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124 results on '"Pozzi, Ernesto"'

3. Rescue use of beclomethasone and albuterol in a single inhaler for mild asthma

Author

Papi, Alberto, Canonica, Giorgio W., Maestrelli, Piero, Paggiaro, Pierluigi, Olivieri, Dario, Pozzi, Ernesto, Crimi, Nunzio, Vignola, Antonio M., Morelli, Paolo, Nicolini, Gabriele, and Fabbri, Leonardo M.

Subjects
Asthma -- Drug therapy, Beclomethasone dipropionate -- Dosage and administration, Albuterol -- Dosage and administration, Inhalers -- Usage
Abstract

A study to investigate whether the use of a combination of beclomethasone dipropionate and albuterol in a single inhaler would be as effective as the regular use of inhaled beclomethasone, was conducted. The symptom-driven use of inhaled beclomethasone and albuterol in a single inhaler was found to be as effective as regular use of inhaled beclomethasone.

Published
2007

6. Long-term Outcome after Pulmonary Endarterectomy

Author

Corsico, Angelo G., DʼArmini, Andrea M., Cerveri, Isa, Klersy, Catherine, Ansaldo, Elena, Niniano, Rosanna, Gatto, Elena, Monterosso, Cristian, Morsolini, Marco, Nicolardi, Salvatore, Tramontin, Corrado, Pozzi, Ernesto, and Viganò, Mario

Published
2008
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10. Complement Receptor 1 Gene Polymorphisms in Sarcoidosis

Author

Zorzetto, Michele, Bombieri, Cristina, Ferrarotti, Ilaria, Medaglia, Sara, Agostini, Carlo, Tinelli, Carmine, Malerba, Giovanni, Carrabino, Natalia, Beretta, Anna, Casali, Lucio, Pozzi, Ernesto, Pignatti, Pier Franco, Semenzato, Gianpietro, Cuccia, Maria Clara, and Luisetti, Maurizio

Published
2002
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14. Successful whole lung lavage in pulmonary alveolar proteinosis secondary to lysinuric protein intolerance: a case report

Author

Baritussio Aldo, Bolongaro Antonia, Adami Andrea, Stella Giulia M, Rodi Giuseppe, Ceruti Michele, Pozzi Ernesto, and Luisetti Maurizio

Subjects
Medicine
Abstract

Abstract Background Pulmonary alveolar proteinosis (PAP) is a rare disease characterised by accumulation of lipoproteinaceous material within alveoli, occurring in three clinically distinct forms: congenital, acquired and secondary. Among the latter, lysinuric protein intolerance (LPI) is a rare genetic disorder caused by defective transport of cationic amino acids. Whole Lung Lavage (WLL) is currently the gold standard therapy for severe cases of PAP. Case presentation We describe the case of an Italian boy affected by LPI who, by the age of 10, developed digital clubbing and, by the age of 16, a mild restrictive functional impairment associated with a high-resolution computed tomography (HRCT) pattern consistent with pulmonary alveolar proteinosis. After careful assessment, he underwent WLL. Conclusion Two years after WLL, the patient has no clinical, radiological or functional evidence of pulmonary disease recurrence, thus suggesting that WLL may be helpful in the treatment of PAP secondary to LPI.

Published
2007
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16. SP-A binds alpha1-antitrypsin in vitro and reduces the association rate constant for neutrophil elastase

Author

Carrabino Natalia, Dalzoppo Daniele, Rognoni Paola, Santos Conceição, Iadarola Paolo, Lupi Anna, Gorrini Marina, Pozzi Ernesto, Baritussio Aldo, and Luisetti Maurizio

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Background α1-antitrypsin and surfactant protein-A (SP-A) are major lung defense proteins. With the hypothesis that SP-A could bind α1-antitrypsin, we designed a series of in vitro experiments aimed at investigating the nature and consequences of such an interaction. Methods and results At an α1-antitrypsin:SP-A molar ratio of 1:1, the interaction resulted in a calcium-dependent decrease of 84.6% in the association rate constant of α1-antitrypsin for neutrophil elastase. The findings were similar when SP-A was coupled with the Z variant of α1-antitrypsin. The carbohydrate recognition domain of SP-A appeared to be a major determinant of the interaction, by recognizing α1-antitrypsin carbohydrate chains. However, binding of SP-A carbohydrate chains to the α1-antitrypsin amino acid backbone and interaction between carbohydrates of both proteins are also possible. Gel filtration chromatography and turnover per inactivation experiments indicated that one part of SP-A binds several molar parts of α1-antitrypsin. Conclusion We conclude that the binding of SP-A to α1-antitrypsin results in a decrease of the inhibition of neutrophil elastase. This interaction could have potential implications in the physiologic regulation of α1-antitrypsin activity, in the pathogenesis of pulmonary emphysema, and in the defense against infectious agents.

Published
2005
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17. Lomefloxacin versus amoxicillin in the treatment of acute exacerbations of chronic bronchitis: an Italian multicenter study

Author

Grassi, Carlo, Albera, Carlo, and Pozzi, Ernesto

Subjects
Amoxicillin -- Evaluation, Bronchitis -- Drug therapy, Health, Health care industry, Lomefloxacin (Medication) -- Evaluation
Abstract

Nine centers in Italy participated in a worldwide, multicenter study comparing the effectiveness and safety of lomefloxacinand amoxicillin in patients with acute exacerbations of chrionic bronchitis caused mainly by gram-negative pathogens. The 157 enrolled patients received either 400 mg lomefloxacin once daily (n = 78) or 500 mg amoxicillin every 8 hours (n = 79) for 7-10 days. A total of 131 patients were evaluable for bacteriologic efficacy and 154 for clinical efficacy. at 2-4 days after the conclusion of treatment, the bacterial eradication rate was 84.8 [degrees] for lomefloxacin-treated patients and 64.6 [degrees] for amoxicillin-treated patients (p = 0.0065); the clinical success rate (cure plus improvement) for lomeflxacin was 94.7 [degrees] and for amoxicillin was 83.3 [degrees] (p = 0.0212). The reinfection rate was lower in the lomefloxacin group than in the amoxicillin group (3.0 [degrees] vs 13.8 [degrees], p = 0.0382). Both drug regimens were well tolerated. Once-a-day treatment with 400 mg lomefloxacin was more effective than 400 mg amoxicillin three times daily for the treatment of acute exacerbations of chronic bronchitis caused by gram-negative pathogens.

Published
1992

18. Non-neuronal cholinergic system in airways and lung cancer susceptibility

Author

Saracino, Laura, Zorzetto, Michele, Inghilleri, Simona, Pozzi, Ernesto, and Stella, Giulia Maria

Subjects
Review Article
Abstract

In the airway tract acetylcholine (ACh) is known to be the mediator of the parasympathetic nervous system. However ACh is also synthesized by a large variety of non-neuronal cells. Strongest expression is documented in neuroendocrine and in epithelial cells (ciliated, basal and secretory elements). Growing evidence suggests that a cell-type specific Ach expression and release do exist and act with local autoparacrine loop in the non-neuronal airway compartment. Here we review the molecular mechanism by which Ach is involved in regulating various aspects of innate mucosal defense, including mucociliary clearance, regulation of macrophage activation as well as in promoting epithelial cells proliferation and conferring susceptibility to lung carcinoma onset. Importantly this non-neuronal cholinergic machinery is differently regulated than the neuronal one and could be specifically therapeutically targeted.

Published
2013

19. Mutational profiling of EGFR and KRAS oncogenes in non-small cell lung cancer (NSCLC) cells obtained through fine needle aspiration cytology (FNAC)

Author

Cemmi, Francesca, Stella, Giulia Maria, Zorzetto, Michele, Inghilleri, Simona, Morbini, Patrizia, Dore, Roberto, and Pozzi, Ernesto

Abstract

Cancer is a genetic disease and this concept has now been widely exploited by both biologists and clinicians to design new targeted therapeutical approaches. Indeed many data have already allowed us to ameliorate not only our knowledge about cancer onset, but also about patient treatment. Correlation between mutations in cancer alleles and drug response is a crucial point to identify drugs or drug combinations that match the genetic profile of individual tumors. On the other hand, experiences derived from receptor tyrosine kinases (RTKs) inhibition have pointed out that targeted treatment is really successful only in a small subset of tumors. The latter are eventually addicted to the genetic alterations responsible for receptors activation and continued expression of their signaling pathways. Therefore, switching off the oncogenic activity by specific inhibitors will trigger an “oncogenic shock” which eventually will lead tumor cell to die. Overall these observations provide a strong rationale for molecular-based diagnosis and cancer patients selection for targeted treatment. Understanding how the mutational status of oncogenic alleles affects sensibility or resistance to drugs represents the most potential strategy in identifying patients for effective personalized therapies. In consideration of the high incidence and the poor prognosis of affected patients, lung carcinoma has been considered and still identify major objective of the targeted therapeutic approach. Experiences derived from this disease, and mainly from non-small cell lung cancer (NSCLC), represent fundamental achievement of translational research. From this perspective, members of the EGFR signal transduction pathway play a key role in lung carcinogenesis and act as genetic markers predictive of response to anti-EGFR therapy. In unselected NSCLCs EGFR activating mutations are rarely present (10%); mutation frequency increases to over 50% in a restricted subset of NSCLC patients: East-Asian, women, non smokers, affected by ADC (mainly BAC variant). Moreover the incidence of EGFR mutations in NSCLCs increases up to 77% among EGFR TKIs responders, while it is 7% in unsensitive cases. This project aims to evaluate in a cohort of NSCLC patients the prevalence of activating mutations in EGFR and KRAS genes by analyzing tumor cells obtained through transthoracic biopsy by FNAC, which actually represents the most appropriate diagnostic tool for peripheral lesions, such as ADKs that actually account for 40% of NSCLC diagnosis. Validation of sequencing technology on tumor samples constituted by only few cells has two relevant implications. First it might allows routinary tumor molecular profiling as powerful integration of conventional histo-pathological diagnosis. Besides the clinical management of NSCLC will take advantages from the characterization of EGFR-KRAS mutational status in order to develop personalized and effective treatment strategies., Bollettino della Società Medico Chirurgica di Pavia, Vol 123, N° 2 (2010)

Published
2010
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20. The combination of sorafenib and everolimus shows antitumor activity in preclinical models of malignant pleural mesothelioma

Author

Pignochino, Ymera, primary, Dell’Aglio, Carmine, additional, Inghilleri, Simona, additional, Zorzetto, Michele, additional, Basiricò, Marco, additional, Capozzi, Federica, additional, Canta, Marta, additional, Piloni, Davide, additional, Cemmi, Francesca, additional, Sangiolo, Dario, additional, Gammaitoni, Loretta, additional, Soster, Marco, additional, Marchiò, Serena, additional, Pozzi, Ernesto, additional, Morbini, Patrizia, additional, Luisetti, Maurizio, additional, Aglietta, Massimo, additional, Grignani, Giovanni, additional, and Stella, Giulia M, additional

Published
2015
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23. Relationship Between Diffuse Pulmonary Fibrosis, Alveolar Proteinosis, and Granulocyte-Macrophage Colony Stimulating Factor Autoantibodies

Author

Luisetti, Maurizio, primary, Bruno, Pierdonato, additional, Kadija, Zamir, additional, Suzuki, Takuji, additional, Raffa, Salvatore, additional, Torrisi, Maria Rosaria, additional, Campo, Ilaria, additional, Mariani, Francesca, additional, Pozzi, Ernesto, additional, Trapnell, Bruce C, additional, and Mariotta, Salvatore, additional

Published
2011
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24. Targeting The MTOR Pathway In Malignant Pleural Mesothelioma

Author

Stella, Giulia M., primary, Pignochino, Ymera, additional, Inghilleri, Simona, additional, Zorzetto, Michele, additional, Scabini, Roberta, additional, Morbini, Patrizia, additional, Dell'Aglio, Carmine, additional, Basiricò, Marco, additional, Pozzi, Ernesto, additional, Aglietta, Massimo, additional, and Luisetti, Maurizio, additional

Published
2011
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27. MET mutations in cancers of unknown primary origin (CUPs)

Author

Stella, Giulia M., primary, Benvenuti, Silvia, additional, Gramaglia, Daniela, additional, Scarpa, Aldo, additional, Tomezzoli, Anna, additional, Cassoni, Paola, additional, Senetta, Rebecca, additional, Venesio, Tiziana, additional, Pozzi, Ernesto, additional, Bardelli, Alberto, additional, and Comoglio, Paolo M., additional

Published
2010
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28. Aerosol Characterization of Nebulized GM-CSF

Author

Zimlich, William C., primary, Mariani, Francesca, additional, Muellinger, Bernhard, additional, Kadija, Zamir, additional, Gleske, Juliane, additional, Kroneberg, Philipp, additional, Frey, Manuel, additional, Campo, Ilaria, additional, Pozzi, Ernesto, additional, and Luisetti, Maurizio, additional

Published
2010
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29. Association Of CR2/CD21 Polymorphisms With Systemic Sclerosis

Author

Zorzetto, Michele, primary, Ottaviani, Stefania, additional, Bonino, Claudia, additional, Montecucco, Carlomaurizio, additional, Cavagna, Lorenzo, additional, Paracchini, Elena, additional, Pozzi, Ernesto, additional, De Silvestri, Annalisa, additional, and Luisetti, Maurizio, additional

Published
2010
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34. “Nonobstructive” emphysema of the lung

Author

Corsico, Angelo G., primary, Niniano, Rosanna, additional, Gatto, Elena, additional, Zoia, Maria C., additional, Corsico, Andrea, additional, Cremaschi, Paolo, additional, Pozzi, Ernesto, additional, and Cerveri, Isa, additional

Published
2007
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35. Foxp3 Expressing CD4+ CD25+ and CD8+CD28− T Regulatory Cells in the Peripheral Blood of Patients with Lung Cancer and Pleural Mesothelioma

Author

Meloni, Federica, primary, Morosini, Monica, additional, Solari, Nadia, additional, Passadore, Ileana, additional, Nascimbene, Caterina, additional, Novo, Monique, additional, Ferrari, Marco, additional, Cosentino, Marco, additional, Marino, Franca, additional, Pozzi, Ernesto, additional, and Fietta, Anna M., additional

Published
2006
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38. Regulatory CD4+CD25+ T cells in the peripheral blood of lung transplant recipients: correlation with transplant outcome

Author

Meloni, Federica, primary, Vitulo, Patrizio, additional, Bianco, Alessia Marone, additional, Paschetto, Enrica, additional, Morosini, Monica, additional, Cascina, Alessandro, additional, Mazzucchelli, Iolanda, additional, Ciardelli, Laura, additional, Oggionni, Tiberio, additional, Fietta, Anna Maria, additional, Pozzi, Ernesto, additional, and Vigan??, Mario, additional

Published
2004
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40. Phase II study of high-dose paclitaxel and carboplatin in previously untreated, unresectable non-small cell lung cancer

Author

Novello, Silvia, primary, Galli, Luca, additional, Antonuzzo, Andrea, additional, Crinó, Lucio, additional, Pozzi, Ernesto, additional, Selvaggi, Giovanni, additional, Ricci, Sergio, additional, Marrocolo, Francesca, additional, Darwish, Samir, additional, Sorbolini, Sara, additional, Tonato, Maurizio, additional, and Scagliotti, Giorgio V, additional

Published
2001
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45. SP-A binds alpha1-antitrypsin in vitro and reduces the association rate constant for neutrophil elastase.

Author

Gorrini, Marina, Lupi, Anna, Iadarola, Paolo, dos Santos, Conceição, Rognoni, Paola, Dalzoppo, Daniele, Carrabino, Natalia, Pozzi, Ernesto, Baritussio, Aldo, and Luisetti, Maurizio

Subjects
TRYPSIN inhibitors, LEUCOCYTE elastase, OBSTRUCTIVE lung diseases, PULMONARY emphysema, MEDICAL research
Abstract

Background: α1-antitrypsin and surfactant protein-A (SP-A) are major lung defense proteins. With the hypothesis that SP-A could bind α1-antitrypsin, we designed a series of in vitro experiments aimed at investigating the nature and consequences of such an interaction. Methods and results: At an α1-antitrypsin:SP-A molar ratio of 1:1, the interaction resulted in a calcium-dependent decrease of 84.6% in the association rate constant of α1-antitrypsin for neutrophil elastase. The findings were similar when SP-A was coupled with the Z variant of α1-antitrypsin. The carbohydrate recognition domain of SP-A appeared to be a major determinant of the interaction, by recognizing α1-antitrypsin carbohydrate chains. However, binding of SP-A carbohydrate chains to the α1-antitrypsin amino acid backbone and interaction between carbohydrates of both proteins are also possible. Gel filtration chromatography and turnover per inactivation experiments indicated that one part of SP-A binds several molar parts of α1-antitrypsin. Conclusion: We conclude that the binding of SP-A to α1-antitrypsin results in a decrease of the inhibition of neutrophil elastase. This interaction could have potential implications in the physiologic regulation of α1-antitrypsin activity, in the pathogenesis of pulmonary emphysema, and in the defense against infectious agents. [ABSTRACT FROM AUTHOR]

Published
2005
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46. Clinical efficacy of dirithromycin versus miocamycin in the treatment of acute bronchitis or acute exacerbations of chronic bronchitis.

Author

Pozzi, Ernesto

Abstract

A multicentre trial was carried out to compare the efficacy and safety of dirithromycin with miocamycin in the treatment of patients with acute bronchitis or acute exacerbations of chronic bronchitis. The study was a single-blind, randomized, parallel-group study. Dirithromycin was administered orally at a dosage of 500 mg once daily and miocamycin was administered orally at a dosage of 600 mg twice daily; the duration of therapy was five to seven days for both drugs. The results, in 161 assessable patients (78 taking dirithromycin; 83 taking miocamycin), show that dirithromycin and miocamycin have comparable efficacy and safety in the treatment of bronchitis caused by susceptible bacterial pathogens. [ABSTRACT FROM PUBLISHER]

Published
1993

47. The Search for the Genetic Component of COPD: Role of the Clinical Phenotype§

Author

Luisetti, Maurizio, Cerveri, Isa, and Pozzi, Ernesto

Abstract

Chronic obstructive pulmonary disease (COPD) is a common, complex disorder, and dissection of its individual components is considered one of the research priorities for this disease. Several lines of evidence suggest that, in spite of the massive role of cigarette smoking, common COPD is not just an environmental phenocopy of COPD associated with alpha1-antitrypsin deficiency: from the racial/ethnic variability in COPD prevalence to the individual susceptibility to cigarette smoke, from the familial aggregation of lung function levels to the familial clustering of COPD symptoms, all lines tend to point to common COPD having a genetic component. The challenge in the last three decades has been to define the borders of this component, its relative weight with respect to the environmental component, and to identify the susceptibility and/or resistance genes. Taking advantage from the knowledge, albeit limited, of the biochemical basis of COPD, a number of genetic polymorphisms have been investigated, mostly in case-control association studies. Although such a strategy is considered more successful than linkage analysis for investigating complex, non-Mendelian disorders and in spite of the considerable amount of data collected, the overall result of the genetic investigations into COPD has so far been largely disappointing. A critical evaluation of the published reports shows that a number of issues could have affected the outcome of the investigations: among such issues, the choice of the appropriate clinical phenotype is fundamental.

Published
2006

48. Primary human mesothelioma cells express class II MHC, ICAM-1 and B7–2 and can present recall antigens to autologous blood lymphocytes

Author

Mutti, Luciano, Valle, Maria T., Balbi, Bruno, Orengo, Anna M., Lazzaro, Antonio, Alciato, Paolo, Gatti, Emiliano, Betta, Pier G., and Pozzi, Ernesto

Abstract

Mesothelioma cells (MMc) are considered to be weakly immunogenic and the experimental approaches attempting to induce an immune response against these cells have been disappointing. Our aim was to investigate whether MMc possess the surface accessory molecules involved in antigen presentation and whether these cells are capable of presenting recall antigens to autologous blood lymphocytes. Four primary MMc cultures were generated from malignant effusions and examined to assess whether the accessory molecules required for antigen presentation were present on their surfaces. Intercellular adhesion molecule-1 (ICAM-1; CD54); class I and class II major histocompatibility complex-DR (MHCI and MHCII-DR); B7–1 (CD80.3); and B7–2 (CD86) expression by MMc was studied by immunocytochemical and/or FACScan analysis. MMc were pulsed with purified protein derivative (PPD), Tetanus toxoid (TT) and Candida albicans (CA) bodies, and incubated with autologous lymphocytes. Lymphocyte proliferation was estimated by radionucleotide incorporation. Phenotypic analysis showed the presence of MHCII-DR, ICAM-1 and B7–2 on primary MMc cultures, whereas the phenotypic evaluation of 2 established MMc lines did not show the presence of the B7–1 and B7–2 molecules. In addition, MHCII-DR was detectable only after interferon gamma (IFN-γ) stimulation. Primary MMc cultures acquired the capability to induce lymphocyte proliferation after pulse with the recall antigens. To achieve characterization of these lymphocytes, we generated a PPD-specific CD4+ T-cell clone. PPD-pulsed MMc were shown to specifically induce T-cell clone proliferation through a MHCII-DR-mediated process. We conclude that primary MMc possess the surface molecules required for antigen presentation and can present recall antigens to CD4+ lymphocytes. Int. J. Cancer 78:740–749, 1998. © 1998 Wiley-Liss, Inc.

Published
1998
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