[Prevalence of Obstructive Sleep Apnea Syndrome among holders of a category B driver's license and among professionals in the Province of Pesaro-Urbino (Italy)]. / Prevalenza di OSAS nella provincia di Pesaro-Urbino: dati derivati da uno screening su titolari di patente superiore e/o professionale afferenti alla CML dell'Area Vasta 1.

Obstructive Sleep Apnea Syndrome (OSAS) is a sleeping disorder caused by repeated episodes of partial or complete obstruction of the upper airways during sleep. During 2013, a pilot project was performed in the Marche region (Italy), co-jointly by the University "Politecnica delle Marche" and the Italian National Institute of Work Accident Insurance (INAIL), among holders of a category "B" driver's licence and among professionals undergoing screening at an Occupational Medicine Service covering the Province of Pesaro-Urbino (Italy). Nineteen percent of 553 subjects undergoing a screening examination were found to be affected by OSAS. The data collected is of great interest in the phase of implementation of new national laws.

Glucose degradation products increase apoptosis of human mesothelial cells.

BACKGROUND: The heat sterilization of glucose solutions for peritoneal dialysis (PDS) induces the formation of glucose degradation products (GDPs), a phenomenon amplified by lactate and neutral pH. In the new three-compartment bag (3CB) PDS, a glucose solution at pH 3 is kept apart from the buffer until use, and the final solution delivers glucose concentrations that are similar to traditional PDS (TPD), with pH 6 and a lower content of GDPs. As GDPs have oxidant activity that may favour apoptosis, we investigated mesothelial cell apoptosis modulation by 12 h cultures in media supplemented with: (i) two relevant GDPs, methylglyoxal (MGly) and formaldehyde (For) in time and dose-dependence assays, (ii) GDPs at concentrations detected in TPD and 3CB, and (iii) commercial TPD and 3CB PDS, both with 1.36% glucose. METHODS: Apoptosis was evaluated by terminal 3' uridine labelling. Key proteins involved in the apoptotic pathway were investigated by reverse transcription polymerase chain reaction (RT-PCR) mRNA expression and immunoperoxidase staining (caspase 9, tumour suppressor protein p53, inducible cyclooxygenase COX-2). RESULTS: The apoptotic effects of MGly and For were dose and time dependent. GPDs at concentrations detected in TPD induced greater transcription and translation of apoptotic pathway proteins (caspase 9, p53 and COX-2) than GPDs in 3CB. This resulted in a higher apoptotic rate, which was not influenced by addition of sterile glucose. A similar enhancement of apoptosis was detected when mesothelial cells were incubated with TPD, whereas incubation in 3CB PDS resulted in less enhanced apoptosis. The 12 h incubation effect of PDS on cultured mesothelial cells was not related to advanced glycosylated end-product formation. CONCLUSIONS: As the rate of mesothelial cell apoptosis is lower in 3CB than in TPD solutions, the 3CB appears to provide improved biocompatibility.

Effects of growth hormone on leptin metabolism and energy expenditure in hemodialysis patients with protein-calorie malnutrition.

The relationships among growth hormone (GH), leptin, and resting energy expenditure (REE) are not understood. It has been reported that in malnourished hemodialysis patients, GH increases muscle protein synthesis, a process that requires energy. The present study evaluated the arterial levels and the forearm exchange of leptin, as well as the REE of the same patients during their participation in the same study, in four sequential 6-wk periods: I, baseline; II, GH treatment; III, washout; and IV, GH + intradialytic parenteral nutrition. During periods II and IV, patients received GH (5 mg three times per week). REE rose by 5% in period II, declined during period III, and rose by 7% during period IV. Basal leptin levels were low (2.0 +/- 0.19 ng/L). Insulin and leptin levels, as well as leptin release from the forearm, were unchanged during periods I through III but rose (+ 36%; P: < 0.05) during period IV. Changes in arterial leptin were directly related to changes in forearm leptin release (P: < 0.002), indicating a role of leptin production by peripheral tissues on leptinemia. Changes in leptin release were directly related to insulin (P: < 0.001) and, less consistently, to insulin-like growth factor-binding protein-1 levels (P: < 0.02). Similarly, variations in leptin levels were directly related to insulin (P: < 0.01). Variations in REE were not related to variations in leptin or insulin levels but to changes in muscle protein synthesis (P: < 0.025). The data show that in malnourished hemodialysis patients, treatment with GH is not invariably associated with an increase in leptin production. An increase in leptin release by peripheral tissues and leptin levels occurs only in the setting of hyperinsulinemia. The increase in REE that is induced by treatment with GH is not dependent on changes in leptin but is largely accounted for by the energy cost of the stimulation of muscle protein synthesis.