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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.
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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.
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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.
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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.
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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.
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Publication Date:
01/02/1981
on Acta neurologica
by Dell'Aria V, Ciannella L, Melone MA
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Publication Date:
01/01/1981
on Acta neurologica. Quaderni
by Dell'Aria V, Ciannella L, Melone MA
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Publication Date:
01/01/1979
on Acta neurologica. Quaderni
by Brandonisio A, Melone MA, Valiani R
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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
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Publication Date:
01/01/1979
on Acta neurologica. Quaderni
by Melone MA, Brandonisio A, Valiani R, Sepe O
