7 results on '"D. Levacic"'
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2. CLIN-NEURO/MEDICAL ONCOLOGY
- Author
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F. Girardi, C. Braun, Dennis C. Shrieve, Wei Chen, D. Kita, M. F. Fanelli, David Schiff, Sunyoung Ahn, Elizabeth Vera-Bolanos, J. Carrasquillo, S. Singer, James G. Herman, C. Bosa, Julia Selfridge, V. Tohidi, B.-A. Millar, M. Benavides, M. I. D. L. Fuente, Phioanh L. Nghiemphu, Kristin R. Swanson, John P. Kirkpatrick, Jonathan P.S. Knisely, Jörg C. Tonn, Kenneth Aldape, J. C. Streeter, R. Ruda, Seung Hong Choi, R. Curry, J. Yu, Ryo Nishikawa, E. Garoufalis, A. H. Friedman, Kurt A. Jaeckle, W. Zhang, Maryam Fouladi, Y. Odia, Arthur P. Chou, S. Sahebjam, E. Pentsova, Luis Souhami, Y. Yuan, F. N. Santos, C. Mesia, H. Friedman, Jennifer Linn, J. E. Adair, Yong Hwy Kim, Athanasios P. Kyritsis, Zvi Ram, M. G. Muhonen, Tracy T. Batchelor, Alissa A. Thomas, Stuart A. Grossman, M. Nasseri, Pedro Pérez Segura, S. Lacey, S. D. Bell, Helen A. Shih, E. Bit-Ivan, Timothy A. Chan, H. Pentsova, H. Wilson, Fumiko Shimizu, M. Forbes, L. Randolph, S. Kim, Amit Bhatt, Sabina Eigenbrod, T. Seigal, P. Dall'Occa, F. McSherry, R. M. Green, Michael D. Prados, Camilo E. Fadul, A. Guevarra, J.-Y. Han, Guido Reifenberger, E. Franceschi, D. Sageser, Jennie Taylor, Kevin Petrecca, M. K. Nicholas, Teresa Ribalta, Morris D. Groves, J.-Y. Blay, B. C. Beard, C. F. La, A. A. da Costa, K. Murillo-Medina, W. Pfisterer, R. Chu, Nan Lin, M. Ermani, A. J. Neuwelt, Samuel T. Chao, T. Ranjan, W. Taki, Hendrik Janssen, R. Agati, A. Mahta, T. N. Kreisl, E. Perez, J. Fuster, B. D. Fu, David M. Peereboom, N. Gresa-Arribas, Georg Widhalm, M. D'Apuzzo, J. Steinbach, Tom Mikkelsen, Michael Platten, R. Poggi, Sandra Ictech, I. Craven, A. Raghunathan, John B. Fiveash, N. L. Jansen, Rupert Egensperger, B. Badie, S. Medrano, Chul-Kee Park, K. Wong, Tae Min Kim, M. Bartolotti, M. Alejandro, T. Rosser, H.-P. Kiem, Marie-Christine Guiot, S. Gonzalez, J. Ljubimova, T. Furuta, J. Herndon, J. Finlay, Vivian Tabar, M. Hadjivassiliou, Christine Marosi, D. Hammoud, K. Black, S. K. Anderson, F. Bach, Gregory N. Fuller, N. Kased, S. Shpigel, Gianluca Marucci, Michael A. Vogelbaum, S. Bluml, J. Joo, M. D. Groves, X. Ye, Adam L. Cohen, J. A. Butman, M. D. Prados, X. Perez-Martin, R. Sharma, G. Colon-Otero, Richard M. Green, Paul D. Brown, Cornelia Sax, Robert J. Weil, J. Connelly, S. Burri, M. R. Welch, Marc K. Rosenblum, Minesh P. Mehta, Shlomit Yust-Katz, J. Canellas, Ulrich Bogdahn, S. Liker, P. U. Kumthekar, F. Gilles, M. Brock, Aaron T. Wild, A. Guerrero-Maldonado, Janet M. Bruner, A. Balmanoukian, E. Kitzweger, B. Schuknecht, Ayman I. Omar, J. Sampson, R. F. Del Maestro, W. Hruby, Niklas Thon, S. Zhao, F. Aboul-Enein, L. M. Alderson, J. McClain, J. Rudnick, J. Dorr, Vinay K. Puduvalli, Sonia Partap, Y. Hayashi, A. Kessinger, N. A. Shonka, T. Minamoto, D. Z. Lee, L. G. Berriel, T. Xie, J. Shih, J. S. Bubalo, Oscar Lin, J. E. Herndon, Michael Glantz, A. Gupta, H. Sabit, H. Heinrichs, Hans A. Kretzschmar, A. Asher, T. M. Bhavsar, A. Coan, V. A. Levin, M. Landeros, A. K. Choucair, D. Garbossa, G. Stockhammer, Jian Campian, C. J. Vecht, C. Ausch, Linda M. Liau, H. I. Farhat, M. Richards, H. I. Robins, R. Chaudhary, Agnieszka Korfel, Marta Penas-Prado, A. Jensen, I. Lolli, Amar J. Gajjar, K. Papsdorf, L. DeAngelis, Kathryn Beal, L. Phishniak, J. Joyce, Arnab Chakravarti, J. J. Vredenburgh, C. Dealis, A. F. Campos-Gines, Peter Hau, J.-I. Hamada, R. A. Gilbert, T. J. Kaley, Eric T. Wong, Ian F. Pollack, T. Gajewski, A. C. Levy, L. R. Bressler, X. Chen, C. Bernadette, O. Etxaniz, N. Antony, Birgit Flechl, D. Levacic, Byung Se Choi, J. I. Stenner, F. Pinto, Sandra K. Johnston, M. M. Mrugala, David Roberge, M. Wang, P. J. Anderson, H. A. Fine, M. J. Glantz, Alfred Yung, L. Alderson, M. Chamberlain, R. Naor, Jaume Capellades, Se-Hoon Lee, D. G. Brackman, Nathalie Jansen, T. Synold, Terri S. Armstrong, J. Pichler, X.-T. Kong, T. Cloughesy, P. Frankel, R. Valdez-Vazquez, Mathias Kunz, J. Dalmau, A. Baldock, Stewart Goldman, K. Rizzo, M. Nakada, Christoph Meisner, Ryan Merrell, C. Bomprezzi, Tomokazu Aoki, M. R. Gilbert, Jason K. Rockhill, Benjamin Ellezam, C. Sebastian, O. Arrieta, N. Wu, M. Magistrello, T. Patel, Adelheid Wöhrer, M. Sabel, F. Bokstein, V. Gomez-Molinar, S. Yovino, A. Kheder, Gaspar Reynes, R. Packer, M. Ronellenfitsch, Sasan Karimi, David Piccioni, J. M. Stachnik, C. Sebesta, Ryan Shanley, L. T. Chinen, H.-S. Gwak, E. A. Woyshner, D. Reuter, S. Bekker, K. Hunter, B. Haghighi, G. Poepperl, M. C. Chamberlain, W. Massey, M. A. Hamza, R. Cavaliere, Sichen Li, Daniela A. Bota, S. Spiegl-Kreinecker, G. Tatzreiter, Sigmund Hsu, M. Westphal, T. Pietsch, P. D. Barnes, C. Arango, G. Cervantes-Sanchez, C. Grommes, W. Brick, Vera Graute, M. P. Gabay, L. Bertero, Friedrich W. Kreth, F. M. Iwamoto, D. T. Blumenthal, M. Matsutani, K. B. Peters, S. F. Shakur, E. Flanagan, H. T. Kim, M. Simon, Michael Ackerl, Nadia N. Laack, J. Portnow, R. Ruckser, T. F. Cloughesy, H. Wayne Slone, A. A. Erazo-Valle-Solis, Karin Dieckmann, J. Baerhing, R. Soffietti, N. Laperriere, M. J. Gil, R. Fisher, Thierry Muanza, Reema R. Mody, W. Kim, L. Droms, Fabio M. Iwamoto, J. Grimm, Robert B. Jenkins, M. R. Aizenberg, E. Lipp, M. J. Taphoorn, V. Garcia-Navarro, J. H. Suh, Peter Bartenstein, E. Bourekas, Brett Theeler, W. G. Watkin, R. M. Tyson, Mira Zurayk, D. Alexandru, N. Uchiyam, J. Gilreath, A. J. Ramiro, R. Rockne, R. Naruse, M. Krieger, A. Kloet, Petr Kavan, E. Jaffe, D. A. Reardon, Jochen Herms, A. Willson, H. Zwinkels, M. Faedi, A. Moreno-Aspitia, J. Vredenburgh, Herbert H. Engelhard, C. Bridge, Paul W. Sperduto, H. Yoo, P. Friedman, N. Letarte, Tetsuya Ueba, Lisa M. DeAngelis, C. Nolan, Michael Weller, H. Colman, Jürgen Lutz, H. Ian Robins, J. McGregor, Pankaj Jalan, Joseph Landolfi, M. Di Battista, Bogdana Suchorska, Manuela Caroli, G. Nikkhah, A. Leibetseder, K. Aboody, V. Liu, Albert Lai, Yoshiki Arakawa, Kazuhiko Nozaki, G. Dhall, Kenneth R. Hess, Oscar Gallego, A. Naomi, A. Pace, T. M. Nguyen, K. Kawakami, K. DeBraganca, A. A. Brandes, V. K. Puduvalli, Lakshmi Nayak, Charles A. Conrad, Laurie E. Gaspar, P. J. Flynn, S. Ruiz-Gonzalez, Carmen Balana, J. Lange, T. Kaley, Vijay Pandav, J. Herrada, Eugenia Verger, S. Honigschnabel, M. Chen, C. A. Bridge, Yu Jung Kim, Mary Jo T. Necesito-Reyes, Bettina Hentschel, Victor A. Levin, J. Hu, K. Hoang-Xuan, Chae-Yong Kim, W. Sherman, L. Armbruster, T. Yun, C. Carapella, E. L. Diamond, A. Mahapatra, Warren P. Mason, X. Luo, R. C. Rockne, S. G. Crasto, L. Bailey, K. Sanghee, Matthias Preusser, R. Mathew, Jaclyn Wu, D. White, Susumu Miyamoto, A. Omuro, A. Desjardins, P.H. Gutin, J. S. Lee, Andrew D. Trister, Maxwell Lewis Neal, W. Zaky, A. L. Sumrall, C. M. Sperduto, A. L. Baldock, S. Phuphanich, J. Sul, S. H. Shin, E. A. Neuwelt, Heinrich Elinzano, C. Huang, H. S. Friedman, Laura Guyman, Sean Grimm, C. Sanchez, H. Newton, G. Oberhauser, Chunyue Yin, Wolfgang Wick, Caterina Giannini, Veronica Chiang, C. LaFougere, P. Metellus, A. Krauthammer, M. Kinoshita, J. Sheehan, Miguel J. Gil, E. Trevisan, J. Raizer, Shin-Ichi Miyatake, A. Olch, Jin Wook Kim, John L. Villano, Patricia Sneed, Brian P. O'Neill, A. Sahgal, Il Han Kim, A. Brickhouse, K. Herath, C. Zoccoli, M. J. van den Bent, T. Tsukahara, M. Heaney, B. Hassanzadeh, J. Quan, David R. Macdonald, Percy Ivy, D. Liue, John H. Suh, K. Miyashita, T. J. Fraum, W. A. Yung, I. Melguizo-Gavilanes, Maciej M. Mrugala, Matthew J. Matasar, and P. Garciarena
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Cancer Research ,medicine.medical_specialty ,Abstracts ,Oncology ,business.industry ,medicine ,Medical physics ,Neurology (clinical) ,business - Published
- 2012
3. The N-methyl-D-aspartate-evoked cytoplasmic calcium increase in adult rat dorsal root ganglion neuronal somata was potentiated by substance P pretreatment in a protein kinase C-dependent manner
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Jose V. Montoya-Gacharna, D. Levacic, M. Dubois, C. Castillo, Thomas J. J. Blanck, J. Baquero-Buitrago, Monica Norcini, Esperanza Recio-Pinto, and R. Medina
- Subjects
Bisindolylmaleimide ,medicine.medical_specialty ,Cytoplasm ,N-Methylaspartate ,Sensory Receptor Cells ,Neuropeptide ,Biology ,Substance P ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Dorsal root ganglion ,Internal medicine ,Ganglia, Spinal ,medicine ,Animals ,Calcium Signaling ,Protein kinase C ,Cells, Cultured ,Protein Kinase C ,General Neuroscience ,Long-term potentiation ,Drug Synergism ,Sensory neuron ,Rats ,Up-Regulation ,Nerve growth factor ,medicine.anatomical_structure ,Endocrinology ,nervous system ,chemistry ,NMDA receptor ,Neuroscience - Abstract
The involvement of substance P (SP) in neuronal sensitization through the activation of the neurokinin-1-receptor (NK1r) in postsynaptic dorsal horn neurons has been well established. In contrast, the role of SP and NK1r in primary sensory dorsal root ganglion (DRG) neurons, in particular in the soma, is not well understood. In this study, we evaluated whether SP modulated the NMDA-evoked transient increase in cytoplasmic Ca 2+ ([Ca 2+ ] cyt ) in the soma of dissociated adult DRG neurons. Cultures were treated with nerve growth factor (NGF), prostaglandin E 2 (PGE 2 ) or both NGF+PGE 2 . Treatment with NGF+PGE 2 increased the percentage of N-methyl- d -aspartate (NMDA) responsive neurons. There was no correlation between the percentage of NMDA responsive neurons and the level of expression of the NR1 and NR2B subunits of the NMDA receptor or of the NK1r. Pretreatment with SP did not alter the percentage of NMDA responsive neurons; while it potentiated the NMDA-evoked [Ca 2+ ] cyt transient by increasing its magnitude and by prolonging the period during which small- and some medium-sized neurons remained NMDA responsive. The SP-mediated potentiation was blocked by the SP-antagonist ([D-Pro 4 , D-Trp 7,9 ]-SP (4–11)) and by the protein kinase C (PKC) blocker bisindolylmaleimide I (BIM); and correlated with the phosphorylation of PKCe. The Nk1r agonist [Sar 9 , Met(O 2 ) 11 ]-SP (SarMet-SP) also potentiated the NMDA-evoked [Ca 2+ ] cyt transient. Exposure to SP or SarMet-SP produced a rapid increase in the labeling of phosphorylated-PKCe. In none of the conditions we detected phosphorylation of the NR2B subunit at Ser-1303. Phosphorylation of the NR2B subunit at Tyr1472 was enhanced to a similar extent in cells exposed to NMDA, SP or NMDA+SP, and that enhancement was blocked by BIM. Our findings suggest that NGF and PGE 2 may contribute to the injury-evoked sensitization of DRG neurons in part by enhancing their NMDA-evoked [Ca 2+ ] cyt transient in all sized DRG neurons; and that SP may further contribute to the DRG sensitization by enhancing and prolonging the NMDA-evoked increase in [Ca 2+ ] cyt in small- and medium-sized DRG neurons.
- Published
- 2010
4. Olutasidenib (FT-2102) in patients with relapsed or refractory IDH1-mutant glioma: A multicenter, open-label, phase Ib/II trial.
- Author
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de la Fuente MI, Colman H, Rosenthal M, Van Tine BA, Levacic D, Walbert T, Gan HK, Vieito M, Milhem MM, Lipford K, Forsyth S, Guichard SM, Mikhailov Y, Sedkov A, Brevard J, Kelly PF, Mohamed H, and Monga V
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- Humans, Pyridines, Isocitrate Dehydrogenase genetics, Quinolines, Glioma drug therapy, Glioma genetics
- Abstract
Background: Olutasidenib (FT-2102) is a highly potent, orally bioavailable, brain-penetrant and selective inhibitor of mutant isocitrate dehydrogenase 1 (IDH1). The aim of the study was to determine the safety and clinical activity of olutasidenib in patients with relapsed/refractory gliomas harboring an IDH1R132X mutation., Methods: This was an open-label, multicenter, nonrandomized, phase Ib/II clinical trial. Eligible patients (≥18 years) had histologically confirmed IDH1R132X-mutated glioma that relapsed or progressed on or following standard therapy and had measurable disease. Patients received olutasidenib, 150 mg orally twice daily (BID) in continuous 28-day cycles. The primary endpoints were dose-limiting toxicities (DLTs) (cycle 1) and safety in phase I and objective response rate using the Modified Response Assessment in Neuro-Oncology criteria in phase II., Results: Twenty-six patients were enrolled and followed for a median 15.1 months (7.3‒19.4). No DLTs were observed in the single-agent glioma cohort and the pharmacokinetic relationship supported olutasidenib 150 mg BID as the recommended phase II dose. In the response-evaluable population, disease control rate (objective response plus stable disease) was 48%. Two (8%) patients demonstrated a best response of partial response and eight (32%) had stable disease for at least 4 months. Grade 3‒4 adverse events (≥10%) included alanine aminotransferase increased and aspartate aminotransferase increased (three [12%], each)., Conclusions: Olutasidenib 150 mg BID was well tolerated in patients with relapsed/refractory gliomas harboring an IDH1R132X mutation and demonstrated preliminary evidence of clinical activity in this heavily pretreated population., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Neuro-Oncology.)
- Published
- 2023
- Full Text
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5. Inclusion-body myositis associated with Alzheimer's disease.
- Author
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Levacic D, Peddareddygari LR, Nochlin D, Sharer LR, and Grewal RP
- Abstract
Sporadic inclusion-body myositis (s-IBM) is a myopathy that is characterized by progressive weakness and muscle pathology demonstrating inflammation and rimmed vacuoles. In addition, similar to the pathology observed in the brains of patients with Alzheimer's disease, the deposition of beta-amyloid and phosphorylated tau proteins in muscle fibers has been reported. These shared pathologic features have prompted hypotheses suggesting a shared etiology of these two conditions. We report a case of a 73-year-old woman initially diagnosed with s-IBM who later developed Alzheimer's disease.
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- 2013
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6. The N-methyl-D-aspartate-evoked cytoplasmic calcium increase in adult rat dorsal root ganglion neuronal somata was potentiated by substance P pretreatment in a protein kinase C-dependent manner.
- Author
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Castillo C, Norcini M, Baquero-Buitrago J, Levacic D, Medina R, Montoya-Gacharna JV, Blanck TJ, Dubois M, and Recio-Pinto E
- Subjects
- Animals, Calcium Signaling drug effects, Calcium Signaling physiology, Cells, Cultured, Cytoplasm drug effects, Cytoplasm enzymology, Drug Synergism, Ganglia, Spinal drug effects, Protein Kinase C drug effects, Rats, Rats, Sprague-Dawley, Sensory Receptor Cells drug effects, Sensory Receptor Cells enzymology, Substance P antagonists & inhibitors, Substance P metabolism, Cytoplasm metabolism, Ganglia, Spinal cytology, Ganglia, Spinal metabolism, N-Methylaspartate pharmacology, Protein Kinase C physiology, Sensory Receptor Cells metabolism, Substance P physiology, Up-Regulation physiology
- Abstract
The involvement of substance P (SP) in neuronal sensitization through the activation of the neurokinin-1-receptor (NK1r) in postsynaptic dorsal horn neurons has been well established. In contrast, the role of SP and NK1r in primary sensory dorsal root ganglion (DRG) neurons, in particular in the soma, is not well understood. In this study, we evaluated whether SP modulated the NMDA-evoked transient increase in cytoplasmic Ca2+ ([Ca2+]cyt) in the soma of dissociated adult DRG neurons. Cultures were treated with nerve growth factor (NGF), prostaglandin E2 (PGE2) or both NGF+PGE2. Treatment with NGF+PGE2 increased the percentage of N-methyl-D-aspartate (NMDA) responsive neurons. There was no correlation between the percentage of NMDA responsive neurons and the level of expression of the NR1 and NR2B subunits of the NMDA receptor or of the NK1r. Pretreatment with SP did not alter the percentage of NMDA responsive neurons; while it potentiated the NMDA-evoked [Ca2+]cyt transient by increasing its magnitude and by prolonging the period during which small- and some medium-sized neurons remained NMDA responsive. The SP-mediated potentiation was blocked by the SP-antagonist ([D-Pro4, D-Trp7,9]-SP (4-11)) and by the protein kinase C (PKC) blocker bisindolylmaleimide I (BIM); and correlated with the phosphorylation of PKCε. The Nk1r agonist [Sar9, Met(O2)11]-SP (SarMet-SP) also potentiated the NMDA-evoked [Ca2+]cyt transient. Exposure to SP or SarMet-SP produced a rapid increase in the labeling of phosphorylated-PKCε. In none of the conditions we detected phosphorylation of the NR2B subunit at Ser-1303. Phosphorylation of the NR2B subunit at Tyr1472 was enhanced to a similar extent in cells exposed to NMDA, SP or NMDA+SP, and that enhancement was blocked by BIM. Our findings suggest that NGF and PGE2 may contribute to the injury-evoked sensitization of DRG neurons in part by enhancing their NMDA-evoked [Ca2+]cyt transient in all sized DRG neurons; and that SP may further contribute to the DRG sensitization by enhancing and prolonging the NMDA-evoked increase in [Ca2+]cyt in small- and medium-sized DRG neurons., (Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
7. Open-label exploration of an intravenous nalbuphine and naloxone mixture as an analgesic agent following gynecologic surgery.
- Author
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Gordon AT, Levine JD, Dubois MY, D'Angelo R, Conlon AM, Levacic D, and Lebovits A
- Subjects
- Adult, Dose-Response Relationship, Drug, Drug Combinations, Female, Humans, Infusions, Intravenous, Middle Aged, Pain, Postoperative etiology, Analgesics administration & dosage, Gynecologic Surgical Procedures adverse effects, Nalbuphine administration & dosage, Naloxone administration & dosage, Pain, Postoperative drug therapy
- Abstract
Objective: The purpose of this series was to explore a 12.5:1 fixed-dose ratio of an intravenous nalbuphine and naloxone mixture (NNM) for use in patients following gynecologic surgery., Design and Patients: Open-label, nonrandomized case series. The first series was a dose-ranging investigation for 12 patients following elective total abdominal hysterectomy or myomectomy. In this series, fentanyl was used for intraoperative analgesia, and patients were assigned to a lower NNM (2.5 mg/0.2 mg) or to a higher NNM (5 mg/0.4 mg) dose group. The second series evaluated the fixed dose of 5 mg nalbuphine/0.4 mg naloxone for four patients undergoing ambulatory gynecologic procedures. In the second series, no opioid agents were administered intraoperatively to eliminate the possibility of mu-opioid reversal by naloxone postoperatively., Outcome Measures: Pain control was assessed using a Verbal Pain Scale (0-10). Vital signs, side effects, and adverse events were recorded to determine drug safety., Results: In the first series, there were no adverse events; however, each patient required rescue medication (either morphine or fentanyl). In the second series, two of the four patients reported a reduction in pain following drug administration and did not require any further analgesic agents in the 3-hour postoperative period. One patient had an asymptomatic lowering of heart rate after receiving the drug., Conclusion: Additional research of the unique combination therapy of nalbuphine and naloxone is warranted to further determine its potential clinical efficacy and safety.
- Published
- 2007
- Full Text
- View/download PDF
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