Search

Your search keyword '"Lecchini Sergio"' showing total 363 results
Start Over Author "Lecchini Sergio"
363 results on '"Lecchini Sergio"'

1. Medical healthcare use in Parkinson's disease: survey in a cohort of ambulatory patients in Italy

Author

Frigo Gianmario, Pacchetti Claudio, Riboldazzi Giulio, Calandrella Daniela, Michielotto Donatella, Martignoni Emilia, Cosentino Marco, Nappi Giuseppe, and Lecchini Sergio

Subjects
Public aspects of medicine, RA1-1270
Abstract

Abstract Background Parkinson's disease (PD) is a chronic neurodegenerative disease which at present has no cure, and it usually results in severe disability. The burden of PD increases as the illness progresses, resulting in the extensive utilisation of both health and community services. Knowledge of healthcare use patterns and of their determinants may greatly contribute to improve patient care, however few studies have examined this issue in PD. The present study was devised to describe the type of and reasons for medical healthcare resource use in persons with PD attending a Centre for PD and Movement Disorders, and to examine drug prescriptions issued on such occasions. Methods The study was a retrospective, cross-sectional survey in a cohort of ambulatory patients with PD, conducted by means of standard interviews. Results In the year before the study, 92 (70.8%) of 130 patients used medical healthcare resources: 1/5 of the patients was admitted to hospital, 1/5 to emergency room, 2/5 were visited by a non-neurology specialist, and 1/4 by the GP. Reasons were: nearly 20% programmed hospital admissions and visits, and more than 25% injuries and musculo-skeletal diseases. Other conditions typically occurring in PD (e.g. dementia, diabetes and cardio- and cerebro-vascular disease) were less frequently involved. On such occasions, drugs for PD were occasionally changed, however drug prescriptions for other indications were issued to more than 66% of the patients. Conclusion Several physicians other than the neurologist may take care of PD patients on different occasions, thus emphasising the need for communication between the reference neurologist and other physicians who from time to time may visit the patient.

Published
2005
Full Text
View/download PDF

2. Intracellular calcium changes induced by the endozepine triakontatetraneuropeptide in human polymorphonuclear leukocytes: role of protein kinase C and effect of calcium channel blockers

Author

Fietta Anna M, Frigo Giuseppina, Cattaneo Simona, Ferrari Marco, Cosentino Marco, Marino Franca, Lecchini Sergio, and Frigo Gian

Subjects
polymorphonuclear leukocytes, triakontatetraneuropeptide, intracellular Ca++, interleukin-8, protein kinase C, Ca++ channel blockers, T-type Ca++-channels., Medicine, Cytology, QH573-671
Abstract

Abstract Background The endozepine triakontatetraneuropeptide (TTN) induces intracellular calcium ([Ca++]i) changes followed by activation in human polymorphonuclear leukocytes (PMNs). The present study was undertaken to investigate the role of protein kinase (PK) C in the modulation of the response to TTN by human PMNs, and to examine the pharmacology of TTN-induced Ca++ entry through the plasma membrane of these cells. Results The PKC activator 12-O-tetradecanoylphorbol-13-acetate (PMA) concentration-dependently inhibited TTN-induced [Ca++]i rise, and this effect was reverted by the PKC inhibitors rottlerin (partially) and Ro 32-0432 (completely). PMA also inhibited TTN-induced IL-8 mRNA expression. In the absence of PMA, however, rottlerin (but not Ro 32-0432) per se partially inhibited TTN-induced [Ca++]i rise. The response of [Ca++]i to TTN was also sensitive to mibefradil and flunarizine (T-type Ca++-channel blockers), but not to nifedipine, verapamil (L-type) or ω-conotoxin GVIA (N-type). In agreement with this observation, PCR analysis showed the expression in human PMNs of the mRNA for all the α1 subunits of T-type Ca++ channels (namely, α1G, α1H, and α1I). Conclusions In human PMNs TTN activates PKC-modulated pathways leading to Ca++ entry possibly through T-type Ca++ channels.

Published
2004
Full Text
View/download PDF

44. Role of neuronal and inducible nitric oxide synthases in the guinea pig ileum myenteric plexus during in vitro ischemia and reperfusion

Author

Giaroni, Cristina, Marchet, S., Carpanese, E., Prandoni, V., Oldrini, R., Bartolini, B., Moro, E., Vigetti, Davide, Crema, F., Lecchini, Sergio, and Frigo, G. M.

Subjects
Male, guinea pig ileum, nitric oxide synthase, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Guinea Pigs, Myenteric Plexus, Nitric Oxide Synthase Type II, in vitro ischemia/reperfusion, myenteric plexus, nitric oxide, Nitric Oxide Synthase Type I, Nitric Oxide, Real-Time Polymerase Chain Reaction, Immunohistochemistry, Ileum, Reperfusion Injury, Animals, RNA, Messenger
Abstract

Intestinal ischemia and reperfusion (I/R) injury leads to abnormalities in motility, namely delay of transit, caused by damage to myenteric neurons. Alterations of the nitrergic transmission may occur in these conditions. This study investigated whether an in vitro I/R injury may affect nitric oxide (NO) production from the myenteric plexus of the guinea pig ileum and which NO synthase (NOS) isoform is involved.The distribution of the neuronal (n) and inducible (i) NOS was determined by immunohistochemistry during 60 min of glucose/oxygen deprivation (in vitro ischemia) followed by 60 min of reperfusion. The protein and mRNA levels of nNOS and iNOS were investigated by Western-immunoblotting and real time RT-PCR, respectively. NO levels were quantified as nitrite/nitrate.After in vitro I/R the proportion of nNOS-expressing neurons and protein levels remained unchanged. nNOS mRNA levels increased 60 min after inducing ischemia and in the following 5 min of reperfusion. iNOS-immunoreactive neurons, protein and mRNA levels were up-regulated during the whole I/R period. A significant increase of nitrite/nitrate levels was observed in the first 5 min after inducing I/R and was significantly reduced by N(ω) -propyl-l-arginine and 1400 W, selective inhibitors of nNOS and iNOS, respectively.Our data demonstrate that both iNOS and nNOS represent sources for NO overproduction in ileal myenteric plexus during I/R, although iNOS undergoes more consistent changes suggesting a more relevant role for this isoform in the alterations occurring in myenteric neurons following I/R.

Published
2013

50. Protein kinase C modulates NMDA receptors in the myenteric plexus of the guinea pig ileum during in vitro ischemia and reperfusion

Author

Giaroni, Cristina, Zanetti, E, Giuliani, D, Oldrini, R, Marchet, S, Moro, E, Borroni, P, Trinchera, MARCO GIUSEPPE, Crema, F, Lecchini, Sergio, and Frigo, G.

Subjects
Benzophenanthridines, Male, Sulfonamides, Guinea Pigs, Myenteric Plexus, In Vitro Techniques, Isoquinolines, Kynurenic Acid, Receptors, N-Methyl-D-Aspartate, 2-Amino-5-phosphonovalerate, Ileum, Reperfusion Injury, Models, Animal, Animals, Phosphorylation, Protein Kinase C
Abstract

Ischemic episodes lead to profound functional and structural alterations of the gastrointestinal tract which may contribute to disorders of intestinal motility. Enhancement of glutamate overflow and the consequent activation of NMDA (N-methyl-D-aspartate) receptors may participate to such changes by modulating different enteric neurotransmitter systems, including cholinergic motor pathways.The molecular mechanism/s underlying activation of NMDA receptors in the guinea pig ileum were investigated after glucose/oxygen deprivation (in vitro ischemia) and during reperfusion.The number of ileal myenteric neurons positive for NR1, the functional subunit of NMDA receptors, and its mRNA levels were unchanged after in vitro ischemia/reperfusion. In these conditions, the protein levels of NR1, and of its phosphorylated form by protein kinase C (PKC), significantly increased in myenteric neurons, whereas, the levels of NR1 phosphorylated by protein kinase A (PKA) did not change, with respect to control values. Spontaneous glutamate overflow increased during in vitro ischemia/reperfusion. In these conditions, the NMDA receptor antagonists, D(-)-2-amino-5-phosphonopentanoic acid [(D)-AP5] (10 μmol L(-1)) and 5,7-dichlorokynurenic acid (5,7-diClKyn acid) (10 μmol L(-1)) and the PKC antagonist, chelerythrine (1 μmol L(-1)), but not the PKA antagonist, H-89 (1 μmol L(-1)), were able to significantly depress the increased glutamate efflux.The present data suggest that in the guinea pig ileum during in vitro ischemia/reperfusion, NR1 protein levels increase. Such event may rely upon posttranscriptional events involving NR1 phosphorylation by PKC. Increased NR1 levels may, at least in part, explain the ability of NMDA receptors to modulate a positive feedback on ischemia/reperfusion-induced glutamate overflow.

Published
2010

Catalog

Books, media, physical & digital resources
See catalog results