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BIBLIOGRAFIA [1] Kiessling, M.; Gauss, P. Stimulus-trascription coupling in focal cerebral ischemia.

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BIBLIOGRAFIA

[1] Kiessling, M.; Gauss, P. Stimulus-trascription coupling in focal cerebral ischemia. Brain Pathol. 4(1), 77-83, 1994.

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[18] Yelin, R. & S. Schuldiner. The pharmacological profile of the vesicular monoamine transporter resembles that of multidrug transporters. FEBS Lett. 377. 201–217. 1995.

[19] Greenamyre, J.T. Mitochondrial dysfunction in Parkinson’s disease. Biochem. Soc. Symp. 66. 85–97. 1999.

[20] Mohanakumar K. P & D. Muralikrishnan. Neurochemical mechanisms underlying neuroprotective actions of bromocriptine, salicylate, D- and L-deprenyl in neurodegeneration caused by MPTP. In Neurotoxic Factors in Parkinson’s Disease and Related Disorders. M.A. Collins & A. Storch. 289–293. 2000.

[21] Dykens, J.A. Isolated cerebral and cerebellar mitochondria produce free radicals when exposed to elevated Ca2+ and Na+: implications for neurodegeneration. J. Neurochem. 63. 584–591. 1994.

[22] Alderton, W.K., Cooper, C.E. and Knowles. Biochem. J. 357. 593–615. 2001. [23] Willmot, M., Gray. Nitrix Oxide. 12. 141-149. 2005.

[24] Furfine, E. S.; Harmon, M. F.; Selective inhibition of constitutive nitric oxide synthase by L-N-nitroarginina. Biochemistry. 32. 8512-8517. 1993.

[25] Yamamoto, K.; Shimamura, K. Effects of N-nitro-L-arginine on the blood pressure of spontaneously hypertensive rats with different degrees of hypertension. Clin. Exp. Hypertens. 23 (7). 533-544. 2001.

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53 [26] Huang, H.; Martasek, P. Syntheses and evaluation of dipeptide amides containing N-nitroarginine and D-2,4-diaminobutyric acid as inhibitors of neuronal nitric oxide synthase. J. Enzyme Inhib. 16. 233-239. 2001.

[27] Griffith, O.W. & D.J. Stuehr. Nitric oxide synthase: properties and catalytic mechanism. Annu. Rev. Physiol. 57. 707–736. 1995.

[28] Garthwaite, G. & J. Garthwaite. NO does not mediate glutamate neurotoxicity, nor is it neuroprotective, in rat brain slices. Neuropharmacology 33. 1431–1438. 1994.

[29] Stamler, J.S. Redox signaling: nitrosylation and related target interactions of nitric oxide. Cell 78. 931–936. 1994.

[30] Lipton, S.A. & J.S. Stamler. Actions of redox-related congeners of nitric oxide at the NMDA receptor. Neuropharmacology. 33. 1229–1233. 1994.

[31] Lipton , S.A. Neuronal protection and descruction by NO. Cell Death Differ. 6. 943-951 . 1999 .

[32] Lipton , S.A. Neuronal protection and descruction by NO. Cell Death Differ. 6. 943-951 . 1999 .

[33] Ontèniente, B ;Couriaud. The mechanisms of cell death in focal cerebral ischemia higlihght neuroprotective perpectives by anti-caspase therapy. Biochem Pharmacol. 66(8).1643-9. 2003.

[34] Kruidering , M.& G . I. Evan. Caspase-8 in apoptostis: the beginning of the and? IUBMB Life. 50 . 85-90. 2000.

[35] Willmot, M; Gipson . Free Radical . Biol . Med . 39.402-425 . 2005.

[36] Fiorucci, S. NO-releasing NSAIDs are caspase inhibitors. Trends Immunol. 22. 232-235. 2001.

[37] Khaldi, A., A. Zauner. Measurement of nitric oxide and brain tissue oxygen tension in patiens after severe subarachnoid hemorrhage. Neurosurgery. 49. 33-40- 2001.

[38] Iadecola, C. Bright and dark sides of nitric oxide in ischemic brain injury. Trend. Neurosci. 20. 132-139. 1993.

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