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1. NMR microscopy of tissue in organic and mixed solvents

Author

Macura Slobodan, Mishra Prasanna K., Gamez Jeffrey D., and Pirko Istvan

Subjects
NMR, MRI, MRM, nuclear magnetic resonance, NMR imaging, NMR microscopy, magnetization transfer, cross-relaxation, Chemistry, QD1-999
Abstract

We propose to use organic and mixed solvents for nuclear magnetic resonance microscopy of fixed tissue as a means for improving image information content. NMR properties of some standard solvents (methanol, acetone, DMSO) and solvents in use for tissue processing in pathology (xylenes, paraffin, ‘Clearify’) have been measured, reviewed, and analyzed. It was found that DMSO and paraffin are very useful solvents that provide images of better quality than those obtained in water (neutralized formalin buffer). This is illustrated on the formalin fixed mouse brain sections imaged at 16.4 teslas (700 MHz).

Published
2013
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3. Contributors

Author

Alexander, Jonathan S., primary, Al-Louzi, Omar, additional, Arima, Yasunobu, additional, Atsumi, Toru, additional, Bando, Hidenori, additional, Becker, Felix, additional, Bonab, Mandana Mohyeddin, additional, Campos, Yesica, additional, Carare, Roxana O., additional, Ciric, Bogoljub, additional, Dehghanian, Fariba, additional, Denic, Aleksandar, additional, Dubois, Bénédicte, additional, Galea, Ian, additional, Gangloff, Steven, additional, Garg, Ravindra Kumar, additional, Gonzalez-Toledo, Eduardo, additional, Goris, An, additional, Hawkes, Cheryl A., additional, Hilven, Kelly, additional, Hojati, Zohreh, additional, Huseby, Eric S., additional, Jaffe, S.L., additional, Javalkar, Vijaykumar, additional, Jiang, Jing-Jing, additional, Kamimura, Daisuke, additional, Kay, Maryam, additional, Kolb, Channa, additional, Kumar, Neeraj, additional, Lucchinetti, Claudia F., additional, Malhotra, Hardeep Singh, additional, Mangalam, Ashutosh, additional, McGee, Jeanie, additional, Meng, Jie, additional, Minagar, Alireza, additional, Murakami, Masaaki, additional, Nadeem, Mohammed, additional, Nikbin, Behrouz, additional, Nourbakhsh, Bardia, additional, Ogura, Hideki, additional, Omura, Seiichi, additional, Pirko, Istvan, additional, Popescu, Bogdan F. Gh., additional, Ramanathan, Murali, additional, Rasouli, Javad, additional, Rostami, Abdolmohamad, additional, Sabharwal, Lavannya, additional, Saidha, Shiv, additional, Saini, Vasu, additional, Sato, Fumitaka, additional, Shakiba, Yadollah, additional, Sheremata, William, additional, Stevenson, Emily V., additional, Talebian, Fatemeh, additional, Tsunoda, Ikuo, additional, Waubant, Emmanuelle, additional, Weinstock-Guttman, Bianca, additional, Weller, Roy O., additional, Wootla, Bharath, additional, Yun, J. Winny, additional, and Zivadinov, Robert, additional

Published
2016
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9. Contributors

Author

Abdel-Aziz, Khaled, primary, Alexander, Daniel C., additional, Assaf, Yaniv, additional, Backes, Walter H., additional, Bammer, Roland, additional, Barry, Robert L., additional, Brooks, Jonathan C.W., additional, Cadotte, David W., additional, Cercignani, Mara, additional, Ciccarelli, Olga, additional, Cohen-Adad, Julien, additional, Curt, Armin, additional, De Vita, Enrico, additional, Dortch, Richard D., additional, Ellingson, Benjamin M., additional, Fehlings, Michael G., additional, Filippi, Massimo, additional, Finsterbusch, Jürgen, additional, Freund, Patrick, additional, Gore, John C., additional, Guttmann, Charles R.G., additional, Holdsworth, Samantha J., additional, Horsfield, Mark A., additional, Kim, Mina, additional, Kramer, John, additional, Laule, Cornelia, additional, MacKay, Alex, additional, Nijenhuis, Robbert J., additional, Pirko, Istvan, additional, Saritas, Emine U., additional, Schneider, Torben, additional, Smith, Seth A., additional, Solanky, Bhavana S., additional, Summers, Paul E., additional, Wald, Lawrence L., additional, and Wheeler-Kingshott, Claudia A.M., additional

Published
2014
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29. CONTRIBUTING AUTHORS

Author

Abou Zeid, Nuhad E., primary, Ascherio, Alberto, additional, Banwell, Brenda, additional, Bates, Angela, additional, Ben-Hur, Tamir, additional, Bowling, Allen C., additional, Davis, Scott L., additional, De Jager, Philip L., additional, Dutta, Ranjan, additional, Edan, Gilles, additional, Frohman, Elliot M., additional, Frohman, Teresa C., additional, Gold, Ralf, additional, Hafler, David A., additional, Jacob, Anu, additional, jelČiĆ, Ilijas, additional, Kaplin, Adam I., additional, Kerr, Douglas A., additional, Kleinschnitz, Christoph, additional, Kozubal, Dana E., additional, Lemack, Gary E., additional, Linker, Ralf A., additional, lucchinetti, Claudia F., additional, Marriott, James J., additional, Martin, Roland, additional, Matiello, Marcelo, additional, Melzer, Nico, additional, Meuth, Sven G., additional, Morrissey, Sean P., additional, Munger, Kassandra L., additional, O'Connor, Paul W., additional, Amato, Maria Pia, additional, Pirko, Istvan, additional, Pittock, Sean Joseph, additional, Schröder, Alexandra, additional, Shah, Anjali, additional, Trapp, Bruce D., additional, Trecker, Carrilin C., additional, Venkateswaran, Sunita, additional, Voskuhl, Rhonda, additional, Weinshenker, Brian G., additional, Wiendl, Heinz, additional, Wingerchuk, Dean M., additional, Young, Nathan P., additional, and Zipoli, Valentina, additional

Published
2010
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34. Contributors

Author

Aminoff, Michael J., primary, Baehring, Joachim M., additional, Barboi, Alexandru C., additional, Bartt, Russell E., additional, Belman, Anita L., additional, Benarroch, Eduardo, additional, Berg, Bruce O., additional, Bhatia, Sanjay, additional, Bianco, Brian A., additional, Biller, José, additional, Bleck, Thomas P., additional, Boeve, Bradley F., additional, Bolla, Karen I., additional, Bönnemann, Carsten G., additional, Brackmann, Derald E., additional, Brewer, James B., additional, Bromley, Steven M., additional, Brown, Paul, additional, Cadet, Jean Lud, additional, Camicioli, Richard, additional, Campero, Mario S., additional, Caplan, Louis R., additional, Caselli, Richard J., additional, Castillo, José Luis, additional, Cea, Gabriel, additional, Chervin, Ronald D., additional, Chou, Kelvin L., additional, Chung, Chin-Sang, additional, Cochrane, Thomas I., additional, Cohen, Bruce H., additional, Consens, Flavia B., additional, Cummings, Jeffrey L., additional, Dastur, Cyrus K., additional, Diener, Hans Christoph, additional, Doty, Richard L., additional, Dyken, Paul Richard, additional, Evans, Randolph W., additional, Fahn, Stanley, additional, Faro, Scott H., additional, Ferrante, Mark A., additional, Feske, Steven K., additional, Fetterman, Bruce L., additional, Fletcher, Jeffrey J., additional, Foldvary-Schaefer, Nancy, additional, Freeman, Roy, additional, Friedman, Joseph H., additional, Gabrieli, John D.E., additional, Galetta, Steven L., additional, Garbern, James Y., additional, Gascon, Generoso G., additional, Golden, Jeffrey A., additional, Gonzalez-Rothi, Leslie J., additional, Goodwin, James, additional, Griggs, Robert C., additional, Hain, Timothy C., additional, Hammerstad, John P., additional, Heilman, Kenneth M., additional, Hening, Wayne A., additional, Hermanowicz, Neal, additional, Hershey, Beverly L., additional, Hochberg, Fred H., additional, Horn, Stacy S., additional, Jankovic, Joseph, additional, Janus, Todd J., additional, Kaufmann, Horacio, additional, Kinsella, Laurence J., additional, Klockgether, Thomas, additional, Koenigsberg, Robert A., additional, Kompoliti, Katie, additional, Kupsky, William J., additional, LeWitt, Peter A., additional, Liu, Grant T., additional, Love, Betsy B., additional, Maertens, Paul, additional, Maletic-Savatic, Mirjana, additional, Mendez, Mario F., additional, Meriggioli, Matthew N., additional, Mohamed, Feroze B., additional, Nasreddine, Ziad S., additional, Nathan, Barnett R., additional, Newman, Nancy J., additional, Noseworthy, John H., additional, Nutt, John G., additional, Osborne, Benjamin J., additional, Ozand, Pinar T., additional, Pirko, Istvan, additional, Prasad, Sashank, additional, Preston, Alison R., additional, Quant, Eudocia, additional, Riley, David E., additional, Roos, Karen L., additional, Rose, Michael, additional, Rosen, Allyson C., additional, Rowin, Julie, additional, Shields, Robert W., additional, Siddique, Nailah, additional, Siddique, Teepu, additional, Siegal, Todd L., additional, Silberstein, Stephen D., additional, Stebbins, Glenn T., additional, Stevens, Suzanne, additional, Stickles, Scott, additional, Sufit, Robert, additional, Swanberg, Lt. Col. Margaret M., additional, Timmann, Dagmar, additional, Topel, Jordan L., additional, Tsai, Fong Y., additional, Vaidya, Chandan J., additional, Verdugo, Renato J., additional, Watson, Robert T., additional, Wilberger, Jack E., additional, Wilbourn, Asa J., additional, Wyllie, Elaine, additional, Young, William B., additional, and Yung, W. K. Alfred, additional

Published
2007
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40. Preserved vascular integrity and enhanced survival following neuropilin-1 inhibition in a mouse model of CD8 T cell-initiated CNS vascular permeability

Author

Suidan Georgette L, Dickerson Jonathan W, Johnson Holly L, Chan Theresa W, Pavelko Kevin D, Pirko Istvan, Seroogy Kim B, and Johnson Aaron J

Subjects
Vascular endothelial growth factor (VEGF), CD8 T cell, CNS vascular permeability, Blood–brain barrier (BBB), Neuropilin-1 (NRP-1), Fetal liver kinase 1 (flk-1), FMS-related tyrosine kinase-1 (flt-1), Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Altered permeability of the blood–brain barrier (BBB) is a feature of numerous neurological conditions including multiple sclerosis, cerebral malaria, viral hemorrhagic fevers and acute hemorrhagic leukoencephalitis. Our laboratory has developed a murine model of CD8 T cell-initiated central nervous system (CNS) vascular permeability in which vascular endothelial growth factor (VEGF) signaling plays a prominent role in BBB disruption. Findings In this study, we addressed the hypothesis that in vivo blockade of VEGF signal transduction through administration of peptide (ATWLPPR) to inhibit neuropilin-1 (NRP-1) would have a therapeutic effect following induction of CD8 T cell-initiated BBB disruption. We report that inhibition of NRP-1, a co-receptor that enhances VEGFR2 (flk-1) receptor activation, decreases vascular permeability, brain hemorrhage, and mortality in this model of CD8 T cell-initiated BBB disruption. We also examine the expression pattern of VEGFR2 (flk-1) and VEGFR1 (flt-1) mRNA expression during a time course of this condition. We find that viral infection of the brain leads to increased expression of flk-1 mRNA. In addition, flk-1 and flt-1 expression levels decrease in the striatum and hippocampus in later time points following induction of CD8 T cell-mediated BBB disruption. Conclusion This study demonstrates that NRP-1 is a potential therapeutic target in neuro-inflammatory diseases involving BBB disruption and brain hemorrhage. Additionally, the reduction in VEGF receptors subsequent to BBB disruption could be involved in compensatory negative feedback as an attempt to reduce vascular permeability.

Published
2012
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41. Advances in understanding gray matter pathology in multiple sclerosis: Are we ready to redefine disease pathogenesis?

Author

Zivadinov Robert and Pirko Istvan

Subjects
Multiple sclerosis, Gray matter, Pathology, Meningeal inflammation, Cortical, Subcortical, MRI, Double inversion recovery, Atrophy, Clinical, Treatment, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract The purpose of this special issue in BMC Neurology is to summarize advances in our understanding of the pathological, immunological, imaging and clinical concepts of gray matter (GM) pathology in patients with multiple sclerosis (MS). Review articles by Lucchinetti and Popescu, Walker and colleagues, Hulst and colleagues and Horakova and colleagues summarize important recent advances in understanding GM damage and its implications to MS pathogenesis. They also raise a number of important new questions and outline comprehensive approaches to addressing those questions in years to come. In the last decade, the use of immunohistochemistry staining methods and more advanced imaging techniques to detect GM lesions, like double inversion recovery, contributed to a surge of studies related to cortical and subcortical GM pathology in MS. It is becoming more apparent from recent biopsy studies that subpial cortical lesions in early MS are highly inflammatory. The mechanisms responsible for triggering meningeal inflammation in MS patients are not yet elucidated, and they should be further investigated in relation to their role in initiating and perpetuating the disease process. Determining the role of antigens, environmental and genetic factors in the pathogenesis of GM involvement in MS is critical. The early involvement of cortical and subcortical GM damage in MS is very intriguing and needs to be further studied. As established in numerous cross-sectional and longitudinal studies, GM damage is a better predictor of physical disability and cognitive impairment than WM damage. Monitoring the evolution of GM damage is becoming an important marker in predicting future disease course and response to therapy in MS patients.

Published
2012
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42. A hematopoietic contribution to microhemorrhage formation during antiviral CD8 T cell-initiated blood-brain barrier disruption

Author

Johnson Holly L, Chen Yi, Suidan Georgette L, McDole Jeremiah R, Lohrey Anne K, Hanson Lisa M, Jin Fang, Pirko Istvan, and Johnson Aaron J

Subjects
Blood-brain barrier, CD8 T cell, Hematopoietic factors, Hemorrhage, MRI, Theiler's murine encephalomyelitis, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background The extent to which susceptibility to brain hemorrhage is derived from blood-derived factors or stromal tissue remains largely unknown. We have developed an inducible model of CD8 T cell-initiated blood-brain barrier (BBB) disruption using a variation of the Theiler's murine encephalomyelitis virus (TMEV) model of multiple sclerosis. This peptide-induced fatal syndrome (PIFS) model results in severe central nervous system (CNS) vascular permeability and death in the C57BL/6 mouse strain, but not in the 129 SvIm mouse strain, despite the two strains' having indistinguishable CD8 T-cell responses. Therefore, we hypothesize that hematopoietic factors contribute to susceptibility to brain hemorrhage, CNS vascular permeability and death following induction of PIFS. Methods PIFS was induced by intravenous injection of VP2121-130 peptide at 7 days post-TMEV infection. We then investigated brain inflammation, astrocyte activation, vascular permeability, functional deficit and microhemorrhage formation using T2*-weighted magnetic resonance imaging (MRI) in C57BL/6 and 129 SvIm mice. To investigate the contribution of hematopoietic cells in this model, hemorrhage-resistant 129 SvIm mice were reconstituted with C57BL/6 or autologous 129 SvIm bone marrow. Gadolinium-enhanced, T1-weighted MRI was used to visualize the extent of CNS vascular permeability after bone marrow transfer. Results C57BL/6 and 129 SvIm mice had similar inflammation in the CNS during acute infection. After administration of VP2121-130 peptide, however, C57BL/6 mice had increased astrocyte activation, CNS vascular permeability, microhemorrhage formation and functional deficits compared to 129 SvIm mice. The 129 SvIm mice reconstituted with C57BL/6 but not autologous bone marrow had increased microhemorrhage formation as measured by T2*-weighted MRI, exhibited a profound increase in CNS vascular permeability as measured by three-dimensional volumetric analysis of gadolinium-enhanced, T1-weighted MRI, and became moribund in this model system. Conclusion C57BL/6 mice are highly susceptible to microhemorrhage formation, severe CNS vascular permeability and morbidity compared to the 129 SvIm mouse. This susceptibility is transferable with the bone marrow compartment, demonstrating that hematopoietic factors are responsible for the onset of brain microhemorrhage and vascular permeability in immune-mediated fatal BBB disruption.

Published
2012
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43. Iron deposition and inflammation in multiple sclerosis. Which one comes first?

Author

Weinstock-Guttman Bianca, Zivadinov Robert, and Pirko Istvan

Subjects
multiple sclerosis, animal model, iron deposition, inflammation, cerebral EAE, CCSVI, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurophysiology and neuropsychology, QP351-495
Abstract

Abstract Whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development remains unclear at this time, and should be studied at the early stages of disease pathogenesis. However, it is difficult to study the relationship between iron deposition and inflammation in early MS due to the delay between the onset of symptoms and diagnosis, and the poor availability of tissue specimens. In a recent article published in BMC Neuroscience, Williams et al. investigated the relationship between inflammation and iron deposition using an original animal model labeled as "cerebral experimental autoimmune encephalomyelitis", which develops CNS perivascular iron deposits. However, the relative contribution of iron deposition vs. inflammation in the pathogenesis and progression of MS remains unknown. Further studies should establish the association between inflammation, reduced blood flow, iron deposition, microglia activation and neurodegeneration. Creating a representative animal model that can study independently such relationship will be the key factor in this endeavor.

Published
2011
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44. Acute hemorrhagic demyelination in a murine model of multiple sclerosis

Author

Rodriguez Moses, Suidan Georgette L, Pirko Istvan, and Johnson Aaron J

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Acute hemorrhagic leukoencephalomyelitis (AHLE) is a rare neurological condition characterized by the development of acute hemorrhagic demyelination and high mortality. The pathomechanism of AHLE, as well as potential therapeutic approaches, have remained elusive due to the lack of suitable animal models. We report the first murine model of AHLE using a variation of the Theiler's Murine Encephalitis Virus (TMEV) MS model. During acute TMEV infection, C57BL/6 mice do not normally undergo demyelination. However, when 7 day TMEV infected C57BL/6 mice are intravenously administered the immunodominant CD8 T cell peptide, VP2121–130, animals develop characteristics of human AHLE based on pathologic, MRI and clinical features including microhemorrhages, increased blood-brain barrier permeability, and demyelination. The animals also develop severe disability as assessed using the rotarod assay. This study demonstrates the development of hemorrhagic demyelination in TMEV infected C57BL/6 mice within 24 hours of inducing this condition through intravenous administration of CD8 T cell restricted peptide. This study is also the first demonstration of rapid demyelination in a TMEV resistant non-demyelinating strain without transgenic alterations or pharmacologically induced immunosuppression.

Published
2008
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47. Neuropilin-1 modulates interferon-γ-stimulated signaling in brain microvascular endothelial cells

Author

Wang, Ying, primary, Cao, Ying, additional, Mangalam, Ashutosh K., additional, Guo, Yong, additional, LaFrance-Corey, Reghann G., additional, Gamez, Jeffrey D., additional, Atanga, Pascal Aliihnui, additional, Clarkson, Benjamin D., additional, Zhang, Yuebo, additional, Wang, Enfeng, additional, Angom, Ramcharan Singh, additional, Dutta, Kirthica, additional, Ji, Baoan, additional, Pirko, Istvan, additional, Lucchinetti, Claudia F., additional, Howe, Charles L., additional, and Mukhopadhyay, Debabrata, additional

Published
2016
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48. Deletion of Beta2-microglobulin Ameliorates Spinal Cord Lesion Load and Promotes Recovery of Brainstem NAA Levels in a Murine Model of Multiple Sclerosis

Author

Denic, Aleksandar, Pirko, Istvan, Wootla, Bharath, Bieber, Allan, Macura, Slobodan, and Rodriguez, Moses

Subjects
Aspartic Acid, Magnetic Resonance Spectroscopy, Multiple Sclerosis, Time Factors, CD8 Antigens, Brain, Mice, Transgenic, Recovery of Function, Article, Axons, Disease Models, Animal, Mice, nervous system, Spinal Cord, Theilovirus, Animals, Humans, beta 2-Microglobulin, Brain Stem
Abstract

We used genetic deletion of β2-microglobulin to study the influence of CD8(+) T cells on spinal cord demyelination, remyelination, axonal loss and brainstem N-acetyl aspartate levels during the acute and chronic phases of Theiler's murine encephalomyelitis virus (TMEV) infection. We used β2m(-/-) and β2m(+/+) B10.Q mice (of H-2(q) background) normally susceptible to TMEV-induced demyelination. Over the disease course, β2m(+/+) mice had increasing levels of demyelination and minimal late-onset remyelination. In contrast, β2m(-/-) mice had steady levels of demyelination from 45-390 dpi and remyelination was extensive and more complete. Early in the disease, brainstem NAA levels drop in both strains, but accordingly with remyelination and axonal preservation, NAA recover in β2m(-/-) mice despite equivalent brainstem pathology. At 270 dpi, β2m(+/+) mice had significantly fewer spinal cord axons than β2m(-/-) mice (up to 28% less). In addition, β2m(+/+) mice lost axons of all calibers, whereas β2m(-/-) mice had a modest loss of only medium- and large-caliber axons. This study further supports the hypothesis that CD8(+) T cells are involved in demyelination, and axonal loss following Theiler's virus-induced demyelination.

Published
2012

49. Poor early relapse recovery affects onset of progressive disease course in multiple sclerosis

Author

Novotna, Martina, primary, Paz Soldán, M. Mateo, additional, Abou Zeid, Nuhad, additional, Kale, Nilufer, additional, Tutuncu, Melih, additional, Crusan, Daniel J., additional, Atkinson, Elizabeth J., additional, Siva, Aksel, additional, Keegan, B. Mark, additional, Pirko, Istvan, additional, Pittock, Sean J., additional, Lucchinetti, Claudia F., additional, Noseworthy, John H., additional, Weinshenker, Brian G., additional, Rodriguez, Moses, additional, and Kantarci, Orhun H., additional

Published
2015
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50. Effective Treatment of Established GL261 Murine Gliomas through Picornavirus Vaccination-Enhanced Tumor Antigen-Specific CD8+ T Cell Responses

Author

Renner, Danielle N., primary, Jin, Fang, additional, Litterman, Adam J., additional, Balgeman, Alexis J., additional, Hanson, Lisa M., additional, Gamez, Jeffrey D., additional, Chae, Michael, additional, Carlson, Brett L., additional, Sarkaria, Jann N., additional, Parney, Ian F., additional, Ohlfest, John R., additional, Pirko, Istvan, additional, Pavelko, Kevin D., additional, and Johnson, Aaron J., additional

Published
2015
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