.;Xie, M.;Yin, X.;Livesey, K. M.;Lotze, M. T.;Tang, D.;Cao, L.*
期刊：
Leukemia,2011年25(1):23-31 ISSN：0887-6924
通讯作者：
Cao, L.
作者机构：
[Yu, Y.; Liu, L.; Kang, R.; Yang, M.; Wang, Z.; Zhao, Y.; Xie, M.; Cao, L.] Cent S Univ, Dept Pediat, Xiangya Hosp, Changsha 410008, Hunan, Peoples R China.;[Yin, X.] Nanhua Univ, Affiliated Hosp 1, Dept Pediat, Hengyang, Hunan, Peoples R China.;[Tang, D.; Lotze, M. T.; Livesey, K. M.] Univ Pittsburgh, Dept Surg, Hillman Canc Ctr, Inst Canc, Pittsburgh, PA USA.;[Cao, L.] Cent S Univ, Dept Pediat, Xiangya Hosp, 110 Xiangya Rd Changsha, Changsha 410008, Hunan, Peoples R China.
通讯机构：
[Cao, L.] Cent S Univ, Dept Pediat, Xiangya Hosp, 110 Xiangya Rd Changsha, Changsha 410008, Hunan, Peoples R China.
关键词：
HMGB1;autophagy;PI3K;ERK;drug resistance
摘要：
Autophagy, a tightly regulated lysosome-dependent catabolic pathway, is important in the regulation of cancer development and progression and in determining the response of tumor cells to anticancer therapy. However, the role of autophagy in leukemia still remains largely unknown. Here we show that high-mobility group box 1 (HMGB1), the best characterized damage-associated molecular pattern, was released from leukemia cell lines after chemotherapy-induced cytotoxicity and activated autophagy to protect against injury. Treatment with HMGB1-neutralizing antibodies increased the sensitivity of leukemia cells to chemotherapy; whereas, exogenous HMGB1 rendered these cells more resistant to drug-induced cytotoxicity. Moreover, exogenous HMGB1 increased autophagy as evaluated by increased expression of the autophagic marker microtubule-associated protein light chain 3-II, degradation of sequestosome 1 (p62) and autophagosome formation. Furthermore, knockdown or pharmacological inhibition of either phosphoinositide 3-kinase-III or extracellular signal-regulated kinase kinase mitogen-activated protein kinase kinase/extracellular signal-regulated protein kinase inhibited HMGB1-induced autophagy. Taken together, these results suggest that HMGB1 release after chemotherapy is a critical regulator of autophagy and a potential drug target for therapeutic interventions in leukemia.
期刊：
Journal of Cellular Biochemistry,2011年112(9):2508-2517 ISSN：1097-4644
通讯作者：
Xiao, Zhi-Qiang
作者机构：
[Wan, Xun-Xun; Qu, Jia-Quan; Zhu, Wei; Yi, Hong; He, Qiu-Yan; Zuo, Jian-Hong; Li, Mao-Yu; Xiao, Zhi-Qiang; Li, Xin-Hui; Zeng, Gu-Qing; Li, Jian-Huang; Chen, Yu] Cent S Univ, Xiangya Hosp, Key Lab Canc Prote, Chinese Minist Hlth, Changsha 410008, Hunan, Peoples R China.;[Zuo, Jian-Hong] Univ S China, Dept Microbiol & Immunol, Sch Med, Hengyang 421001, Peoples R China.;[Zhu, Wei] Univ S China, Affiliated Hosp 1, Dept Oncol, Hengyang 421001, Peoples R China.;[Xiao, Zhi-Qiang] Cent S Univ, Xiangya Hosp, Key Lab Canc Prote, Chinese Minist Hlth, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
通讯机构：
[Xiao, Zhi-Qiang] Cent S Univ, Xiangya Hosp, Key Lab Canc Prote, Chinese Minist Hlth, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China.
关键词：
EGFR;HNSCC;INVASION;MMP-9;E-CADHERIN
摘要：
EGFR is a potent stimulator of invasion and metastasis in head and neck squamous cell carcinomas (HNSCC). However, the mechanism by which EGFR may stimulate tumor cell invasion and metastasis still need to be elucidated. In this study, we showed that activation of EGFR by EGF in HNSCC cell line SCC10A enhanced cell migration and invasion, and induced loss of epitheloid phenotype in parallel with downregulation of E-cadherin and upregulation of N-cadherin and vimentin, indicating that EGFR promoted SCC10A cell migration and invasion possibly by an epithelial to mesenchymal transition (EMT)-like phenotype change. Interestingly, activation of EGFR by EGF induced production of matrix metalloproteinase-9 (MMP-9) and soluble E-cadherin (sE-cad), and knockdown of MMP-9 by siRNA inhibited sE-cad production induced by EGF in SCC10A. Moreover, both MMP-9 knockdown and E-cadherin overexpression inhibited cell migration and invasion induced by EGF in SCC10A. The results indicate that EGFR activation promoted cell migration and invasion through inducing MMP-9-mediated degradation of E-cadherin into sE-cad. Pharmacologic inhibition of EGFR, MEK, and PI3K kinase activity in SCC10A reduced phosphorylated levels of ERK-1/2 and AKT, production of MMP-9 and sE-cad, cell migration and invasion, and expressional changes of EMT markers (E-cadherin and N-cadherin) induced by EGF, indicating that EGFR activation promotes cell migration and invasion via ERK1/2 and PI3K-regulated MMP-9/E-cadherin signaling pathways. Taken together, the data suggest that EGFR activation promotes HNSCC SCC10A cell migration and invasion by inducing EMT-like phenotype change and MMP-9-mediated degradation of E-cadherin into sE-cad related to activation of ERK-1/2 and PI3K signaling pathways. J. Cell. Biochem. 112: 2508-2517, 2011. (C) 2011 Wiley-Liss, Inc.
期刊：
Clinical Cancer Research,2013年19(20):5602-5612 ISSN：1078-0432
通讯作者：
Xie, Xiaoming
作者机构：
[Tang, Hailin; Xie, Xinhua; Xie, Xiaoming; Kong, Yanan; Guo, Jiaoli; Ye, Feng] Sun Yat Sen Univ, Dept Breast Oncol, Ctr Canc, Guangzhou 510060, Guangdong, Peoples R China.;[Tang, Hailin; Xie, Xinhua; Xie, Xiaoming; Kong, Yanan; Guo, Jiaoli; Ye, Feng] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China.;[Deng, Min] Guangzhou Med Univ, Canc Hosp, Guangzhou, Guangdong, Peoples R China.;[Deng, Min] Guangzhou Med Univ, Canc Res Inst, Guangzhou, Guangdong, Peoples R China.;[Tang, Hailin; Tang, Yunyun; Deng, Min; Su, Qi] Univ South China, Canc Res Inst, Hengyang, Hunan, Peoples R China.
通讯机构：
[Xie, Xiaoming] Sun Yat Sen Univ, Dept Breast Oncol, State Key Lab Oncol South China, Ctr Canc, 651 East Dongfeng Rd, Guangzhou 510060, Guangdong, Peoples R China.
摘要：
AIM:To compare the effects of four Bifidobacteria strains(Bifidobacteria L66-5,L75-4,M13-4 and FS31-12,originated from normal human intestines) on weight gain,lipid metabolism,glucose metabolism in an obese murine model induced by high-fat diet.METHODS:Forty-eight Sprague-Dawley rats were randomly divided into six groups.Control group received standard chow,model group received high-fat diet,and intervention groups received high-fat diet added with different Bifidobacteria strains isolated from healthy volunteers’ fresh feces.All rats were executed at the 6th weekend.Body weight(BW),obese indexes,oral glucose tolerance test,serum and liver lipid and serum insulin(INS) were tested.Liver lipid deposition was classif ied pathologically.RESULTS:Compared with the model group,B.M13-4 improved BW gains(264.27 ± 26.91 vs 212.55 ± 18.54,P = 0.001) while B.L66-5 induced a decrease in BW(188.47 ± 11.96 vs 212.55 ± 18.54,P = 0.043).The rest two strains had no significant change in BW.All the four strains can reduce serum and liver triglyceride and significantly alleviate the lipid deposition in liver.All strains showed a trend of lowing serum and liver total cholesterol while B.L66-5 and B.FS31-12 did so more significantly.In addition,all the four strains showed no significant differences in serum INS and glucose level.CONCLUSION:The response of energy metabolism to administration of Bifidobacteria is strain dependent.Different strains of Bifidobacteria might drive different directions of fat distribution.
通讯机构：
[Xiao, Xianzhong] Cent S Univ, Xiangya Sch Med, Dept Pathophysiol, 110 Xiangya Rd, Changsha 410078, Hunan, Peoples R China.
关键词：
Apoptosis;Doxorubicin;Resveratrol;SIRT1;p53
摘要：
Aims Doxorubicin (DOX) is an anthracycline drug with a wide spectrum of clinical antineoplastic activity, but increased apoptosis has been implicated in its cardiotoxicity. Resveratrol (RES) was shown to harbour major health benefits in diseases associated with oxidative stress. In this study, we aimed to determine the effect of RES on DOX-induced myocardial apoptosis in mice. Methods and results Male Balb/c mice were randomized to one of the following four treatments: saline, RES, DOX, or RES plus DOX (10 mice in each group). DOX treatment markedly depressed cardiac function, decreased the heart weight, the body weight, and the ratio of heart weight to body weight, but inversely increased the level of protein carbonyl, malondialdehyde, and serum lactate dehydrogenase, and induced mitochondrial cytochrome c release and cardiomyocyte apoptosis. However, these effects of DOX were ameliorated by its combination with RES. Further studies with a co-immunoprecipitation assay revealed an interaction between p53 and Sirtuin 1 (SIRT1). It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects. Conclusion The protective effect of RES against DOX-induced cardiomyocyte apoptosis is associated with the up-regulation of SIRT1-mediated p53 deacetylation.
摘要：
Osteosarcoma (OS) is the most common nonhematologic bone malignancy in children and adolescents. Despite the advances of adjuvant chemotherapy and significant improvement of survival, the prognosis remains generally poor. As such, the search for more effective anti-OS agents is urgent. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is thought to be one of the most important oncogenic pathways in human cancer. An increasing body of evidence has shown that this pathway is frequently hyperactivated in OS and contributes to disease initiation and development, including tumorigenesis, proliferation, invasion, cell cycle progression, inhibition of apoptosis, angiogenesis, metastasis and chemoresistance. Inhibition of this pathway through small molecule compounds represents an attractive potential therapeutic approach for OS. The aim of this review is to summarize the roles of the PI3K/Akt pathway in the development and progression of OS, and to highlight the therapeutic potential of targeting this signaling pathway. Knowledge obtained from the application of these compounds will help in further understanding the pathogenesis of OS and designing subsequent treatment strategies. (C) 2015 Elsevier B.V. All rights reserved.
