Marina Melone

Professor of Neurology
Former Director of the CIRN

Name Marina
Surname Melone
Institution Università degli Studi della Campania Luigi Vanvitelli
Telephone +39 081 566 6810
Mobile +39 333 956 6365
Address Department of Medical, Surgical, Neurological, Metabolic Sciences, and Aging, 2nd Division of Neurology, Center for Rare Diseases, University of Campania "Luigi Vanvitelli", Napoli, Italy
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Marina Melone


  • Modulation of cytokine production in activated human monocytes by somatostatin.

    Publication Date: 01/10/1996 on Neuropeptides
    by Peluso G, Petillo O, Melone MA, Mazzarella G, Ranieri M, Tajana GF

    The immunosuppressor effects of the widely distributed neuropeptide somatostatin were examined on purified peripheral blood human monocytes. Somatostatin, at concentrations thought to be physiologic (10(-10)-10(-7) M), regulated monocyte/macrophage responses to (LPS) stimulation, as reflected by interleukin production. In particular, somatostatin had direct inhibitory effects on TNF-alpha, IL-1 beta, and IL-6 secretion by LPS-activated monocytes, while the decrease on IL-8 synthesis was modulated mainly by the action of somatostatin on TNF-alpha and IL-1 beta. In fact, the addition of these two inflammatory cytokines to the monocyte culture medium was able to induce IL-8 expression, as demonstrated by mRNA analysis, also in presence of the neuropeptide. Although somatostatin affected IL-8 production in an indirect way, it suppressed directly the chemotactic response of neutrophils to IL-8. Finally, somatostatin downregulation of monocyte activation was confirmed by the decrease of HLA-DR expression on cell plasma membranes (52% versus 33%). Our results confirm that somatostatin exerts preferential effects on the suppression of immunoreactions by modulating cytokine production and activity.

  • Myotonic dystrophy: antisense oligonucleotide inhibition of DMPK gene expression in vitro.

    Publication Date: 25/04/1996 on Biochemical and biophysical research communications
    by Galderisi U, Cipollaro M, Melone MA, Iacomino G, Di Bernardo G, Galano G, Contrufo R, Zappia V, Cascino A
    DOI: 10.1006/bbrc.1996.0668

    Antisense phosphorothioate oligonucleotides, targeted against the first codon starting region of DMPK mRNA, were successfully used in K562 and HepG2 cells to decrease DMPK expression. The most effective antisense oligo, MIO1, when added to K562 cells, shows a 75% reduction of the DMPK gene expression 6 hours after addition. The same molecule, when encapsulated in liposomes, delays myotonin mRNA decrease at 24 hours after cell treatment. This considerable success with such inhibition in vitro could be utilised to generate a cell model to study myotonic dystrophy (DM) chemio-physiological alterations.

  • Regenerated EDL muscle of rats requires innervation to maintain AChE molecular forms.

    Publication Date: 01/08/1990 on Muscle & nerve
    by Melone MA, De Lucia D, Fratta M, Cotrufo R
    DOI: 10.1002/mus.880130809

    Extensores digitorum longi of rats, infarcted and denervated by different surgical procedures, were used to analyze by biochemical and cytochemical methods the acetylcholinesterase (AChE) changes during muscle degeneration, regeneration, and early or delayed reinnervation. Biochemical tests showed that the regenerating muscle produces globular AChE forms (36% of controls) and small amounts of A12 (16S) asymmetric form (5% of controls); at the end of the regeneration, innervation and electromechanical function are required for the complete recovery of globular forms, and are absolutely critical to prevent A12 (16S) disappearance. Cytochemical observations showed that, unlike nicotinic receptor, AChE deposited at the neuromuscular junction before ischemic necrosis is protected from breakdown, as is the basal lamina of muscle fibers. Taken together, these observations contribute to the understanding of the factors that play a critical role in muscle repair and are, therefore, of clinical relevance.

  • Phenotype heterogeneity among hemizygotes in a family biochemically screened for adrenoleukodystrophy.

    Publication Date: 01/04/1987 on American journal of medical genetics
    by Cotrufo R, Melone MA, Monsurro MR, Di Iorio G, Carella C, Moser HW
    DOI: 10.1002/ajmg.1320260410

    We report on two clinically, neurologically normal relatives of a boy affected by adrenoleukodystrophy (ALD); they were found repeatedly to have the biochemical defect of an ALD hemizygote. The assay consisted in the determination of very-long-chain fatty acids in lyophilized and reconstituted plasma. While no evidence of neurologic disease (leukodystrophy or myeloneuropathy) was present in these hemizygotes, adrenocortical insufficiency provoking compensatory high ACTH release was found in both. These findings should be taken into consideration when counseling families in which cases with clinically expressed ALD are represented in several generations.

  • Acetylcholinesterase in neuroblastoma and neuroblastoma x glioma hybrid cells: cellular localization and molecular forms.

    Publication Date: 01/01/1987 on International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
    by Melone MA, Longo A, Taddei C, Augusti-Tocco G

    The cellular localization of acetylcholinesterase (AChE) was investigated at the electron microscope (E.M.) in a neuroblastoma and neuroblastoma x glioma hybrid line, which differ for their ability to establish synaptic contacts. Only cells of the latter line show association of AChE to the plasmamembrane, while in the former the activity is mainly intracellular. Sucrose sedimentation analysis of AChE molecular forms has shown no significant differences in the distribution of the two forms, G2 and G4, between the two cell lines. On the contrary a marked difference is observed in the ability of the cell to release the enzyme in the culture medium. In fact the cells lacking AChE on their surface release in the medium a much higher proportion of their enzyme, than the cells showing AChE association to their plamamembrane. The possible role of two alternative fates for AChE, secretion or membrane insertion, in determining the observed differences of enzyme localization is discussed.

  • [L-dopa-resistant parkinsonism with cerebral atrophy: striato-nigral degeneration? 2 cases].

    Publication Date: 01/02/1981 on Acta neurologica
    by Dell'Aria V, Ciannella L, Melone MA
  • [L-dopa-resistant Parkinson's disease with cerebral atrophy: striato-nigral degeneration?].

    Publication Date: 01/01/1981 on Acta neurologica. Quaderni
    by Dell'Aria V, Ciannella L, Melone MA
  • [Some aspects of hysteria: a clinical study].

    Publication Date: 01/01/1979 on Acta neurologica. Quaderni
    by Brandonisio A, Melone MA, Valiani R
  • [Preliminary results of isolation and identification of rat sarcolemma and the effect of denervation on membrane-bound neuraminidase activity].

    Publication Date: 01/01/1979 on Acta neurologica. Quaderni
    by Monsurrò MR, Cotrufo R, Melone MA, Metafora S, Felsani A, Prisco PP, Del Rio A, Tajana GF
  • [An unusual case of poisoning due to dithiocarbamates with serious neurological symptoms. Analogy with poisoning due to organo-phosphate substances].

    Publication Date: 01/01/1979 on Acta neurologica. Quaderni
    by Melone MA, Brandonisio A, Valiani R, Sepe O