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Distribution of cysteinyl leukotriene receptor 2 in human traumatic brain injury and brain tumors

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Acta Pharmacologica Sinica 2005年第6期26卷 685-690页

作者： Hua HU~(2,3), Gao CHEN~2, Jian-min ZHANG~2, Wei-ping ZHANG~3, Lei ZHANG~3, Qiu-fu GE~3, Hong-tian YAO~4, WeiDING~4, Zhong CHEN~3, Er-qing WEI~(3,5) ~2 department of Neurosurgery, the Second Affiliated Hospital, school of medicine, Zhejiang university, Hangzhou 310009 ~3 department of pharmacology school of medicine, Zhejiang university, Hangzhou 310031 ~4 department of Pathology, the First Affiliated Hospital, school of medicine, Zhejiang university, Hangzhou 310003, China department of Neurosurgery the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou China department of pharmacology School of Medicine Zhejiang University Hangzhou China department of Pathology the First Affiliated Hospital School of Medicine Zhejiang University Hangzhou China

Aim: To determine the distribution of cysteinyl leukotriene receptor 2 （CysLT2）, one of the cysteinyl leukotriene receptors, in human brains with traumatic injury and tumors. Methods: Brain specimens were obtained from patients who underwent brain surgery. CysLT2in brain tissues was examined using immunohis-tochemical analysis. Results: CysLT2was expressed in the smooth muscle cells （not in the endothelial cells） of arteries and veins. CysLT2was also expressed in the granulocytes in both vessels and in the brain parenchyma. In addition, CysLT2was detected in neuron- and glial-appearing cells in either the late stages of traumatic injury or in the area surrounding the tumors. Microvessels regenerated 8 d after trauma and CysLT2expression was recorded in their endothelial cells. Conclusion: CysLT2is distributed in vascular smooth muscle cells and granulocytes, and brain trauma and tumor can induce its expression in vascular endothelial cells and in a number of other cells.

关键词： cysteinyl leukotriene receptor 2 brain injuries brain neoplasms vascular smooth muscle cell

New Concepts in Tumor Antigens:Their Significance in Future Immunotherapies for Tumors

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Cellular & Molecular Immunology 2005年第5期2卷 331-341页

作者： Fan Yang~(1,2) Xiao-Feng Yang~(1,2,3) ~1department of pharmacology,Temple university school of medicine,Philadelphia,Pennsylvania 19140,usa ~2departments of medicine and Immunology,Baylor College of medicine,Houston,Texas 77030,usa department of pharmacology,Temple university school of medicine,3420 N.Broad Street,Philadelphia,Pennsylvania 19140, department of pharmacology Temple University School of Medicine Philadelphia Pennsylvania 19140 USA.

The identification and molecular characterization of self-antigens expressed by human malignancies that are capable of elicitation of anti-tumor immune responses in patients have been an active field in tumor immunology. More than 2,000 tumor antigens have been identified, and most of these antigens are self-antigens. These significant progresses have led to the renaissance of tumor immunology and studies on anti-tumor immunotherapy. However, despite of the progress in the identification of self-tumor antigens, current antigen-specific immunotherapies for tumors are far less satisfied than expected, which reflects the urgent need to improve our understanding on self-tumor antigens. In order to develop more effective antigen specific anti-tumor immunotherapies and to monitor the responses to these immunotherapies in patients with tumors, many important fundamental questions need to be addressed. We propose for the first time that the studies in addressing the characteristics of self-tumor antigens and autoantigens are grouped as a new subject termed ＂antigenology＂. In this brief review, we would outline the progress in the identification of tumor antigens in solid tumors and hematologic malignancies, and overview the new concepts and principles of antigenology and their significance for future immunotherapies to these malignancies.

关键词： tumor tumor antigen new concept anti-tumor immune response immunotherapy

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Axial Cone Beam Reconstruction with Asymptotic Trajectory Extrapolation Implemented by 3-D Weighting Scheme

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Tsinghua Science and Technology 2010年第1期15卷 114-119页

作者： TANG Xiangyang department of Radiology,emory university school of medicine,Atlanta 30322,usa Computed Tomography and Molecular Imaging,GE Healthcare,Waukesha 53188,usa department of Radiology Emory University School of Medicine Atlanta 30322 USA Computed Tomography and Molecular Imaging GE Healthcare Waukesha 53188 USA

Axial scan along circular trajectory has been the most desirable in clinical and preclinical applications. However, due to the violation of the data sufficiency condition, the reconstruction accuracy of axial scan deteriorates rapidly with increasing detector z-dimension. A number of algorithms have been proposed thus far to improve the reconstruction accuracy. It is well understood that, the larger the radius of circular trajectory the more accurate the reconstruction. Ultimately, the reconstruction becomes accurate if the trajectory radius reaches infinite. Inspired by such observations, an asymptotic weighting scheme is proposed here for axial scan at large cone angles to improve reconstruction accuracy. In practice, there may be other ways to im- plement the asymptotic 3-D weighting scheme, and we present one approach in this paper with preliminary results. Further investigation may enable this asymptotic weighting scheme to improve reconstruction accuracy significantly, enabling numerous applications in which axial scan at large z-dimension is desired.

关键词： computed tomography (CT) cone beam volumetric CT volumetric.CT image reconstruction tomography cone beam reconstruction axial scan

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Metallothionein mediates cardioprotection of isoliquiritigenin against ischemia-reperfusion through JAK2/STAT3 activation

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Acta Pharmacologica Sinica 2006年第11期27卷 1431-1437页

作者： Wei AN Jing YANG~1 Ying AO department of pharmacology,school of medicine,Wuhan university,Wuhan 430071,China department of pharmacology School of Medicine Wuhan University Wuhan China

Aim:To examine whether isoliquiritigenin(ISL)can attenuate myocardial ischemia-reperfusion(MI/R)injury in rats by inducing metallothionein(MT)through acti-vation of janus kinase 2(JAK 2)/signal transducers and activators of transcription3(STAT 3)***:The experimental model of MI/R in rats was gener-ated by 30 min of ischemia and reperfusion for 2 *** mRNA expression of MT,COX-2,and iNOS were measured by *** protein expressions of MT,JAK/STAT,extracellular signal-regulated kinase(ERK),and Akt were determinedby Western blotting in the absence or presence of a JAK kinase inhibitor,tyrphostinAG490(1.0 mg/kg,iv,1h before ischemia).Results:Pretreatment with ISL mark-edly decreased the severity of reperfusion-induced arrhythmias and myocardialinfarct *** the ISL 20 mg/kg group,the activities of lactate dehydrogenase(LDH)and creatinine phosphokinase(CPK)were reduced by 38.4% and 51.3%when compared with the vehicle *** JAK 2/STAT 3 phosphoryla-tion was accompanied by increased synthesis of MT but not of COX-2 or iNOS inISL-treated ***490 can significantly weaken ISL-induced cardioprotectionand prevent the increase of MT expression and JAK 2/STAT 3 ***:ISL protected MI/R injury through activation of JAK 2/STAT 3 sig-nal transduction pathway,which might be involved in mediating the upregulationof MT expression.

关键词： isoliquiritigenin myocardial ischemiareperfusion metallothionein janus kinase STAT3 transcription factors

ONO-1078 reduces NMDA-induced brain injury and vascular cell adhesion molecule-1 expression in rats

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Acta Pharmacologica Sinica 2005年第4期26卷 435-440页

作者： Li-hui ZHANG~(2,3) Er-qing WEI~(2,4) 2 department of pharmacology,school of medicine,Zhejiang university,Hangzhou 310031 3 Medical school,Hangzhou Normal university,Hangzhou 310018,China department of pharmacology School of Medicine Zhejiang University Hangzhou China Medical school Hangzhou Normal University Hangzhou China

Aim:To determine whether ONO-1078 （pranlukast）,a potent cysteinyl leukotrienereceptor 1 （CysLTI） antagonist,has an effect on N-methyl-D-aspartate （NMDA）-induced brain injury and vascular cell adhesion molecule-1 （VCAM-1） expres-sion in ***:Brain injury was induced by direct microinjection of NMDA（0.3 μmol in 1 μL of sterile 0.1 mol/L PBS,pH 7.4） into the cerebral *** volume （area）,brain edema and neuron density were assessed by an imageanalyzer and the expression of VCAM-1 in the cortex was detected by Westernblot 24 h after NMDA ***-1078 （0.03,0.1,or 0.3 mg/kg） andedaravone （MCI-186,10 mg/kg）,a neuroprotective agent,were ip injected 30rain before and after NMDA ***:NMDA microinjection producedwell-defined focal lesions （Figure 1） dose- and ***-1078（0.1,0.3 mg/kg） and edaravone （10 mg/kg） decreased the total lesion volume,lesion area and brain edema induced by ***,ONO-1078 （0.1,0.3mg/kg） significantly inhibited the enhanced expression of VCAM-1 in the injuredcortices,but edaravone did not have this ***:CysLT1receptorantagonist ONO-1078 at tenufftes NMDA-induced brain damage in rats,and thismight relate to the attenuation of NMDA receptor-dependent neurotoxicity andthe inhibition of the upregulation of VCAM-1 expression.

关键词： leukotriene antagonists pranlukast N-methylaspartate vascular cell adhesion molecule-1 neurotoxicity brain injuries

Signal transduction mediated by Bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways

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Cell Research 2000年第3期10卷 161-167页

作者： YIN XIAO-MING (department of Pathology, university of Pittsburgh school of medicine, 3550 Terrace Street, Pittsburgh, PA 15261, usa) department of Pathology University of Pittsburgh School of Medicine Pittsburgh USA

Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.

关键词： Apoptosis Bcl-2 family proteins Bid Fas TNF.

Quality Control System of the Endoplasmic Reticulum and Related Diseases

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Acta Biochimica et Biophysica Sinica 2006年第4期38卷 219-226页

作者： Jun-Chao WU Zhong-Qin LIANG Zheng-Hong QIN* department of pharmacology,school of medicine,Soochow university,Suzhou 215123,China department of pharmacology School of Medicine Soochow UniversitySuzhou 215123 China

The quality control (QC) system of the endoplasmic reticulum (ER) is an important monitoringmechanism in the protein maturation process,which ensures export of properly folded proteins from the *** or incompletely folded proteins are retained in the ER for refolding or degradation by the ER-residing *** calnexin/calreticulin cycle and ER-associated degradation are the key elements *** two mechanisms work together to allow incorrectly folded proteins have additional opportunitiesto achieve their native *** QC dysfunction is involved in many diseases caused by mutantproteins,many of which are causes of neurodegenerative disorders.A better understanding of molecularregulation in the QC system will uncover the molecular pathogenic mechanisms of many diseases caused byprotein misfolding and help discover novel strategies for preventing or treating these diseases.

关键词： protein folding quality control calnexin/calreticulin cycle endoplasmic reticulum-associated degradation protein misfolding disease

Growth suppression and radiosensitivity increase by HMGB1 in breast cancer

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Acta Pharmacologica Sinica 2007年第12期28卷 1957-1967页

作者： Yang JIAO~2,Hai-chao WANG~3,Sai-jun FAN~(2,4,5)~2 school of Radiology and Public Health,Soochow university,Suzhou 215123,China ~3 department of Emergency medicine,North Shoreuniversity Hospital,New York university school of medicine,Manhasset,New York 11030,usa ~4 department of Oncology,LombardiComprehensive Cancer Center,Georgetown university,Washington DC,Washington 20057,usa school of Radiology and Public Health Soochow University Suzhou China department of Emergency medicine North Shore University Hospital New York University School of Medicine Manhasset USA department of Oncology Lombardi Comprehensive Cancer Center Georgetown University Washington DC USA

Aim:HMGB 1 （high-mobility group box-1） is a nuclear protein containing a con-sensus RB （retinoblastoma）-binding LXCXE *** this study,we studied thepotential association of HMGB 1 and RB and the in vitro and in vivo activities ofHMGB 1 in human breast cancer ***:The protein-protein interactionwas determined by immunoprecipitation-Western blotting and glutathione-S-trans-ferase capture assays;cell growth and radiosensitivity were examined by cellcounts,MTT assay,and clonogenic assay;cell cycle progression and apoptosiswere evaluated using flow cytometry;and the antitumor activity of HMGB 1 wasexamined with tumor xenografts in nude ***:HMGB 1 was associatedwith RB via a LXCXE motif-dependent *** 1 enhanced the abilityof RB for E2F and cyclin A transcription *** increased expression ofHMGB 1 conferred an altered phenotypes characterized by the suppression of cellgrowth;G1arrest and apoptosis was induced in MCF-7 cells containing the wild-type retinoblastoma （Rb） gene,but showed no activities in BT-549 cells contain-ing the Rb gene *** HMGB 1-induced apoptosis accompanied by caspase3 activation and PARP (poly（ADP-ribose）polymerase) *** 1 elevatedthe radiosensitivity of breast cancer cells in both the MCF-7 and BT-549 cell *** enhanced expression of HMGB 1 caused a suppression of growth of MCF-7tumor xenografts in nude mice,while LXCXE-defective HMGB 1 completely lostantitumor growth ***:HMGB 1 functions as a tumor suppressorand radiosensitizer in breast cancer.A HMGB 1-RB interaction is critical for theHMGB 1-mediated transcriptional repression,cell growth inhibition,G1cell cyclearrest,apoptosis induction,and tumor growth suppression,but is not required ***,it may be possible to design new therapies for thetreatment of breast cancer that exert their effects by modulating the HMGB 1 andRB regulatory pathway and HMGB 1-related gene therapy.

关键词： HMGBI RB breast cancer cell growth

Emerging roles of deubiquitinating enzymes in human cancer

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Acta Pharmacologica Sinica 2007年第9期28卷 1325-1330页

作者： Jin-ming YANG department of pharmacology,The Cancer Institute of New Jersey,university of medicine and Dentistry of New Jersey/Robert Wood Johnson Medical school,New Brunswick,New Jersey 08903,usa department of pharmacology The Cancer Institute of New Jersey University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School New Brunswick USA

Protein modifications by the covalent linkage of ubiquitin have significant in-volvement in many cellular processes,including stress response,oncogenesis,viral infection,transcription,protein turnover,organelle biogenesis,DNA repair,cellular differentiation,and cell cycle *** ubiquitination and subse-quent degradation by the proteasome require the participation of bothubiquitinating enzymes and deubiquitinating *** deubiquitinatingenzymes constitute a large family in the ubiquitin system,the study of this class ofproteins is still in its infant *** studies have revealed a variety ofmolecular and biological functions of deubiquitinating enzymes and their associa-tion with human *** this review we will discuss the possible roles thatdeubiquitinating enzymes may play in cancers.

关键词： ubiquitin cancer deubiquitinating enzymes