University of Malta
 

Dr Mario Valentino
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Dr Mario Valentino

Qualification and Experience

Senior lecturer in neuroscience at the University of Malta, Department of Pathology. Dr Mario Valentino obtained his Ph.D. in 2001 with distinction through a scholarship awarded from the Max Planck Institute for Neurological Research ,Cologne Germany following a brief training period as Research Guest Fellow. Under the supervision of renowned neuroscientists, W.-D Heiss and R.Graf, his work involved the investigation of the haemodynamic and molecular mechanisms of ischemic brain damage caused by strokes during ischemia and reperfusion in live animals. After his return to Malta, he was awarded a 3-year post-doctoral fellowship in the Dept of Neurology, Washington University, St.Louis. MO (D.W Choi and M.P. Goldberg) and the Hope Centre For Neurological Disorders, St.Louis, MO, USA to study the neurobiology of glial-axon interactions in white matter injury.  He is currently an active member of The Society of Neuroscience and COSIB- an international group of clinical and basic scientists working on various kinds of brain injury. Dr Valentino has served as ad hoc reviewer for the editorial boards of the journals, Stroke and Journal of Cerebral Blood Flow and Metabolism and supervised several student doctoral projects in his field.
Research in his laboratory is directed to understanding cellular mechanisms of brain damage and recovery in acute neurological disorders. His current work focuses on hypoxic-ischemic injury of the brain's white matter. The research focus involves a multiparametric approach based on a combination of techniques broadly aimed to shed some light on specific pathways of damage to both axonal and glial damage. Relatively little is known about specific pathways leading to structural and functional disruption of axons and glial cells in white matter. Experimental methods used in the lab include cell culture, brain slice, and in vivo stroke models along with the development of methods for the visualization of cell-specific expression of fluorescent proteins from transgenic mice with advanced optical microscopy techniques. The laboratory benefits tremendously from the collaborative environment provided by the Washington University's neuroscience community and the Max Planck Institute for Neurological Research.


Research Capacity

Facilities to perform in vitro and in vivo models of spinal cord injury and stroke on mice and rats. Imaging of brain slices from transgenic mice in interface and submersible chambers with combined electrophysiological recordings and drug maniplulation during oxygen-glucose deprivation and glucose deprivation.

Available equipment – Major items for collaborative Sharing include Vibratome, Fluoresence microscopy, Multiple electrophysiological rigs and setups (Harvard Instruments), Horizontal electrode puller, Brain slice chambers (Harvard Instruments), Fast Cyclic Voltammetry (Millar Voltameters), Microdialysis, Nitric oxide and free radical analyser (WPI, Apollo 4000).

Expertise include In vivo models of stroke (intra-luminal approach and trans-orbital approach) in rodent and higher animals; Surgical techniques; Brain slices; Immunocytochemistry; Microdialysis with combined off-line HPLC anylsis of neuroactive compounds; Monitoring of nitric oxide in vivo through the use of porphyrin-based electrodes; Electrode fabrication (ion-selective, NO, calomel electrodes) for in vivo monitoring; Advanced imaging techniques, including confocal and multiphoton microscopy, deconvolution; Voltammetry and amperommetry.

Research Interests



Selected References

Borg I, Valentino M, Fiorini A, Felice AE. Hb Setif [alpha 94(G1)Asp-->Tyr] in Malta.  Hemoglobin, 1997, 21(1): 91-96.
 
Valentino M, Graf R, Toyota S, W.-D. Heiss. Glutamate and purine catabolites in relation to free radical production during focal ischemia-reperfusion: an in vivo study in cats.  J. Cereb. Blood Flow Metab. 2001, Suppl.
 
Toyota S, Valentino M, Graf R, W.-D. Heiss.  J. Cereb. Blood Flow Metab. 2001, Suppl.   
Malignant edema formation following transient MCA occlusion: decrease of cerebral perfusion pressure causes secondary elevation of glutamate.
 
Toyota S, Valentino M, Graf R, W.-D. Heiss. Extracellular glutamate accumulates only in final, ischemic stage of progressive epidural mass lesion in cats.  J. Cereb Blood Flow Metab. 2001, Suppl.
 
Toyota S, Graf R, Dohmen C, Valentino M, Grond M, Wienhard K, Heiss W.-D. Elevation of extracellular glutamate in the final, ischemic stage of progressive epidural mass lesion in cats.  J.Neurotrauma, 2001; 18(12): 1349-57.
 
Brain activation and CBF control (Tomida M, Kanno I and Hamel E, editors, 2001; ISBN:0444508740). Ischemic depression of neuronal activity: real time comparison between DC potential changes and alterations of ion and transmitter homeostasis pp 465-474.
 
Toyota S,Valentino M, Graf R, Yoshimine T, Heiss W.-D. Malignant infarction in cats after prolonged middle cerebral artery occlusion: glutamate elevation related to decrease of cerebral perfusion pressure. Stroke, 2002; 33(5): 1383-91.
 
Graf R, Toyota S, Valentino M, Dohmen C, Heiss W-D.  Malignant infarction in cats following prolonged middle cerebral artery occlusion: volumes of severe blood flow reduction predict fatal outcome.  PET 2003, Conference.
 
Heiss W.-D, Dohmen C, Sobesky J, Kracht L, Bosche B, Staub F, Toyota S, Valentino M, Graf R.Identification of malignant brain edema after hemispheric stroke by PET-imaging and microdialysis.    Acta Neurochir 2003; 86: 237-40.
 
Toyota S, Valentino M, Graf R, Yoshimine T, Heiss W.-D. Prediction of malignant infarction: perifocal neurochemical monitoring following prolonged MCA occlusion in cats.   Acta Neurochir, 2003; 86: 153-7.
 
Valentino M, Inoue I, Macklin W.B, Kirchhoff F, and Goldberg M.P.  White matter hypoglycemic injury revealed by multiphoton microscopy in transgenic mice.  Program No. 1018.6, 2004 Abstract Viewer/Itenary Planner, Washington DC: Society for Neuroscience, San Diego, Oct 2004.
 
Ness J.K, Valentino M, McIver S and  Goldberg M.P. Identification of oligodendrocytes in experimental disease models.  Glia. 2005; 50(4):321-8.
 
Valentino M,.Tenkova T, Inauoe I,Yang P, Yamada K.A and Goldberg M Delayed axonal degeneration after glucose deprivation is attenuated by AMPA/Kainate receptor blockade.. (Submitted to J.Neuroscience).
 
M.Valentino and M.P.Goldberg.Transient oxygen glucose deprivation in Plp-EGFP transgenic mice induces irreversible oligodendrocyte injury during the early stage of energy deprivation. (Submitted to  J. Comp. Neurol).

Research Funds

1) Deutsche Forschungsgemeinschaft (BMBF Kompetenznetz Schlaganfall): Cerebral Ischemia (1999-2001)EUR 90,000.
 
2) NIH grants P01 NS032636 (2003-2005).Mechanisms of injury to oligodendrocytes and axons in cerebral ischaemia $ 100,000.
 
3) American Heart Association postdoctoral research grant, R01 NS36265 (2003-2005) $ 30,000.
 
4) University of Malta Research Grant-Pathophysiology and treatment of stroke (2001)EUR 90,000.
 
5) University of Malta Research Grant-The pathophysiology and neurobiology of cerebral deep white matter stroke (2006) EUR 65,000.
 
6) Max Planck Society (2007). Research project: COSIB. Periinfarct depolarizations. EUR 3000 as travel grant.

Calendar
 
 
Last Updated: 19 February 2010

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