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Modena, Italy

The University of Modena and Reggio Emilia , located in Modena and Reggio Emilia, Emilia-Romagna, Italy, is one of the oldest universities in Italy, founded in 1175, with a population of more than 20,000 students.The medieval university disappeared by 1338 and was replaced by "three public lectureships" which did not award degrees and were suspended in the 1590s "for lack of money". The university was not reestablished in Modena until the 1680s and did not receive an imperial charter until 1685. Wikipedia.


Pietrangelo A.,University of Modena and Reggio Emilia
Gastroenterology | Year: 2010

In the late 1800s, hemochromatosis was considered an odd autoptic finding. More than a century later, it was finally recognized as a hereditary, multi-organ disorder associated with a polymorphism that is common among white people: a 845G→A change in HFE that results in C282Y in the gene product. Hemochromatosis is now a well-defined syndrome characterized by normal iron-driven erythropoiesis and the toxic accumulation of iron in parenchymal cells of liver, heart, and endocrine glands. It can be caused by mutations that affect any of the proteins that limit the entry of iron into the blood. In mice, deletion of the iron hormone hepcidin and any of 8 genes that regulate its biology, including Hfe, transferrin receptor 2 (Tfr2), and hemojuvelin (Hjv) (which all sense the accumulation of iron that hepcidin corrects) or ferroportin (Fpn) (the cellular iron exporter down-regulated by hepcidin), cause iron overload but not organ disease. In humans, loss of TfR2, HJV, and hepcidin itself or FPN mutations result in full-blown hemochromatosis. Unlike these rare instances, in white people, homozygotes for C282Y polymorphism in HFE are numerous, but they are only predisposed to hemochromatosis; complete organ disease develops in a minority, when these individuals abuse alcohol or from other unidentified modifying factors. HFE gene testing can be used to diagnose hemochromatosis, but analyses of liver histology and clinical features are still required to identify patients with rare, non-HFE forms of the disease. The role of hepcidin in the pathogenesis of hemochromatosis reveals its similarities to endocrine diseases such as diabetes and indicates new approaches to diagnosis and management of this common disorder in iron metabolism. © 2010 AGA Institute. Source


Pietrangelo A.,University of Modena and Reggio Emilia
Journal of Hepatology | Year: 2011

The discovery of hepcidin has triggered a virtual explosion of studies on iron metabolism and related disorders, the results of which have profoundly changed our view of human diseases associated with excess of iron, iron deficiency or iron misdistribution. Not only has new light been shed on the pathogenesis of these disorders, but therapeutic applications from these advances are now foreseen. The notion that hepcidin excess or deficiency may contribute to the dysregulation of iron homeostasis in hereditary and acquired iron disorders raises the possibility that hepcidin-lowering or enhancing agents may be an effective strategy for curing the main consequences of hepcidinopathies, anemia or iron overload, respectively. Experimental pre-clinical and clinical studies have shown that hepcidin antibodies, agonists or antagonists, cytokine receptor antibodies and small-molecules that modify hepcidin expression also reverse iron abnormalities in vivo, in a number of disease models. While future studies addressing safety and long-term efficacy of hepcidin-targeted treatments will clarify risks and benefits, a new era has begun based on the treatment of disorders of iron homeostasis through the modulation of its regulatory hormone, hepcidin. © 2010 European Association for the Study of the Liver. Source


Pietrangelo A.,University of Modena and Reggio Emilia
Gastroenterology | Year: 2015

The discovery of hepcidin in 2000 and the subsequent unprecedented explosion of research and discoveries in the iron field have dramatically changed our understanding of human disorders of iron metabolism. Today, hereditary hemochromatosis, the paradigmatic iron-loading disorder, is recognized as an endocrine disease due to the genetic loss of hepcidin, the iron hormone produced by the liver. This syndrome is due to unchecked transfer of iron into the bloodstream in the absence of increased erythropoietic needs and its toxic effects in parenchymatous organs. It is caused by mutations that affect any of the proteins that help hepcidin to monitor serum iron, including HFE and, in rarer instances, transferrin-receptor 2 and hemojuvelin, or make its receptor ferroportin, resistant to the hormone. In Caucasians, C282Y HFE homozygotes are numerous, but they are only predisposed to hemochromatosis; complete organ disease develops in a minority, due to alcohol abuse or concurrent genetic modifiers that are now being identified. HFE gene testing can be used to diagnose hemochromatosis in symptomatic patients, but analyses of liver histology and full gene sequencing are required to identify patients with rare, non-HFE forms of the disease. Due to the central pathogenic role of hepcidin, it is anticipated that nongenetic causes of hepcidin loss (eg, end-stage liver disease) can cause acquired forms of hemochromatosis. The mainstay of hemochromatosis management is still removal of iron by phlebotomy, first introduced in 1950s, but identification of hepcidin has not only shed new light on the pathogenesis of the disease and the approach to diagnosis, but etiologic therapeutic applications from these advances are now foreseen. © 2015 AGA Institute. Source


Patent
University of Modena and Reggio Emilia | Date: 2012-03-20

A control system for controlling horizontal trim of a flying saucer comprises a plurality of horizontal vanes, automatically and passively selectively movable between a first rest configuration and a perturbed configuration, in response to an undesired variation in a flight trim of the flying saucer.


A nozzle is capable of producing a mixing of two primitive fluid jets and a selective and controllable angular deviation of the synthetic jet obtained by mixing the primitive jets without any moving mechanical part. The nozzle is also capable of generating a controllable deviation of the synthetic jet and of changing the direction of this jet in a continuous and dynamic manner so as to allow the jet to sweep a preset and arbitrary angle. The nozzle is constituted, in a first part thereof, by a conduit divided into two channels by a central baffle and, in a second part thereof, by a convergence zone and an outflow mouth whose walls have a curvilinear profile and are connected seamlessly to the walls of the conduit.

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