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On average, radon concentrations are substantially higher in schools in villages than in schools located in towns (double,on average). Annual radon concentrations exceeding 300 Bq/m3 were found in 5% of primary schools (generally on ground floors of schools in villages). The considerable variability of radon concentration observed between and within floors indicates a need to monitor concentrations in several rooms for each floor. A single radon detector for each room can be used provided that the measurement error is considerable lower than variability of radon concentration between rooms.

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Intrauterine growth retardation (IUGR) has been linked to the development of type 2 diabetes in later life. The mechanisms underlying this phenomenon are unknown. Recent data suggest that some of the molecular defects underlying type 2 diabetes reside in the CNS. The enzyme carnitine palmitoyltransferase-1 (CPT1) regulates long-chain fatty acid (LCFA) entry into mitochondria, where LCFA undergo ␤-oxidation. Hypothalamic inhibition of CPT1 decreases food intake and suppresses endogenous glucose production. Our aim was to investigate the effects of uterine artery ligation, a procedure that mimics uteroplacental insufficiency, on the CNS expression of CPT1 and other key enzymes of LCFA metabolism. Bilateral uterine artery ligation was performed on d 19 of gestation in the pregnant rat; sham-operated pregnant rats served as controls. Hypothalamus, cerebellum, hippocampus, and cortex were dissected and analyzed at birth by real-time PCR. Nonesterified fatty acid (NEFA) serum levels were significantly higher in IUGR pups (p Ͻ 0.0001). In IUGR rats, the hypothalamic expression of CPT1 isoform C (p ϭ 0.005) and acetyl-CoA carboxylase (ACC) isoforms alpha (p Ͻ 0.05) and beta (p ϭ 0.005) were significantly decreased. The data presented here support the hypothesis that an abnormal intrauterine milieu can induce changes in hypothalamic lipid sensing. E pidemiologic studies in man have shown that impaired intrauterine growth is associated with an increased incidence of insulin resistance, type 2 diabetes, and cardiovascular disease in the adult (1-5). These observations have led to the hypothesis that adult disease arises in utero, in part, as a result of changes in the development of key endocrine and metabolic pathways during suboptimal intrauterine conditions associated with impaired fetal growth. This hypothesis has been tested experimentally in a number of species, using a range of techniques to impair fetal growth. Inducing IUGR by placental insufficiency or by undernutrition, stress, or hormone treatment of the mother leads to endocrine and metabolic alterations in the adult offspring in several species (6). These findings have led to the "fetal origins" hypothesis, which suggests that an adverse intrauterine environment would program or imprint the development of fetal tissues, permanently determining responses producing later dysfunction and disease (7).The hypothalamus is emerging as a critical site for the integration of nutritional, endocrine, and neural cues signaling the body's metabolic and nutritional status. Neurons in the hypothalamus (particularly in the arcuate nucleus) are primary targets of a number of key hormones and metabolic signals. Hypothalamic neurons, in turn, target several downstream sites to influence the coordinated autonomic, behavioral, and endocrine responses. These signals should normally activate a negative feedback loop between the availability of nutrients and their intake and metabolism (8 -10). A major breakthrough in the understanding of mechanisms leading to type 2 diabe...