Maturity-onset diabetes of the young (MODY) is an unusual form of diabetes with specific features that distinguish it from type 1 and type 2 diabetes. There are 14 known subtypes of MODY, and mutations in three genes (HNF1A, HNF4A, GCK) account for about 95% of all MODY cases. Diagnosis usually occurs before the age of 25 years, although less frequent forms may occur more often-but not necessarilylater in life. The molecular diagnosis may tailor the choice of the most appropriate treatment, with the aim to optimize blood glucose control, reduce the risk of hypoglycemic events and long-term complications, and enable proper genetic counseling. Treatment is usually unnecessary for patients with mutations in the GCK gene, while oral hypoglycemic agents (generally sulphonylureas) are recommended for patients with mutations in the HNF4A and HNF1A genes. More recent data show that other glucose-lowering agents can be effective in the latter patients, and additional and alternative therapies have been proposed. Proper management guidelines during pregnancy have been developed for carriers of GCK gene mutations, but such guidelines are still a subject of debate in other cases, although some recommendations are available. The other subtypes of MODY are even more rare, and very little data are available in the literature. In this review we summarize the most pertinent findings and recommendations on the treatment of patients with the different subtypes of MODY. Our aim is to provide the reader with an easy-to-read update that can be used to drive the clinician's therapeutical approach to these patients after the molecular diagnosis.

Monilinia spp. are responsible for brown rot decay of stone and pome fruit in the field as well as in postharvest. Monilinia laxa and M. fructigena are considered indigenous to Europe, while M. fructicola is a quarantine pathogen in the European and Mediterranean Plant Protection Organization area included in the A2 List. In Italy, it was first reported in 2009 in Piedmont (northern Italy) and rapidly spread to central Italy. We carried out a monitoring program on the occurrence of Monilinia spp. in southern Italy and a comparative characterization of the three main fungal pathogens. Molecular assays based on direct polymerase chain reaction (PCR) and real-time quantitative PCR for molecular identification of Monilinia spp. from rotted fruit were set up, validated, and applied in a monitoring program. Of the tested 519 isolates from 26 orchards, 388 (74.8%) were identified as M. fructicola, 118 (22.7%) as M. laxa, 10 (1.9%) as M. fructigena, and 3 (0.6%) were M. polystroma. M. fructicola colonies grew faster and had a higher optimal temperature for growth (26°C) than M. laxa (23°C) and M. fructigena (20°C). No relevant difference in virulence could be observed on artificially inoculated apricot, cherry, and peach fruit. The fungal species showed different responses to fungicides, because M. fructicola was more sensitive than M. laxa, especially to cyflufenamid, and M. fructigena revealed a lower sensitivity to succinate dehydrogenase inhibitors (boscalid, fluopyram, and fluxapyroxad) and quinone outside inhibitors (mandestrobin). In summary, the two species M. fructicola and M. polystroma were first detected in southern Italy where M. fructicola has largely displaced the two indigenous pathogens M. laxa and M. fructigena; the relative proportions of the three pathogens in orchards should be considered when defining the management of brown rot of stone fruit due to differences in their responses to fungicides.

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Childhood obesity is a modern worldwide epidemic with significant burden for health. It is a chronic metabolic disorder associated with multiple cardiovascular risk factors such as dyslipidemia, hypertension, stroke, and insulin resistance. Many obese adolescents remain obese into adulthood, with increased morbidity and mortality. As childhood obesity is a risk factor for adult obesity, the childhood obesity-related disorders account for an increased risk of cardiovascular consequences in adults, in addition to the effects already exerted by the fat mass in adulthood. Several papers have already described the cardiovascular implications of idiopathic obesity, while few data are available about syndromic obesity, due to the small sample size, not homogeneous phenotypes, and younger age at death. The aim of this mini-review is to give a comprehensive overview on knowledge about cardiovascular implications of idiopathic and syndromic obesity to allow the reader a quick comparison between them. The similarities and differences will be highlighted.