Search

Your search keyword '"Tartari, S"' showing total 132 results
Start Over Author "Tartari, S"
132 results on '"Tartari, S"'

9. Abdominal ultrasonography as first-line examination in patients with non-specific abdominal pain from emergency department (ED): concordance with CT findings

Author

Vizzuso, A., Ribuffo, D., Pellegrino, F., Ferrante, Z., Tartari, S., Giganti, M., and Benea, G.

Subjects
genetic structures, Gastrointestinal tract, Emergency, Abdomen, Ultrasound, Diagnostic procedure, CT, NO
Abstract

Aims and objectives Methods and materials Results Conclusion Personal information References, Aims and objectives: Acute abdominal pain of non-traumatic origin is one of the most common causes of Emergency Department (ED) admission [1] . Acute appendicitis, diverticulitis, cholecystitis and bowel obstruction are common causes of acute abdominal pain. Other...

Published
2018

10. Corrigendum to “Vascular pentraxin 3 controls arterial thrombosis by targeting collagen and fibrinogen induced platelets aggregation” [Biochim. Biophys. Acta, 1862 (2016) 1182–1190]

Author

Bonacina, F., primary, Barbieri, S.S., additional, Cutuli, L., additional, Amadi, P., additional, Don, A., additional, Sironi, M., additional, Tartari, S., additional, Mantovani, A., additional, Bottazzi, B., additional, Garlanda, C., additional, Tremoli, E., additional, Catapano, A.L., additional, and Norata, G.D., additional

Published
2019
Full Text
View/download PDF

13. An acidic microenvironment sets the humoral pattern recognition molecule PTX3 in a tissue repair mode

Author

Doni, A, Musso, T, Morone, D, Bastone, A, Zambelli, V, Sironi, M, Castagnoli, C, Cambieri, I, Stravalaci, M, Pasqualini, F, Laface, I, Valentino, S, Tartari, S, Ponzetta, A, Maina, V, Barbieri, S, Tremoli, E, Catapano, A, Norata, G, Bottazzi, B, Garlanda, C, Mantovani, A, Mantovani, A., ZAMBELLI, VANESSA, Doni, A, Musso, T, Morone, D, Bastone, A, Zambelli, V, Sironi, M, Castagnoli, C, Cambieri, I, Stravalaci, M, Pasqualini, F, Laface, I, Valentino, S, Tartari, S, Ponzetta, A, Maina, V, Barbieri, S, Tremoli, E, Catapano, A, Norata, G, Bottazzi, B, Garlanda, C, Mantovani, A, Mantovani, A., and ZAMBELLI, VANESSA

Abstract

Pentraxin 3 (PTX3) is a fluid-phase pattern recognition molecule and a key component of the humoral arm of innate immunity. In four different models of tissue damage in mice, PTX3 deficiency was associated with increased fibrin deposition and persistence, and thicker clots, followed by increased collagen deposition, when compared with controls. Ptx3-deficient macrophages showed defective pericellular fibrinolysis in vitro. PTX3-bound fibrinogen/fibrin and plasminogen at acidic pH and increased plasmin-mediated fibrinolysis. The second exon-encoded N-terminal domain of PTX3 recapitulated the activity of the intact molecule. Thus, a prototypic component of humoral innate immunity, PTX3, plays a nonredundant role in the orchestration of tissue repair and remodeling. Tissue acidification resulting from metabolic adaptation during tissue repair sets PTX3 in a tissue remodeling and repair mode, suggesting that matrix and microbial recognition are common, ancestral features of the humoral arm of innate immunity.

Published
2015

14. An acidic microenvironment sets the humoral pattern recognition molecule PTX3 in a tissue repair mode

Author

Doni, A., Musso, T., Morone, D., Bastone, A., Zambelli, V., Sironi, M., Castagnoli, C., Cambieri, I., Stravalaci, M., Pasqualini, F., Laface, I., Valentino, S., Tartari, S., Ponzetta, A., Maina, V., Barbieri, S., Tremoli, E., Catapano, A., Norata, Giuseppe, Bottazzi, B., Garlanda, C., Mantovani, A., Doni, A., Musso, T., Morone, D., Bastone, A., Zambelli, V., Sironi, M., Castagnoli, C., Cambieri, I., Stravalaci, M., Pasqualini, F., Laface, I., Valentino, S., Tartari, S., Ponzetta, A., Maina, V., Barbieri, S., Tremoli, E., Catapano, A., Norata, Giuseppe, Bottazzi, B., Garlanda, C., and Mantovani, A.

Abstract

Pentraxin 3 (PTX3) is a fluid-phase pattern recognition molecule and a key component of the humoral arm of innate immunity. In four different models of tissue damage in mice, PTX3 deficiency was associated with increased fibrin deposition and persistence, and thicker clots, followed by increased collagen deposition, when compared with controls. Ptx3-deficient macrophages showed defective pericellular fibrinolysis in vitro. PTX3-bound fibrinogen/fibrin and plasminogen at acidic pH and increased plasmin-mediated fibrinolysis. The second exon-encoded N-terminal domain of PTX3 recapitulated the activity of the intact molecule. Thus, a prototypic component of humoral innate immunity, PTX3, plays a nonredundant role in the orchestration of tissue repair and remodeling. Tissue acidification resulting from metabolic adaptation during tissue repair sets PTX3 in a tissue remodeling and repair mode, suggesting that matrix and microbial recognition are common, ancestral features of the humoral arm of innate immunity.

Published
2015

15. End-of-life decision-making and quality of ICU performance: an observational study in 84 Italian units

Author

Bertolini, G, Boffelli, S, Malacarne, P, Peta, M, Marchesi, M, Barbisan, C, Tomelleri, S, Spada, S, Satolli, R, Gridelli, B, Lizzola, I, Gianni M, Mazzon D., Nasso, A, Perno, S, Cocco, L, Caracciolo, A, Di Masi, P, Moretti, M, Mazzon, D, Luise, C, Abate, C, Morigi, A, Zotti, Mc, Natalini, G, Antonini, B, Pedemonte, A, Brizio, E, Rossi, M, Ruggeri, P, Vitale, Mr, Garofalo, G, Bonaccorso, V, Cocciolo, F, Gamberini, E, Bufalini, M, Pedullà, A, Barbagli, R, Pelagatti, C, Oggioni, R, Barattini, M, Giuntini, R, Isetta, M, Cinque, E, Tavola, M, Negro, G, Ferrari, F, Chiarello, M, David, Antonio, Solca, M, Cattaneo, A, Bassini, E, Pinciroli, D, Negri, G, Ughi, L, Sicignano, A, Rotelli, S, Reineke, R, Rossi, S, Clementi, S, Bellocchio, E, Antonelli, S, Furfori, P, Guadagnucci, A, Postiglione, M, Catanzaro, P, Burgio, G, Todesco, L, Spina, T, Zava, R, Simeoni, C, Mosca, C, Bandini, M, Breschi, C, Casalini, P, Cosimati, F, Davini, D, Alampi, D, Alberti, A, Malengo, S, Tartari, S, Mastroianni, A, Perino, P, Belloni, Ug, Salcuni, R, Fiore, G, Odetto, L, Pastorelli, M, Agnelli, E, Vacca, M, Segala, V, Arbinolo, Ma, Vaj, M, Larghero, E, Vergano, M, Roncato, P, Lugano, M, Cominotti, S, Deprado, A, and Badii, F.

Subjects
Adult, Male, medicine.medical_specialty, Critical Care, Critical Illness, Decision Making, Critical Care and Intensive Care Medicine, Logistic regression, law.invention, Young Adult, law, Intensive care, medicine, Humans, Prospective Studies, Organ donation, Intensive care medicine, Critically ill, Decision-making, End-of-life, Ethics, Intensive care units, Aged, Resuscitation Orders, Aged, 80 and over, business.industry, Odds ratio, Middle Aged, Euthanasia, Passive, Intensive care unit, Confidence interval, Life Support Care, Standardized mortality ratio, Italy, Withholding Treatment, Female, Observational study, Settore SPS/07 - Sociologia Generale, Family Relations, business
Abstract

To appraise the end-of-life decision-making in several intensive care units (ICUs) and to evaluate the association between the average inclination to limit treatment and overall survival at ICU level. Prospective, multicenter, observational study, lasting 12 months. Eighty-four Italian, adult ICUs. Consecutive patients (3,793) who died in ICU or were discharged in terminal condition, in 2005. Data collection included patient description, treatment limitation and decision-makers, involvement of patients and relatives in the decision, and organ donation. A logistic regression model was used to identify predictors of treatment limitation and develop a measure of the inclination to limit treatment for each ICU. This was compared with the standardized mortality ratio, an index of the overall performance of the unit. Treatment limitation preceded 62% of deaths. In 25% of cases, nurses were involved in the decision. Half the limitations were do-not-resuscitate orders, with the remaining half almost equally split between withholding and withdrawing treatment. Units less inclined to limit treatments (odds ratio

Published
2010

16. External validation of the Simplified Acute Physiology Score (SAPS) 3 in a cohort of 28,357 patients from 147 Italian intensive care units

Author

Poole, D, Rossi, C, Anghileri, A, Giardino, M, Latronico, N, Radrizzani, D, Langer, M, Bertolini, G, Acciarri, C, Acquarolo, A, Adorni, A, Alberti, A, Alborghetti, A, Antonini, B, Archi, D, Arditi, E, Badii, F, Balata, A, Barattini, M, Barbagli, R, Barbieri, P, Baroncia, M, Bartoccini, A, Bartoli, T, Bassi, F, Beck, E, Bellato, V, Bellorini, M, Belluomo Anello, C, Benanti, C, Berardino, M, Bernasconi, Mo, Besozzi, A, Bianchin, A, Bindi, Ml, Biolino, P, Blasetti, A, Boccalatte, D, Bonaccorso, G, Bonfà, A, Bonfiglio, M, Boniotti, C, Bonizzoli, M, Bottari, V, Breschi, C, Brunori, E, Buonanno, R, Buzzetti, V, Calicchio, G, Calva, S, Capannolo, B, Caracciolo, A, Carnevale, L, Carsana, C, Casadei, E, Casagli, S, Casagrande, L, Casalini, P, Castiglione, G, Cavallo, R, Chiarello, M, Chieregato, A, Chinelli, E, Cigada, M, Coaloa, M, Colombo, R, Colombo, S, Corsini, W, Corvi, D, Cosentino, E, Costa, R, Costanzo, E, Cottignoli, T, Crema, L, Crestan, E, Da Re, D, Dal Cero, P, Dal Ferro, M, David, Antonio, De Blasi RA, De Blasio, E, De Luca, A, De Negri, P, Dei Poli, M, Del Sarto, P, Di Lorenzo, G, Di Masi, P, Di Pasquale, D, Di Serafino, G, Donato, I, Fabbri, L, Fabbri, E, Fabbri, Pg, Fabi, Mc, Faccio, L, Ferla, F, Ferri, F, Fiore, G, Fognani, G, Galeotti, E, Gamberini, E, Garelli, A, Garofalo, G, Garzilli, T, Giacopuzzi, L, Gianni, M, Giannoni, S, Giugiaro, Pm, Gorietti, A, Grassi, P, Greco, M, Guadagnucci, A, Guagliardi, C, Isetta, M, Lapolla, A, Lefons, U, Livigni, S, Madonna, R, Maestrone, C, Magatti, Mf, Maggiolo, C, Malacarne, P, Mancosu, S, Mangani, Va, Mantovani, G, Marafon, S, Martinez Escobar, R, Mastroianni, A, Mastropierro, R, Meloni, A, Messina, M, Miglioranzi, R, Molino, Fm, Morigi, A, Mosca, C, Murri, V, Nardi, G, Nascimben, E, Natalini, G, Negri, G, Negro, G, Neri, M, Nicolini, A, Nuovo, D, Odetto, L, Olivieri, C, Ortoleva, A, Pacini, Dm, Paganini, G, Paganoni, G, Palmer, M, Papiri, S, Parma, A, Parrini, V, Pastorelli, M, Pastorini, S, Pegoraro, M, Pezzi, A, Pinciroli, D, Piredda, G, Piva, S, Pizzaballa, M, Possamai, C, Postiglione, M, Potalivo, A, Pulici, M, Quattrocchi, P, Raffaeli, M, Ranzini, L, Righini, E, Rona, R, Rossi, G, Rossi, S, Rossi, M, Rottoli, F, Salcuni, R, Salvi, G, Savioli, M, Scarrone, S, Schellino, Mm, Segala, V, Segalini, Pa, Sera, G, Sforza, D, Sicignano, A, Sorbara, C, Spadini, E, Staccioli, P, Stefani, M, Sucre, Mj, Tartari, S, Tavola, M, Tetamo, R, Tibaldi, G, Tinacci, S, Todesco, L, Torta, M, Tosi, L, Tripepi, C, Ughi, L, Vaj, M, Vecchiarelli, P, Vespignani, Mg, Visconti, Mg, Vulcano, Ga, Zappa, S, Zocaro, R, and Zuccaro, F.

Subjects
Male, medicine.medical_specialty, Time Factors, genetic structures, Critical Care, Critical Illness, Critical Care and Intensive Care Medicine, law.invention, Bias, law, Predictive Value of Tests, Risk Factors, Intensive care, Anesthesiology, Outcome Assessment, Health Care, medicine, Humans, Hospital Mortality, Prospective Studies, Simplified Acute Physiology Score, Intensive care medicine, Prospective cohort study, Diagnosis-Related Groups, APACHE, Aged, Chi-Square Distribution, business.industry, Data Collection, Benchmarking, Critical care, Hospital mortality, Outcome assessment, Validation study, Discriminant Analysis, Middle Aged, Prognosis, Intensive care unit, Intensive Care Units, Logistic Models, Italy, ROC Curve, Predictive value of tests, Cohort, Calibration, Female, business, Chi-squared distribution
Abstract

To evaluate the SAPS 3 score predictive ability of hospital mortality in a large external validation cohort.Prospective observational study.A total of 28,357 patients from 147 Italian ICUs joining the Project Margherita national database of the Gruppo italiano per la Valutazione degli interventi in Terapia Intensiva (GiViTI).None.Evaluation of discrimination through ROC analysis and of overall goodness-of-fit through the Cox calibration test.Although discrimination was good, calibration turned out to be poor. The general and the South-Europe Mediterranean countries equations overestimated hospital mortality overall (SMR values 0.73 with 95% CI 0.72-0.75 for both equations) and homogeneously across risk classes. Overprediction was confirmed among important subgroups, with SMR values ranging between 0.47 and 0.82.The result strictly supported by our data is that the SAPS 3 score calibrates inadequately in a large sample of Italian ICU patients and thus should not be used for benchmarking, at least in Italian settings.

Published
2009

22. Hind limb muscle atrophy precedes cerebral neuronal degeneration in G93A-SOD1 mouse model of amyotrophic lateral sclerosis: A longitudinal MRI study

Author

Marcuzzo, S, Zucca, I, Mastropietro, A, de Rosbo, N, Cavalcante, P, Tartari, S, Bonanno, S, Preite, L, Mantegazza, R, Bernasconi, P, Bernasconi, P., BONANNO, SILVIA, Marcuzzo, S, Zucca, I, Mastropietro, A, de Rosbo, N, Cavalcante, P, Tartari, S, Bonanno, S, Preite, L, Mantegazza, R, Bernasconi, P, Bernasconi, P., and BONANNO, SILVIA

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive, fatal, neurodegenerative disorder caused by the degeneration of motor neurons in the CNS, which results in complete paralysis of skeletal muscles. Recent experimental studies have suggested that the disease could initiate in skeletal muscle, rather than in the motor neurons. To establish the timeframe of motor neuron degeneration in relation to muscle atrophy in motor neuron disease, we have used MRI to monitor changes throughout disease in brain and skeletal muscle of G93A-SOD1 mice, a purported model of ALS. Longitudinal MRI examination of the same animals indicated that muscle volume in the G93A-SOD1 mice was significantly reduced from as early as week 8 of life, 4. weeks prior to clinical onset. Progressive muscle atrophy from week 8 onwards was confirmed by histological analysis. In contrast, brain MRI indicated that neurodegeneration occurs later in G93A-SOD1 mice, with hyperintensity MRI signals detected only at weeks 10-18. Neurodegenerative changes were observed only in the motor nuclei areas of the brainstem; MRI changes indicative of neurodegeneration were not detected in the motor cortex where first motor neurons originate, even at the late disease stage. This longitudinal MRI study establishes unequivocally that, in the experimental murine model of ALS, muscle degeneration occurs before any evidence of neurodegeneration and clinical signs, supporting the postulate that motor neuron disease can initiate from muscle damage and result from retrograde dying-back of the motor neurons. © 2011 Elsevier Inc.

Published
2011

25. 70

Author

Doni, A., primary, Sironi, M., additional, Musso, T., additional, Castagnoli, C., additional, Gobbi, M., additional, Valentino, S., additional, Tartari, S., additional, Bottazzi, B., additional, Garlanda, C., additional, and Mantovani, A., additional

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results