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16 results on '"Bernardini N"'

2. How lockdown measures, during COVID-19 pandemic, matter on psoriatic patient’s perception: Study on 600 patients on biologic therapy

Author

Bernardini, N., primary, Skroza, N., additional, Spagnoli, A., additional, Marchesiello, A., additional, Balduzzi, V., additional, Tolino, E., additional, Mambrin, A., additional, Michelini, S., additional, Maddalena, P., additional, Volpe, S., additional, Proietti, I., additional, Vestri, A., additional, and Potenza, C., additional

Published
2021
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3. OC.05.3 HISTOMORPHOLOGICAL AND MOLECULAR CHARACTERIZATION OF PARKINSON'S DISEASE PATIENTS WITH CONSTIPATION: A PILOT STUDY

Author

Fani, B., primary, Bellini, G., additional, Fornai, M., additional, Ippolito, C., additional, Segnani, C., additional, Frosini, D., additional, Pellegrini, C., additional, Benvenuti, L., additional, Gambaccini, D., additional, Bernardini, N., additional, Ceravolo, R., additional, Blandizzi, C., additional, Marchi, S., additional, and Bellini, M., additional

Published
2019
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4. Effects of L-DOPA/benserazide co-treatment on colonic excitatory cholinergic motility and enteric inflammation following dopaminergic nigrostriatal neurodegeneration

Author

Pellegrini, C., primary, Antonioli, L., additional, Colucci, R., additional, Tirotta, E., additional, Gentile, D., additional, Ippolito, C., additional, Segnani, C., additional, Levandis, G., additional, Cerri, S., additional, Blandini, F., additional, Barocelli, E., additional, Ballabeni, V., additional, Bernardini, N., additional, Blandizzi, C., additional, and Fornai, M., additional

Published
2017
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15. Emerging role of cyclooxygenase isoforms in the control of gastrointestinal neuromuscular functions

Author

Roberto De Giorgio, Luca Antonioli, Mario Del Tacca, Corrado Blandizzi, Rocchina Colucci, Marco Tuccori, Matteo Fornai, Nunzia Bernardini, Narcisa Ghisu, Fornai M, Antonioli L, Colucci R, Bernardini N, Ghisu N, Tuccori M, De Giorgio R, Del Tacca M, and Blandizzi C.

Subjects
Gene isoform, cyclooxygenase isoforms, gastrointestinal motility, enteric nervous system, intestinal inflammation, postoperative ileus, Postoperative ileus, Gastrointestinal Diseases, Motility, Biology, Bioinformatics, Enteric Nervous System, NO, postoperative ileus, intestinal inflammation, Animals, Humans, Cyclooxygenase Inhibitors, Pharmacology (medical), Pharmacology, Mucous Membrane, Inflammatory Bowel Diseases, Muscle, Smooth, cyclooxygenase isoforms, Neuromuscular compartment, Pathophysiology, Gastrointestinal Tract, Isoenzymes, gastrointestinal motility, enteric nervous system, Prostaglandin-Endoperoxide Synthases, Immunology, biology.protein, Enteric nervous system, Cyclooxygenase, Gastrointestinal Motility
Abstract

Since the discovery of two cyclooxygenase isoforms (COX-1, COX-2), efforts have been made to characterize the roles played by these enzymes in the regulation of physiological functions, as well as to explore their involvement in the pathophysiology of inflammatory disorders. In the digestive tract, the majority of evidence has been obtained at mucosal level, where both isoforms regulate various functions, and contribute to the development of inflammatory and neoplastic disorders. The role of COX isoforms in the gut neuromuscular compartment, where their expression has been detected in different species, is still unclear. However, the characterization of actions exerted by COX-derived prostanoids on gut motility has been under investigation for many years, and it is becoming increasingly appreciated that these mediators subserve complex regulatory patterns of COX on digestive motility. More recently, several studies have strengthened the concept that both COX-1 and COX-2 are involved in the modulation of gastrointestinal neuromuscular activity under normal conditions, and that changes in their regulatory activities occur in the presence of various digestive disorders, including inflammatory bowel diseases and postoperative ileus. Despite a large body of preclinical evidence, studies aimed at translating these findings into clinically relevant applications are needed, in an attempt to identify novel therapeutic approaches for treatment of gut disorders associated with motility alterations. This review illustrates and discusses current knowledge of the roles played by COX pathways in the regulation of gastrointestinal neuromuscular functions, both under normal conditions and in the presence of gut disorders.

Published
2010

16. Thyroid dysfunction in megalin deficient mice

Author

Claudio Marcocci, Amelio Dolfi, Cristina Segnani, Nunzia Bernardini, Michele Marinò, Letizia Mattii, Robert T. McCluskey, R. Botta, Simonetta Lisi, Aldo Pinchera, Lisi, Simonetta, Segnani, C, Mattii, L, Botta, R, Marcocci, C, Dolfi, A, Mccluskey, Rt, Pinchera, A, Bernardini, N, and Marino', M.

Subjects
Heterozygote, Thyroid Hormones, endocrine system, medicine.medical_specialty, Goiter, endocrine system diseases, medicine.medical_treatment, Thyroid Gland, Thyrotropin, urologic and male genital diseases, Thyroglobulin, Biochemistry, Mice, Megalin, Endocrinology, Hypothyroidism, Internal medicine, medicine, Animals, Secretion, Molecular Biology, Thyroid, Mice, Knockout, Thyroid, Thyroglobulin, Hypothyroidism, Megalin, Mice, Chemistry, Homozygote, Histology, medicine.disease, Low Density Lipoprotein Receptor-Related Protein-2, Thyroxine, medicine.anatomical_structure, Transcytosis, Thyroid function, Hormone
Abstract

Megalin mediates transcytosis of thyroglobulin (Tg), the thyroid hormone precursor, resulting in its passage into the bloodstream. The process involves especially hormone-poor Tg, which may favour hormone secretion by preventing competition with hormone-rich Tg for proteolytic degradation. To gain more insight into the role of megalin, here we studied thyroid function and histology in megalin deficient mice compared with WT mice. As expected from the knowledge that megalin mediates Tg transcytosis, serum Tg levels were significantly reduced in homozygous (megalin −/− ) mice, which, more importantly, were found to be hypothyroid, as demonstrated by significantly reduced serum free thyroxine and significantly increased serum thyroid stimulating hormone (TSH) levels. In heterozygous (megalin +/− ) mice, in which megalin expression was normal, thyroid function was unaffected. Although the serological phenotype in megalin −/− mice was not associated with histological alterations or goiter, our results support a major role of megalin in thyroid hormone secretion.

Published
2005

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