[Effect of physical exercise training on the arterial pressure in normotensive subjects]. / Effetto dell'allenamento all'esercizio fisico sulla pressione arteriosa in soggetti normotesi.

To determine the effect of exercise training on blood pressure at rest and during maximal exercise 15 adolescent and 15 adult normotensive cyclists were studied after a period of detraining and of physical activity. In the lying position resting blood pressure did not change with training, while a slight but significant decrease in blood pressure (p less than 0.05) was observed on standing up. At the same absolute work rate, after training exertional blood pressure was lower than before training, but at peak exercise the same blood pressure levels were achieved before and after training. These results indicate that, contrary to what has been reported in the sedentary subject, resuming exercise training after a period of detraining brings about in the normotensive athlete only minor changes in blood pressure.

Metabolic effects of glucagon in endogenous hypertriglyceridemia.

The metabolic effects of glucagon, administered i.v. in doses of 1 microgram/kg, were evaluated in two groups of patients with endogenous hypertriglyceridemia (Types IV and V according to Fredrickson) with normal and reduced glucose tolerance and in a control group. Glucagon had a lipolytic effect, evaluated as the plasma increase of free fatty acids (FFA) during the first 20 min in normal subjects, but not in the two hyperlipemic groups. A negative correlation was observed between fasting IRI level and FFA mobilization. The ketogenic and hypotriglyceridemic effects of glucagon were demonstrated in normal and hyperlipemic groups. It would seem, therefore, that at the pharmacological doses injected, there is no resistance to the hypotriglyceridemic effect of glucagon in endogenous hypertriglyceridemia.

Neonatal respiratory morbidity risk and mode of delivery at term: influence of timing of elective caesarean delivery.

AIM: To establish whether the timing of delivery between 37 + 0 and 41 + 6 wk gestation influences neonatal respiratory outcome in elective caesarean delivery, following uncomplicated pregnancy, thus providing information that can be used to aid planning of elective delivery at term. METHODS: All pregnant women who were delivered by elective caesarean delivery at term during a 3-y period were identified from a perinatal database and compared retrospectively with pregnant women matched for week of gestation, who were vaginally delivered. Maternal characteristics, neonatal outcome, incidence of respiratory distress syndrome (RDS) and transient tachypnea of the newborn (TTN) were analysed. During this time, 1284 elective caesarean section deliveries occurred at or after 37 + 0 wk of gestation. RESULTS: Neonatal respiratory morbidity risk (odds ratio, OR), including RDS and TTN, was significantly higher in the infant group delivered by elective caesarean delivery compared with vaginal delivery (OR 2.6; 95% CI: 1.35-5.9; p < 0.01). While TTN risk in caesarean delivery was not increased (OR 1.19; 95% CI: 0.58-2.4; p > 0.05), the RDS risk was significantly increased (OR 5.85; 95% CI: 2.27-32.4; p < 0.01). This RDS risk is greatly increased in weeks 37 + 0 to 38 + 6 (OR 12.9; 95% CI: 3.57-35.53; p < 0.01). After 39 + 0 wk, there was no significant difference in RDS risk. CONCLUSIONS: Infants born by elective caesarean delivery at term are at increased risk for developing respiratory disorders compared with those born by vaginal delivery. A significant reduction in neonatal RDS would be obtained if elective caesarean delivery were performed after 39 + 0 gestational weeks of pregnancy.

Characterization of the genomic structure of the human neuronal nicotinic acetylcholine receptor CHRNA5/A3/B4 gene cluster and identification of novel intragenic polymorphisms.

Genes coding for the alpha5, alpha3, and beta4 subunits (CHRNA5, CHRNA3, and CHRNB4) of the neuronal nicotinic acetylcholine receptors (nAChRs) are clustered on chromosome 15q24. Linkage of this chromosomal region to autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), an idiopathic partial epilepsy, was reported in one family. Moreover, mutations in other neuronal nAChR subunit genes coding for the alpha4 (CHRNA4) and the beta2 (CHRNB2) subunits were associated with ADNFLE. Apart from the exon-intron structure of CHRNA3, the genomic organization of this gene cluster was unknown, making comprehensive mutational analyses impossible. The genomic structure of CHRNA5 and CHRNB4 is here reported. Moreover, two hitherto unknown introns were identified within the 3' untranslated region of CHRNA3, causing a partial tail-to-tail overlap with CHRNA5. Four novel intragenic polymorphisms were identified and characterized in the cluster.