Rajiv Ratan

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Antioxidants, HIF prolyl hydroxylase inhibitors or short interfering RNAs to BNIP3 or PUMA, can prevent prodeath effects of the transcriptional activator, HIF-1alpha, in a mouse hippocampal neuronal line
    Leila R Aminova
    Department of Neurology, Harvard Medical School and BIDMC, Boston, Massachusetts, USA
    Antioxid Redox Signal 10:1989-98. 2008
  2. ncbi request reprint Translation of ischemic preconditioning to the patient: prolyl hydroxylase inhibition and hypoxia inducible factor-1 as novel targets for stroke therapy
    Rajiv R Ratan
    Department of Neurology and Neuroscience, Burke Cornell Medical Research Institute, Weill Medical College of Cornell, White Plains, NY 10605, USA
    Stroke 35:2687-9. 2004
  3. ncbi request reprint Mining genome databases for therapeutic gold: SIM2 is a novel target for treatment of solid tumors
    Rajiv R Ratan
    Department of Neurology, Program in Neuroscience, and Center for Neurodegeneration and Repair, Harvard Medical School and Burke Cornell Medical Research Institute, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Trends Pharmacol Sci 24:508-10. 2003
  4. pmc Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection
    Brett Langley
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 28:163-76. 2008
  5. pmc A large-scale chemical screen for regulators of the arginase 1 promoter identifies the soy isoflavone daidzeinas a clinically approved small molecule that can promote neuronal protection or regeneration via a cAMP-independent pathway
    Thong C Ma
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 30:739-48. 2010
  6. pmc HIF prolyl hydroxylase inhibitors prevent neuronal death induced by mitochondrial toxins: therapeutic implications for Huntington's disease and Alzheimer's disease
    Zoya Niatsetskaya
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    Antioxid Redox Signal 12:435-43. 2010
  7. pmc CD36 is involved in astrocyte activation and astroglial scar formation
    Yi Bao
    Burke Cornell Medical Research Institute, White Plains, New York, USA
    J Cereb Blood Flow Metab 32:1567-77. 2012
  8. pmc Prolyl 4-hydroxylase activity-responsive transcription factors: from hydroxylation to gene expression and neuroprotection
    Ambreena Siddiq
    Burke Medical Research Institute, White Plains, New York 10605, USA
    Front Biosci 13:2875-87. 2008
  9. pmc Hypoxia-inducible factor prolyl 4-hydroxylase inhibition. A target for neuroprotection in the central nervous system
    Ambreena Siddiq
    Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:41732-43. 2005
  10. ncbi request reprint Prosurvival and prodeath effects of hypoxia-inducible factor-1alpha stabilization in a murine hippocampal cell line
    Leila R Aminova
    Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:3996-4003. 2005

Research Grants

Collaborators

Detail Information

Publications49

  1. pmc Antioxidants, HIF prolyl hydroxylase inhibitors or short interfering RNAs to BNIP3 or PUMA, can prevent prodeath effects of the transcriptional activator, HIF-1alpha, in a mouse hippocampal neuronal line
    Leila R Aminova
    Department of Neurology, Harvard Medical School and BIDMC, Boston, Massachusetts, USA
    Antioxid Redox Signal 10:1989-98. 2008
    ..The findings offer strategies for minimizing the prodeath effects of HIF-1 in neurologic conditions associated with hypoxia and oxidative stress, such as stroke and spinal cord injury...
  2. ncbi request reprint Translation of ischemic preconditioning to the patient: prolyl hydroxylase inhibition and hypoxia inducible factor-1 as novel targets for stroke therapy
    Rajiv R Ratan
    Department of Neurology and Neuroscience, Burke Cornell Medical Research Institute, Weill Medical College of Cornell, White Plains, NY 10605, USA
    Stroke 35:2687-9. 2004
    ..Here, we review evidence suggesting that the HIF-1 prolyl hyroxylases are inhibited during ischemic preconditioning and that pharmacological inhibitors of these enzymes are viable targets for stroke therapy...
  3. ncbi request reprint Mining genome databases for therapeutic gold: SIM2 is a novel target for treatment of solid tumors
    Rajiv R Ratan
    Department of Neurology, Program in Neuroscience, and Center for Neurodegeneration and Repair, Harvard Medical School and Burke Cornell Medical Research Institute, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Trends Pharmacol Sci 24:508-10. 2003
  4. pmc Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection
    Brett Langley
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 28:163-76. 2008
    ....
  5. pmc A large-scale chemical screen for regulators of the arginase 1 promoter identifies the soy isoflavone daidzeinas a clinically approved small molecule that can promote neuronal protection or regeneration via a cAMP-independent pathway
    Thong C Ma
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 30:739-48. 2010
    ....
  6. pmc HIF prolyl hydroxylase inhibitors prevent neuronal death induced by mitochondrial toxins: therapeutic implications for Huntington's disease and Alzheimer's disease
    Zoya Niatsetskaya
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    Antioxid Redox Signal 12:435-43. 2010
    ....
  7. pmc CD36 is involved in astrocyte activation and astroglial scar formation
    Yi Bao
    Burke Cornell Medical Research Institute, White Plains, New York, USA
    J Cereb Blood Flow Metab 32:1567-77. 2012
    ..These findings identify CD36 as a novel mediator for injury-induced astrogliosis and scar formation. Targeting CD36 may serve as a potential strategy to reduce glial scar formation in stroke...
  8. pmc Prolyl 4-hydroxylase activity-responsive transcription factors: from hydroxylation to gene expression and neuroprotection
    Ambreena Siddiq
    Burke Medical Research Institute, White Plains, New York 10605, USA
    Front Biosci 13:2875-87. 2008
    ....
  9. pmc Hypoxia-inducible factor prolyl 4-hydroxylase inhibition. A target for neuroprotection in the central nervous system
    Ambreena Siddiq
    Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:41732-43. 2005
    ..Taken together these findings identified low molecular weight and peptide HIF prolyl 4-hydroxylase inhibitors as novel neurological therapeutics for stroke as well as other diseases associated with oxidative stress...
  10. ncbi request reprint Prosurvival and prodeath effects of hypoxia-inducible factor-1alpha stabilization in a murine hippocampal cell line
    Leila R Aminova
    Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:3996-4003. 2005
    ..Together, these data demonstrate that HIF-1 can mediate prodeath or prosurvival responses in the same cell type depending on the injury stimulus...
  11. pmc Proteasome inhibition protects HT22 neuronal cells from oxidative glutamate toxicity
    Klaus van Leyen
    Neuroprotection Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Neurochem 92:824-30. 2005
    ..These findings suggest that caspases can be decoupled from oxidative stress under some conditions, and implicate the ubiquitin/proteasome pathway in neuronal cell death caused by oxidative glutamate toxicity...
  12. ncbi request reprint Remodeling chromatin and stress resistance in the central nervous system: histone deacetylase inhibitors as novel and broadly effective neuroprotective agents
    Brett Langley
    Burke Medical Research Institute, White Plains, NY 10605, USA
    Curr Drug Targets CNS Neurol Disord 4:41-50. 2005
    ..These studies demonstrate that pharmacological HDAC inhibition is a promising therapeutic approach for the treatment of a range of central nervous system disorders...
  13. ncbi request reprint Novel roles for arginase in cell survival, regeneration, and translation in the central nervous system
    Philipp S Lange
    Department of Neurology, Harvard Medical School and the Beth Israel Deaconess Medical Center, Boston MA 02115, USA
    J Nutr 134:2812S-2817S; discussion 2818S-2819S. 2004
    ..Beyond molecular mechanisms, this review will also include relevant clinical findings in patients with neurodegenerative diseases...
  14. ncbi request reprint Oxidative stress-induced death in the nervous system: cell cycle dependent or independent?
    Brett Langley
    Department of Neurology, Harvard Medical School and the Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    J Neurosci Res 77:621-9. 2004
    ..The determining factor for which or how many pathways are induced appears to be context dependent and determined by the level and duration of oxidative stress...
  15. ncbi request reprint The role of iron neurotoxicity in ischemic stroke
    Magdy H Selim
    Department of Neurology, Division of Cerebrovascular Diseases, Harvard Medical School, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Palmer 127, Boston, MA 02215, USA
    Ageing Res Rev 3:345-53. 2004
    ..Understanding the changes in brain iron metabolism and its relationship to neuronal injury in ischemic stroke could provide new therapeutic targets to improve the outcome of stroke patients...
  16. ncbi request reprint Sp1 and Sp3 are oxidative stress-inducible, antideath transcription factors in cortical neurons
    Hoon Ryu
    Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 23:3597-606. 2003
    ..Taken together, these results establish Sp1 and Sp3 as oxidative stress-induced transcription factors in cortical neurons that positively regulate neuronal survival...
  17. pmc Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathway
    Hoon Ryu
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:4281-6. 2003
    ..Together, these results demonstrate that HDAC inhibitors inhibit oxidative death independent of polyglutamine expansions by activating an Sp1-dependent adaptive response...
  18. pmc Effects of intravenous dimethyl sulfoxide on ischemia evolution in a rat permanent occlusion model
    Juergen Bardutzky
    Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
    J Cereb Blood Flow Metab 25:968-77. 2005
    ..This effect was mainly observed in the cortex. Our data suggest that DMSO represents an interesting candidate for acute stroke treatment...
  19. pmc Harnessing hypoxic adaptation to prevent, treat, and repair stroke
    Rajiv R Ratan
    Winifred Masterson Burke Medical Research Institute, White Plains, NY 10605, USA
    J Mol Med (Berl) 85:1331-8. 2007
    ..The breadth and depth of this homeostatic program offers a hopeful alternative to the current pessimism towards stroke therapeutics...
  20. pmc ATF4 is an oxidative stress-inducible, prodeath transcription factor in neurons in vitro and in vivo
    Philipp S Lange
    Burke Medical Research Institute, White Plains, NY 10605, USA
    J Exp Med 205:1227-42. 2008
    ..Collectively, these findings establish ATF4 as a redox-regulated, prodeath transcriptional activator in the nervous system that propagates death responses to oxidative stress in vitro and to stroke in vivo...
  21. pmc Selective inhibition of hypoxia-inducible factor (HIF) prolyl-hydroxylase 1 mediates neuroprotection against normoxic oxidative death via HIF- and CREB-independent pathways
    Ambreena Siddiq
    Department of Neurosciences, Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 29:8828-38. 2009
    ....
  22. pmc Hypoxia inducible factor prolyl 4-hydroxylase enzymes: center stage in the battle against hypoxia, metabolic compromise and oxidative stress
    Ambreena Siddiq
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Neurochem Res 32:931-46. 2007
    ....
  23. pmc HDAC6 is a target for protection and regeneration following injury in the nervous system
    Mark A Rivieccio
    Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Proc Natl Acad Sci U S A 106:19599-604. 2009
    ..Together, these findings define HDAC6 as a potential nontoxic therapeutic target for ameliorating CNS injury characterized by oxidative stress-induced neurodegeneration and insufficient axonal regeneration...
  24. ncbi request reprint In vitro model of oxidative stress in cortical neurons
    Rajiv R Ratan
    Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Methods Enzymol 352:183-90. 2002
  25. doi request reprint Utilization of an in vivo reporter for high throughput identification of branched small molecule regulators of hypoxic adaptation
    Natalya A Smirnova
    Burke Medical Research Institute, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Chem Biol 17:380-91. 2010
    ....
  26. pmc Arginase 1 regulation of nitric oxide production is key to survival of trophic factor-deprived motor neurons
    ALVARO G ESTEVEZ
    Burke Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 26:8512-6. 2006
    ..They also suggest that the resistance of motor neuron subpopulations to trophic factor deprivation may result from increased arginase activity...
  27. pmc Controlled enzymatic production of astrocytic hydrogen peroxide protects neurons from oxidative stress via an Nrf2-independent pathway
    RENEE E HASKEW-LAYTON
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, The Burke Medical Research Institute, White Plains, NY 10605, USA
    Proc Natl Acad Sci U S A 107:17385-90. 2010
    ..These findings demonstrate the utility of rgDAAO for spatially and temporally controlling intracellular H(2)O(2) concentrations to uncover unique astrocyte-dependent neuroprotective mechanisms...
  28. pmc The histone deacetylase inhibitor sodium butyrate protects against cisplatin-induced hearing loss in guinea pigs
    Marie Drottar
    Department of Otolaryngology, Children s Hospital, and the Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Laryngoscope 116:292-6. 2006
    ..The goal of this study was to determine if the antitumor agent sodium butyrate (a histone deacetylase inhibitor) protects against cisplatin ototoxicity when administered systemically...
  29. ncbi request reprint Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis
    Sandra Camelo
    Laboratory of Transcriptional and Immune Regulation, Brigham and Women s Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02139, USA
    J Neuroimmunol 164:10-21. 2005
    ..A transcriptional imbalance in MS may contribute to immune dysregulation and neurodegeneration, and we identify HDAC inhibition as a transcriptional intervention to ameliorate this imbalance...
  30. pmc Mitochondrial cyclic AMP response element-binding protein (CREB) mediates mitochondrial gene expression and neuronal survival
    Junghee Lee
    Neurology Department, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 280:40398-401. 2005
    ....
  31. pmc Genetic variant of BDNF (Val66Met) polymorphism attenuates stroke-induced angiogenic responses by enhancing anti-angiogenic mediator CD36 expression
    Luye Qin
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    J Neurosci 31:775-83. 2011
    ..The results suggest that CD36 inhibition may be a viable strategy to enhance angiogenesis and possible recovery in human stroke victims who are Met homozygotes at codon 66 of the BDNF locus...
  32. ncbi request reprint New perspectives on developing acute stroke therapy
    Marc Fisher
    Department of Neurology, University of Massachusetts Medical School, Worcester 01605, USA
    Ann Neurol 53:10-20. 2003
    ..Combining knowledge from these three areas provides optimism that additional acute stroke therapies can be developed to maximize beneficial functional outcome in the greatest proportion of acute stroke patients possible...
  33. pmc Cause and consequence: mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases
    Gary E Gibson
    Department of Neurology and Neuroscience, Weill Cornell Medical College of Cornell University at Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Biochim Biophys Acta 1802:122-34. 2010
    ..Altogether, our results suggest that increasing KGDHC via inhibition of TGase or via a host of other strategies to be described would be effective therapeutic approaches in age-associated neurodegenerative diseases...
  34. ncbi request reprint Neuroprotective effects of phenylbutyrate in the N171-82Q transgenic mouse model of Huntington's disease
    Gabriella Gardian
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, New York 10021, USA
    J Biol Chem 280:556-63. 2005
    ....
  35. ncbi request reprint The metabolic coupling of arginine metabolism to nitric oxide generation by astrocytes
    Joann M Gensert
    Burke Cornell Medical Research Institute, White Plains, New York 10605, USA
    Antioxid Redox Signal 8:919-28. 2006
    ..Thus, neural and nonneural cells act in concert to affect neuron physiology in an elegantly integrated system. This review focuses on the components of the interaction between astrocytes and neurons in nitric oxide biology...
  36. ncbi request reprint CD81, a cell cycle regulator, is a novel target for histone deacetylase inhibition in glioma cells
    Joann M Gensert
    The Winifred Masterson Burke Cornell Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Neurobiol Dis 26:671-80. 2007
    ..Induction of CD81 expression through HDAC inhibition is a novel strategy to promote growth arrest in glioma cells...
  37. pmc Histone deacetylase inhibitors de-repress tyrosine hydroxylase expression in the olfactory bulb and rostral migratory stream
    Yosuke Akiba
    Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA
    Biochem Biophys Res Commun 393:673-7. 2010
    ....
  38. pmc Novel multi-modal strategies to promote brain and spinal cord injury recovery
    Rajiv R Ratan
    Winifred Masterson Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, USA
    Stroke 40:S130-2. 2009
    ..We conclude that combinations of interventions will be needed to surmount the multiple barriers to recovery in stroke and other types of brain and spinal cord injury recovery...
  39. pmc Translational control of inducible nitric oxide synthase expression by arginine can explain the arginine paradox
    Junghee Lee
    Deparment of Neurology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:4843-8. 2003
    ..These results provide an explanation for the arginine paradox for iNOS and define a distinct mechanism by which a substrate can regulate the activity of its associated enzyme...
  40. ncbi request reprint The c-Raf inhibitor GW5074 provides neuroprotection in vitro and in an animal model of neurodegeneration through a MEK-ERK and Akt-independent mechanism
    Paul C Chin
    Department of Molecular and Cell Biology, University of Texas at Dallas, Richardson, Texas 75083, USA
    J Neurochem 90:595-608. 2004
    ....
  41. pmc Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration
    Savita Khanna
    Laboratory of Molecular Medicine, Department of Surgery, Dorothy M Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, Ohio 43210, USA
    J Biol Chem 278:43508-15. 2003
    ..These findings lend further support to alpha-tocotrienol as a potent neuroprotective form of vitamin E...
  42. ncbi request reprint Role of cyclooxygenase-2 induction by transcription factor Sp1 and Sp3 in neuronal oxidative and DNA damage response
    Junghee Lee
    Geriatric Research Education and Clinical Center, Bedford Veteran s Affairs Medical Center, 200 Springs Rd, Bedford, MA 01730, USA
    FASEB J 20:2375-7. 2006
    ..These results indicate that in primary neurons Sp1 and Sp3 play an essential role in the modulation of COX-2 transcription, which mediates neuronal homeostasis and survival by preventing DNA damage in response to neuronal stress...
  43. ncbi request reprint Arginase I and polyamines act downstream from cyclic AMP in overcoming inhibition of axonal growth MAG and myelin in vitro
    Dongming Cai
    Biology Department, Hunter College, City University of New York, 695 Park Avenue, New York, NY 10024, USA
    Neuron 35:711-9. 2002
    ..Over-expressing Arginase I in maturing DRGs blocks that switch. Arginase I and polyamines are more specific targets than cAMP for intervention to encourage regeneration after CNS injury...
  44. ncbi request reprint Therapeutic effects of cystamine in a murine model of Huntington's disease
    Alpaslan Dedeoglu
    Geriatric Research Education and Clinical Center, Bedford Veterans Affairs Medical Center, Bedford, Massachusetts 01730, USA
    J Neurosci 22:8942-50. 2002
    ..These findings are consistent with the hypothesis that transglutaminase activity may play a role in the pathogenesis of HD, and they identify cystamine as a potential therapeutic strategy for treating HD patients...
  45. ncbi request reprint Novel changes in gene expression following axotomy of a sympathetic ganglion: a microarray analysis
    Kristen L Boeshore
    Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA
    J Neurobiol 59:216-35. 2004
    ..In addition, the data suggest a potential role for putrescine and spermidine, acting downstream of arg I, in the regenerative process...
  46. ncbi request reprint cAMP response element binding protein family transcription factors: the Holy Grail of neurological therapeutics?
    Rajiv R Ratan
    Ann Neurol 56:607-8. 2004
  47. pmc Oxygen-sensitive reset of hypoxia-inducible factor transactivation response: prolyl hydroxylases tune the biological normoxic set point
    Savita Khanna
    Laboratory of Molecular Medicine, Davis Heart and Lung Research Institute, Department of Surgery, The Ohio State University Medical Center, Columbus, 43210, USA
    Free Radic Biol Med 40:2147-54. 2006
    ..siRNA dependent knockdown of PHD expression revealed that O(2)-sensitive regulation of PHD may contribute to tuning the normoxic set point in biological cells...
  48. pmc Chemotherapy for the brain: the antitumor antibiotic mithramycin prolongs survival in a mouse model of Huntington's disease
    Robert J Ferrante
    Geriatric Research and Education and Clinical Center, Veterans Administration Medical Center, Bedford, MA, USA
    J Neurosci 24:10335-42. 2004
    ..Because it is Food and Drug Administration-approved, mithramycin is a promising drug for the treatment of HD...
  49. pmc Antioxidants modulate mitochondrial PKA and increase CREB binding to D-loop DNA of the mitochondrial genome in neurons
    Hoon Ryu
    Geriatric Research Education and Clinical Center, Veteran s Affairs Medical Center, Bedford, MA 01730, USA
    Proc Natl Acad Sci U S A 102:13915-20. 2005
    ..These results suggest that the regulation of mitochondrial function via the mitochondrial PKA and CREB pathways may underlie some of the salutary effects of DFO in neurons...

Research Grants9

  1. NEUROPROTECTIVE GENE INDUCTION BY ANTIOXIDANT IRON CHELA
    Rajiv Ratan; Fiscal Year: 2002
    ..Furthermore, these studies also promise to further define mechanisms of protection by small molecule iron chelators. ..
  2. Arginase and Regulation of Nitric Oxide Synthase in ALS
    Rajiv Ratan; Fiscal Year: 2004
    ..These studies promise to enhance our understanding of how arginine about metabolism, including the synthesis of NO, is regulated in the normal and abnormal nervous system. ..