Summary.A 4-month-old baby girl, after a period of apparent good health, began to have aphonia, dyspnea, difficulties with swallowing, cyanosis, apnea, and hypopnea during sleep that resulted in admission to an intensive care unit for intubation and mechanical ventilation. At the age of 9 months she was admitted to our hospital with a possible diagnosis of central hypoventilation syndrome. A polysomnographic study showed apnea and hypopnea (apnea + hypopnea index = 47.1), hypercapnia (mean end-tidal PCO 2 89 ± 15.0 mmHg), and arterial desaturation (mean SaO 2 91 ± 1.7%; lowest SaO 2 < 50%; 68% of total sleep time at SaO 2 below 93%); the study also showed an absent ventilatory response to CO 2 , absent cardiac responses to apnea during sleep, and right ventricular hypertrophy.Nocturnal nasal bi-level positive airway pressure (BiPAP), applied initially at 6 cmH 2 O and gradually increased to 16 cmH 2 O, caused the sleep-related abnormal respiratory events to disappear. End-tidal PCO 2 decreased to 39 mmHg, and SaO 2 increased to 94%. After 6 months of nocturnal BiPAP ventricular right hypertrophy reversed and arrested growth and hypotonia normalized. The child has tolerated and has remained on BiPAP support up to her current age of 3 years and continues to use this form of ventilatory assistance without difficulties. Pediatr.

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A G1-conforming finite element formulation based on the Kirchhoff beam model suitable for the analysis of structures composed by coupling of slender beams is presented. A new set of kinematic parameters is introduced in order to account for the continuity required by the rod model. This new set of kinematic parameters defines the G1-map that guarantees continuity of the rotations at the ends of the beam. The tangent stiffness matrix for the proposed Kirchhoff beam model is derived in a consistent way. It is shown that an additional geometric term, specific for the G1-conforming formulation, appears in the tangent stiffness matrix. In order to avoid the singularities arising with the introduction of the G1-map, an updated Lagrangian formulation is adopted. In this way, a G1-conforming Bézier finite element based on the Kirchhoff beam model able to model large deformations of space rod systems is obtained. Several numerical examples show the high accuracy and the robustness of the proposed conforming formulation.

In humans beta-adrenergic receptors mediate an inhibitory effect on somatotropic function, likely via stimulation of hypothalamic somatostatin release. Accordingly, salbutamol (SAL), a beta 2-agonist, given iv abolishes the GH response to GH-releasing hormone (GHRH) in adults. Taking into account that in bronchial asthma an alteration in the beta-adrenergic neural control of airways has been hypothesized, we aimed to verify whether, in asthmatic children, beta-adrenergic activation inhibits or not GH secretion. To this goal, we studied the effect of therapeutical doses of SAL on GH response to GHRH in 15 asthmatic children (12 M and 3 F, 5.9-11.1 yr, pubertal stage I-II). All children underwent a GHRH test (1 microgram/kg iv). Moreover, in 7 children (group A), SAL was administered orally (0.125 mg/kg) 1 h before GHRH, while in 8 (group B) by inhaled aerosol (2 mg) 30 min before GHRH. Oral SAL (group A) abolished the GHRH-induced GH rise (AUC, mean +/- SE 165.1 +/- 33.3 vs 959.9 +/- 158.1 micrograms/L/h; p < 0.03). In group B, the GH response to GHRH was only blunted by inhaled SAL (938.6 +/- 284.6 vs 1378.8 +/- 315.6 micrograms/L/h; p < 0.02). In conclusion, our data show that in asthmatic children, therapeutical doses of SAL exert a marked inhibitory effect on GH secretion. Further studies are needed to exclude detrimental effects of chronic treatment with beta 2-agonists on GH secretion and growth velocity in asthmatic children.

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