A new Caenorhabditis elegans model to study copper toxicity in Wilson disease.

Wilson disease (WD) is caused by mutations in the ATP7B gene that encodes a copper (Cu) transporting ATPase whose trafficking from the Golgi to endo-lysosomal compartments drives sequestration of excess Cu and its further excretion from hepatocytes into the bile. Loss of ATP7B function leads to toxic Cu overload in the liver and subsequently in the brain, causing fatal hepatic and neurological abnormalities. The limitations of existing WD therapies call for the development of new therapeutic approaches, which require an amenable animal model system for screening and validation of drugs and molecular targets.

Nasal and systemic eosinophilia associated with solid intestinal tumors, a case report and review of the literature.

The authors report the study of a clinical case, which presented eosinophilia both in the secretion of the nasal mucosa and in the blood count. After a careful examination of all the pathologies related to hypereosinophilia, through a clinical study, they have documented the presence of an adenocarcinoma located in the ileocecal junction of the colon. From what has been documented it is clear that only a clinical observation of precision, carried out above all through nasal cytology and colonoscopy, is able to diagnose an important pathology, such as oncology.