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2. List of Contributors

Author

Abbatemarco, J.A., primary, Adams, R.J., additional, Adkins, D.L., additional, Akamatsu, Y., additional, Akyol, O., additional, Alexandrov, A.V., additional, Alim, I., additional, Alkhachroum, A.M., additional, Amin-Hanjani, S., additional, Andjelkovic, A.V., additional, Anrather, J., additional, Applegate, R., additional, Arai, K., additional, Ayata, C., additional, Aziz-Sultan, M.A., additional, Ballesteros, I., additional, Bar, B., additional, Barone, F.C., additional, Barrow, D.L., additional, Başkaya, M.K., additional, Bateman, K., additional, Bazan, N.G., additional, Beecher, J.S., additional, Beer-Furlan, A., additional, Belayev, L., additional, Bhattacharya, P., additional, Bhole, R., additional, Biller, J., additional, Biousse, V., additional, Borlongan, C.V., additional, Bouts, M.J.R.J., additional, Brey, R.L., additional, Bronstein, R., additional, Bryer, A., additional, Bulsara, K.R., additional, Can, A., additional, Canhão, P., additional, Caplan, L.R., additional, Carmichael, S.T., additional, Carrau, R., additional, Castaldo, J., additional, Catanese, L., additional, Chabriat, H., additional, Chaturvedi, S., additional, Chaudhary, N., additional, Chen, Jieli, additional, Chen, S., additional, Chen, Jun, additional, Choi, D.W., additional, Choi, B., additional, Chopp, M., additional, Chung, D.Y., additional, Chung, C.-P., additional, Cipolla, M.J., additional, Colbourne, F., additional, Colburn, Q., additional, Cord, B.J., additional, Coull, B.M., additional, Cuartero, M.I., additional, Cummings, J.L., additional, Dafer, R.M., additional, Dalkara, T., additional, Daou, B., additional, Dave, K.R., additional, Davis, T.P., additional, De Georgia, M., additional, De Silva, T.M., additional, Dharap, A., additional, Di Tullio, M.R., additional, Dietrich, W.D., additional, Dijkhuizen, R.M., additional, Dobkin, B.H., additional, Du, R., additional, Ducruet, A.F., additional, Duncan, K.R., additional, Edvinsson, L., additional, Edwards, M.J., additional, Egemen, E., additional, El-Hunjul, M., additional, Emanuele, M., additional, Emanuele, N., additional, Erdman, M.K., additional, Ergul, A., additional, Fagan, S.C., additional, Faraci, F.M., additional, Federau, C., additional, Ferro, J.M., additional, Fisher, M., additional, Flemming, K.D., additional, Foerch, C., additional, Freitas, R.S., additional, Friedlander, R.M., additional, Gaberel, T., additional, Gakuba, C., additional, Giffard, R.G., additional, Goldberg, M.P., additional, González, R.G., additional, Gopinath, S., additional, Gorelick, P.B., additional, Goshgarian, C., additional, Greenberg, D.A., additional, Griessenauer, C.J., additional, Groshans, K.A., additional, Gupta, R., additional, Hachem, R.A., additional, Hage, Z.A., additional, Hall, E.D., additional, Hamel, E., additional, Hao, Q., additional, Haqqani, A.S., additional, Hariman, R., additional, Hasan, D., additional, Haussen, D.C., additional, He, L., additional, Heiferman, D.M., additional, Herndon, J.M., additional, Ho, W.M., additional, Hoffmann, S., additional, Howard, B.M., additional, Hu, B.R., additional, Huber, J.D., additional, Huisa, B., additional, Hurn, P.D., additional, Iliff, J.J., additional, Jabbour, P., additional, Jamshidi, A.O., additional, Jankowitz, B., additional, Jickling, G.C., additional, Johansen, M., additional, Jovin, T.G., additional, Karuppagounder, S.S., additional, Kasper, E.M., additional, Keep, R.F., additional, Kim, H.-H., additional, Kim, D.E., additional, Kim, J.S., additional, Kim, J.Y., additional, Klahr, A.C., additional, Koch, M.J., additional, Kole, M., additional, Koleilat, S.M., additional, Kozan, A., additional, Kuroda, S., additional, Lamy, C., additional, Lanzino, G., additional, Larsen, A.G., additional, Laviv, Y., additional, Lawton, M.T., additional, Leary, M.C., additional, Leira, E.C., additional, Li, L., additional, Li, Q., additional, Liebeskind, D.S., additional, Lin, L., additional, Lioutas, V.A., additional, Lippert, T., additional, Liu, R., additional, Liu, J., additional, Liu, C.L., additional, Lizasoain, I., additional, Lo, E.H., additional, Loftus, C.M., additional, Logsdon, A.F., additional, Lucke-Wold, B.P., additional, Madhavan, S., additional, Madhugiri, V., additional, Malhotra, K., additional, Manning, W.J., additional, Marcell, S.J., additional, Mas, J.-L., additional, Masamoto, K., additional, Matute, C., additional, McCullough, L.D., additional, McDowell, M.M., additional, Mehdiratta, M., additional, Mehta, D., additional, Meisel, A., additional, Messegee, J., additional, Miller, B., additional, Mirza, S., additional, Modak, J.M., additional, Moro, M.A., additional, Nagel, M.A., additional, Namura, S., additional, Nedergaard, M., additional, Newell, D.W., additional, Newman, N.J., additional, Ng, K.L., additional, Nguyen, D., additional, Nguyen, H., additional, Nielsen, G., additional, Nishijima, Y., additional, Nishimura, N., additional, Nogueira, R.G., additional, Ogilvy, C.S., additional, Orbach, D.B., additional, Ostendorf, A.P., additional, Otto, B., additional, Ozpinar, A., additional, Panczykowski, D.M., additional, Patel, A.B., additional, Perez, Y., additional, Perez-Pinzon, M.A., additional, Potey, C., additional, Pradillo, J.M., additional, Prevedello, D.M., additional, Rajamani, K., additional, Rangel-Castilla, L., additional, Rao, N.M., additional, Ratan, R.R., additional, Raval, A.P., additional, Reddy, G.D., additional, Reis, C., additional, Roach, E.S., additional, Ronaldson, P.T., additional, Rosen, C.L., additional, Rosenberg, G.A., additional, Rutledge, W.C., additional, Sabzwari, R., additional, Salzano, G., additional, Santucci, P.A., additional, Saver, J.L., additional, Schallert, T., additional, Schermerhorn, M.L., additional, Schneck, M.J., additional, See, A.P., additional, Shakir, H.J., additional, Sharp, F.R., additional, Shuja, F., additional, Siddiqui, A.H., additional, Silva, M.A., additional, Singhal, A.B., additional, Sivakumar, K., additional, Slade, D.H., additional, Smith, E.R., additional, Sohrabji, F., additional, Solaroglu, I., additional, Sriraman, S.K., additional, Stamova, B., additional, Stanimirovic, D.B., additional, Stapleton, C.J., additional, Stary, C.M., additional, Steinberg, G.K., additional, Stephen, C., additional, Stetler, R.A., additional, Stone, J., additional, Sumbria, R., additional, Sweis, R., additional, Tahir, R., additional, Tarawneh, R., additional, Tarsia, J., additional, Tehrani, R., additional, Teo, M.K., additional, Testai, F.D., additional, Thrane, A.S., additional, Tobin, M.K., additional, Tome, M.E., additional, Topcuoglu, M.A., additional, Topel, C.H., additional, Torchilin, V., additional, Traystman, R.J., additional, Tsirka, S.E., additional, Turan, Y., additional, Tymianski, M., additional, van Leyen, K., additional, Varade, P., additional, Veluz, J.S., additional, Vemuganti, R., additional, Venkat, P., additional, Vexler, Z.S., additional, Vial, C.M., additional, Vinters, H.V., additional, Vosko, M.R., additional, Waeber, C., additional, Walcott, B.P., additional, Wang, J., additional, Wang, X., additional, Wang, Y.T., additional, Wei, Z.Z., additional, Wei, L., additional, Welch, B.G., additional, Winn, H.R., additional, Wintermark, M., additional, Wityk, R.J., additional, Wu, O., additional, Wu, K.C., additional, Xi, G., additional, Yacoub, H.A., additional, Yakhkind, A., additional, Yamamoto, Y., additional, Yang, S.-H., additional, Yenari, M., additional, Yigitkanli, K., additional, Yonas, H., additional, Yu, Z., additional, Zettervall, S.L., additional, Zhang, J., additional, Zhang, W., additional, and Zhao, H., additional

Published
2017
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40. Erythropoietin: not just about erythropoiesis

Author

Ghezzi, P., Bernaudin, M., Bernaudinb, M., Bianchi, R., Bianchic, R., Blomgren, K., Brines, M., Campana, W., Cavaletti, G., Cerami, A., Chopp, M., Coleman, T., Digicaylioglu, M., Ehrenreich, H., Erbayraktar, S., Erbayraktar, Z., Gassmann, M., Genc, S., Gokmen, N., Grasso, G., Juul, S., Lipton, S. A., Hand, C. C., Latini, R., Lauria, G., Leist, M., Newton, S. S., Petit, E., Probert, L., Sfacteria, Alessandra, Siren, A., Talan, M., Thiemermann, C., Westenbrink, D., Yaqoob, M., Zhu, C., University of Zurich, Ghezzi, P, Bernaudinb, M, Bianchic, R, Blomgren, K, Brines, M, Campana, W, Cavaletti, G, Cerami, A, Chopp, M, Coleman, T, Digicaylioglu, M, Ehrenreich, H, Erbayraktar, S, Erbayraktar, Z, Gassmann, M, Genc, S, Gokmen, N, Grasso, G, Juul, S, Lipton, S, Hand, C, Latini, R, Lauria, G, Leist, M, Newton, S, Petit, E, Probert, L, Sfacteria, A, Siren, A, Talan, M, Thiemermann, C, Westenbrink, D, Yaqoob, M, and Zhu, C

Subjects
erythropoyetin, Receptors, Cell Surface, 2700 General Medicine, Bioinformatics, Erythropoiesis, Erythropoietin, Humans, Neoplasms, Neuroprotective Agents, Receptors, Cell Surface, Article, 03 medical and health sciences, 0302 clinical medicine, Receptors, Erythropoietin, medicine, Brain function, 030304 developmental biology, 0303 health sciences, business.industry, General Medicine, 10081 Institute of Veterinary Physiology, 3. Good health, Original data, Erythropoietin receptor, Clinical trial, Action (philosophy), Immunology, 570 Life sciences, biology, business, 030217 neurology & neurosurgery, medicine.drug
Abstract

A paper by Sinclair and colleagues1 in Blood challenges, on the basis of observations on cell lines, the concept that erythropoietin has activities unrelated to erythrodifferentiation. Sinclair and colleagues, based at Amgen, have published six papers since 2006 focused on whether the erythropoietin receptor (EPOR) is expressed by tumour cells—a fact that, if true, could have adverse effects for the use of erythropoietin in cancer. They conclude that EPOR is not expressed by many of the cells previously reported to express EPOR and exhibit cytoprotection by erythropoietin, and question the entire concept that erythropoietin is active on non-haemopoietic cells. Although sometimes data from one laboratory are not replicated in another, many investigators have reported trophic or antiapoptotic effects of erythropoietin on many cells, including those that Sinclair and colleagues report in tabular form without presenting their original data. In fact, over the past 10 years, multiple investigators have shown that erythropoietin is tissue-protective, anti-inflammatory, and promotes neurogenesis and angiogenesis. The observation that erythropoietin is neuroprotective in vivo2 ignited substantial interest in its roles and possible therapeutic use in various diseases. Searching for “erythropoietin AND protect*”, PubMed gives 863 hits of which we identified 346 research papers reporting a protective or reparative action, and only ten a lack of extra-haemopoietic effects. Having no data to compare with previous studies, it is difficult to understand whether “inconsistent, irreproducible and at best modest (10–20%) effects”1 refers to the inconsistency of the effect or to Sinclair and colleagues' experimental technique. Sinclair and colleagues expand their conclusions further by stating that in vivo studies of erythropoietin in animal models of damage are faulty and that they “do not believe [that] clinical studies examining an alleged ‘direct’ effect of ESAs [erythropoiesis-stimulating agents] on heart or brain function or repair are well founded”.1 The term “alleged” is a hyperbole when referring to the tissue-protective actions of erythropoietin that, independently of the receptors implicated, are supported by hundreds of studies, two meta-analyses,3,4 and some clinical trials, although we agree that caution should be used because of potential side-effects.5 Cratylus, discussing with Plato, stated that names express the essence of the thing. This is hardly the case for cytokines: look at tumour necrosis factor or inter leukin 1. Although, from a pharmaceutical perspective, it would be convenient if erythropoietin had no activities outside erythropoiesis, this is wishful thinking. The field would be better served by efforts to understand the full spectrum of erythropoietin's actions.

Published
2010

41. Erythropoietin: not just about erythropoiesis

Author

Bernaudin, M, Bianchi, R, Blomgren, K, Brines, M, Campana, W, Cavaletti, G, Cerami, A, Chopp, M, Coleman, T, Digicaylioglu, M, Ehrenreich, H, Erbayraktar, S, Erbayraktar, Z, Gassmann, M, Genc, S, Gokmen, N, Juul, S, Lipton, SA, Hand, CC, Latini, R, Lauria, G, Leist, M, Newton, SS, Petit, E, Probert, L, Sfacteria, A, Siren, AL, Talan, M, Thiemermann, C, Westenbrink, D, Yaqoob, M, Zhu, C, GRASSO, Giovanni, Bernaudin, M, Bianchi, R, Blomgren, K, Brines, M, Campana, W, Cavaletti, G, Cerami, A, Chopp, M, Coleman, T, Digicaylioglu, M, Ehrenreich, H, Erbayraktar, S, Erbayraktar, Z, Gassmann, M, Genc, S, Gokmen, N, Juul, S, Lipton, SA, Hand, CC, Latini, R, Lauria, G, Leist, M, Newton, SS, Petit, E, Probert, L, Sfacteria, A, Siren, AL, Talan, M, Thiemermann, C, Westenbrink, D, Yaqoob, M, Zhu, C, and Grasso, G

Subjects
Erythropoietin, Neuroprotection
Published
2010

42. Stem cells as an emerging paradigm in stroke 3

Author

Savitz, S.I., Cramer, S.C., Wechsler, L., Aronowski, J., Boltze, J., Borlongan, C., Case, C., Chase, T., Chopp, M., Carmichael, S.T., Duncan, P., Finklestein, S., Fischkoff, S., Guzman, R., Hess, D.C., Huang, D., Hinson, J., Kautz, S., Kondziolka, D., Mays, R., Misra, V., Mitsias, P., Modo, M., Muir, K., Sinden, J., Snyder, E., Steinberg, G., Vahidy, F., Willing, A., Wolf, S., Yankee, E., Yavagal, D.R., and Publica

Published
2014

44. Astrocytes mediate bone marrow stromal cell transplantation enhanced glial cell derived neurotrophic factor (GDNF) production in the ischemic boundary zone after stroke in adult rats

Author

Shen, LH, Li, Y, and Chopp, M

Subjects
Male, Neurons, Aging, Doublecortin Protein, Brain, Apoptosis, Infarction, Middle Cerebral Artery, Article, Brain Ischemia, Rats, Stroke, Random Allocation, Astrocytes, Animals, Glial Cell Line-Derived Neurotrophic Factor, Rats, Wistar, Stem Cell Niche, Stromal Cells, Bone Marrow Transplantation
Abstract

Bone marrow stromal cells (BMSCs) facilitate functional recovery in rats after focal ischemic attack. Growing evidence suggests that the secretion of various bioactive factors underlies BMSCs' beneficial effects. This study investigates the expression of glial cell derived neurotrophic factor (GDNF) in the ischemic hemisphere with or without BMSC administration. Adult male Wistar rats were subjected to 2 h of middle cerebral artery occlusion followed by an injection of 3 x 10(6) BMSCs (n = 11) or phosphate-buffered saline (n = 10) into the tail vein 24 h later. Animals were sacrificed seven days later. Single and double immunohistochemical staining was performed to measure GDNF, Ki67, doublecortin, and glial fibrillary acidic protein expression as well as the number of apoptotic cells along the ischemic boundary zone (IBZ) and/or in the subventricular zone (SVZ). BMSC treatment significantly increased GDNF expression and decreased the number of apoptotic cells in the IBZ (P0.05). GDNF expression was colocalized with GFAP. Meanwhile, BMSCs increased the number of Ki-67 positive cells and the density of DCX positive migrating neuroblasts (P0.05). GDNF expression was significantly increased in single astrocytes collected from animals treated with BMSCs, and in astrocytes cocultured with BMSCs after OGD (P0.05). Our data suggest that BMSCs increase GDNF levels in the ischemic hemisphere; the major source of GDNF protein is reactive astrocytes. We propose that the increase of GDNF in response to BMSC administration creates a hospitable environment for local cellular repair as well as for migrating neuroblasts from the SVZ, and thus contributes to the functional improvement.

Published
2010

47. Biology of Vascular Malformations of the Brain

Author

Leblanc, Gg, Golanov, E, Awad, Ia, Young, Wl, Biology of Vascular Malformations of the Brain NINDS Workshop Collaborators:Awad, I, Berg, M, Chopp, M, Gale, Nw, Gunel, M, Lo, Eh, Marchuk, D, Rigamonti, D, Tournier Lasserve, E, Blasig, Ie, Boudreau, N, Ginsberg, M, Jin, K, Johnson, Gl, Kim, H, Lawton, Mt, Letarte, M, Li, Dy, Mohr, Jp, Nishimura, S, Noonan, Douglas, Pawlikowska, L, Plate, Kh, Shenkar, R, Al Shahi Salman, R, Ball, Kl, Clancy, Ms, Connolly SE Jr, Derry, B, Faurobert, E, Gault, J, Hannegan, L, Hashimoto, T, Keep, Rf, Lee, C, Mccarty, J, Morrison, L, Ning, M, Nunn, Mf, Oh, Sp, Plahn, Bk, Pratt, Ca, Pratt, Wb, Spatz, M, Stapf, C, Yang, Gy, and Zhang, J.

Subjects
Intracranial Arteriovenous Malformations, Hemangioma, Cavernous, Central Nervous System, Pathology, medicine.medical_specialty, Angiogenesis, Cerebral arteries, Gene mutation, medicine.disease_cause, Article, medicine, Animals, Humans, Genetic Predisposition to Disease, Telangiectasia, Advanced and Specialized Nursing, Mutation, Neovascularization, Pathologic, business.industry, Gene Expression Regulation, Developmental, Arteriovenous malformation, Cerebral Arteries, medicine.disease, Disease Models, Animal, Etiology, Telangiectasia, Hereditary Hemorrhagic, Neurology (clinical), medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract

Background and Purpose—This review discusses recent research on the genetic, molecular, cellular, and developmental mechanisms underlying the etiology of vascular malformations of the brain (VMBs), including cerebral cavernous malformation, sporadic brain arteriovenous malformation, and the arteriovenous malformations of hereditary hemorrhagic telangiectasia.Summary of Review—The identification of gene mutations and genetic risk factors associated with cerebral cavernous malformation, hereditary hemorrhagic telangiectasia, and sporadic arteriovenous malformation has enabled the development of animal models for these diseases and provided new insights into their etiology. All of the genes associated with VMBs to date have known or plausible roles in angiogenesis and vascular remodeling. Recent work suggests that the angiogenic process most severely disrupted by VMB gene mutation is that of vascular stabilization, the process whereby vascular endothelial cells form capillary tubes, strengthen their intercellular junctions, and recruit smooth muscle cells to the vessel wall. In addition, there is now good evidence that in some cases, cerebral cavernous malformation lesion formation involves a genetic 2-hit mechanism in which a germline mutation in one copy of a cerebral cavernous malformation gene is followed by a somatic mutation in the other copy. There is also increasing evidence that environmental second hits can produce lesions when there is a mutation to a single allele of a VMB gene.Conclusions—Recent findings begin to explain how mutations in VMB genes render vessels vulnerable to rupture when challenged with other inauspicious genetic or environmental factors and have suggested candidate therapeutics. Understanding of the cellular mechanisms of VMB formation and progression in humans has lagged behind that in animal models. New knowledge of lesion biology will spur new translational work. Several well-established clinical and genetic database efforts are already in place, and further progress will be facilitated by collaborative expansion and standardization of these.

Published
2009

49. Multiparametric Iterative Self-Organizing MR Imaging Data Analysis Technique for Assessment of Tissue Viability in Acute Cerebral Ischemia

Author

Mitsias, P. D., Ewing, J. R., Lu, M., Khalighi, M. M., Pasnoor, M., Ebadian, H. B., Zhao, Q., Santhakumar, S., Michael A. Jacobs, Papamitsakis, N., Soltanian-Zadeh, H., Hearshen, D., Patel, S. C., and Chopp, M.

Subjects
Male, Tissue Survival, Brain, Reproducibility of Results, Cerebral Infarction, Middle Aged, Prognosis, Magnetic Resonance Imaging, Cohort Studies, Diffusion Magnetic Resonance Imaging, Logistic Models, Tissue Plasminogen Activator, Acute Disease, Multivariate Analysis, Image Processing, Computer-Assisted, Humans, Brain Damage, Chronic, Female, Thrombolytic Therapy, Prospective Studies, Mathematical Computing, Algorithms, Aged, Follow-Up Studies
Abstract

BACKGROUND AND PURPOSE: Defining viability and the potential for recovery of ischemic brain tissue can be very valuable for patient selection for acute stroke therapies. Multiparametric MR imaging analysis of ischemic lesions indicates that the ischemic lesion is inhomogeneous in degree of ischemic injury and recovery potential. We sought to define MR imaging characteristics of ischemic lesions that are compatible with viable tissue. METHODS: We included patients with supratentorial ischemic stroke who underwent multiparametric MR imaging studies (axial multi-spin-echo T2-weighted imaging, T1-weighted imaging, and diffusion-weighted imaging) at the acute (

Published
2004

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