@article {10573,
	title = {A premenarcheal girl with urogenital bleeding.},
	journal = {Arch Dis Child},
	volume = {102},
	year = {2017},
	month = {2017 May},
	pages = {472},
	issn = {1468-2044},
	doi = {10.1136/archdischild-2016-311730},
	author = {Lora, Angela and Scrimin, Federica and Taddio, Andrea and Ventura, Alessandro and Barbi, Egidio}
}
@article {8075,
	title = {Patients{\textquoteright} Induced Pluripotent Stem Cells to Model Drug Induced Adverse Events: A Role in Predicting Thiopurine Induced Pancreatitis?},
	journal = {Curr Drug Metab},
	volume = {17},
	year = {2015},
	month = {2015},
	pages = {91-8},
	abstract = {<p>Induced pluripotent stem cells (iPSC) can be produced from adult cells by transfecting them with a definite set of pluripotency-associated genes. Under adequate growth conditions and stimulation iPSC can differentiate to almost every somatic lineage in the body. Patients{\textquoteright} derived iPSC are an innovative model to study mechanisms of adverse drug reactions in individual patients and in cell types that cannot be easily obtained from human subjects. Proof-of concept studies with known toxicants have been performed for liver, cardiovascular and central nervous system cells: neurons obtained from iPSC have been used to elucidate the mechanism of chemotherapy-induced peripheral neuropathy by evaluating the effects of neurotoxic drugs such as vincristine. However, no study has been performed yet on pancreatic tissue and drug induced pancreatitis. Thiopurines (azathioprine and mercaptopurine) are immunosuppressive antimetabolite drugs, commonly used to treat Crohn{\textquoteright}s disease. About 5\% of Crohn{\textquoteright}s disease patients treated with thiopurines develop pancreatitis, a severe idiosyncratic adverse event; these patients have to stop thiopurine administration and may require medical treatment, with significant personal and social costs. Molecular mechanism of thiopurine induced pancreatitis (TIP) is currently unknown and no fully validated biomarker is available to assist clinicians in preventing this adverse event. Hence, in this review we have reflected upon the probable research applications of exocrine pancreatic cells generated from patient specific iPS cells. Such pancreatic cells can provide excellent insights into the molecular mechanism of TIP. In particular three hypotheses on the mechanism of TIP could be explored: drug biotransformation, innate immunity and adaptative immunity.</p>},
	issn = {1875-5453},
	author = {Stocco, Gabriele and Lanzi, Gaetana and Yue, Fengming and Giliani, Silvia and Sasaki, Katsunori and Tommasini, Alberto and Pelin, Marco and Martelossi, Stefano and Ventura, Alessandro and Decorti, Giuliana}
}
@article {3526,
	title = {A pneumonia that does not improve.},
	journal = {Arch Dis Child Educ Pract Ed},
	volume = {100},
	year = {2015},
	month = {2015 Feb},
	pages = {18, 55},
	keywords = {Airway Obstruction, Bronchoscopy, Child, Preschool, Foreign Bodies, Humans, Pneumonia, Radiography, Thoracic},
	issn = {1743-0593},
	doi = {10.1136/archdischild-2014-306343},
	author = {Naviglio, Samuele and Chinello, Matteo and Ventura, Alessandro}
}
@article {3516,
	title = {Pharmacogenetics of azathioprine in inflammatory bowel disease: a role for glutathione-S-transferase?},
	journal = {World J Gastroenterol},
	volume = {20},
	year = {2014},
	month = {2014 Apr 7},
	pages = {3534-41},
	abstract = {<p>Azathioprine is a purine antimetabolite drug commonly used to treat inflammatory bowel disease (IBD). In vivo it is active after reaction with reduced glutathione (GSH) and conversion to mercaptopurine. Although this reaction may occur spontaneously, the presence of isoforms M and A of the enzyme glutathione-S-transferase (GST) may increase its speed. Indeed, in pediatric patients with IBD, deletion of GST-M1, which determines reduced enzymatic activity, was recently associated with reduced sensitivity to azathioprine and reduced production of azathioprine active metabolites. In addition to increase the activation of azathioprine to mercaptopurine, GSTs may contribute to azathioprine effects even by modulating GSH consumption, oxidative stress and apoptosis. Therefore, genetic polymorphisms in genes for GSTs may be useful to predict response to azathioprine even if more in vitro and clinical validation studies are needed.</p>},
	keywords = {6-Mercaptopurine, Animals, Apoptosis, Azathioprine, Glutathione, Glutathione Transferase, Humans, Immunosuppressive Agents, Inflammatory Bowel Diseases, Oxidative Stress, Pharmacogenetics, Polymorphism, Genetic},
	issn = {2219-2840},
	doi = {10.3748/wjg.v20.i13.3534},
	author = {Stocco, Gabriele and Pelin, Marco and Franca, Raffaella and De Iudicibus, Sara and Cuzzoni, Eva and Favretto, Diego and Martelossi, Stefano and Ventura, Alessandro and Decorti, Giuliana}
}
@article {1848,
	title = {Pathergy as a cause of false-positive tuberculin skin test.},
	journal = {Pediatr Infect Dis J},
	volume = {31},
	year = {2012},
	month = {2012 Jan},
	pages = {104},
	keywords = {Adolescent, Behcet Syndrome, False Positive Reactions, Female, Humans, Hypersensitivity, Needles, Skin, Skin Tests, Tuberculin Test, Tuberculosis, Gastrointestinal},
	issn = {1532-0987},
	doi = {10.1097/INF.0b013e31823627ad},
	author = {Pastore, Serena and Naviglio, Samuele and Ventura, Alessandro}
}
