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Children and parents evaluate the child's quality of life (QOL) from their own perspectives; therefore, responses may differ, especially in abstract domains. We examined differences between self- and proxy-reported QOL of children with epilepsy. Children with active epilepsy (N=375) and their parents (N=378) separately completed the CHEQOL-25, a condition-specific QOL measure. The intraclass correlation coefficient was used to determine interrater agreement. Concordance on the Total CHEQOL-25 was 0.45 (P<0.01). Discrepancies were greatest for the subscales of Secrecy (0.24, P<0.01) and Present Concerns (0.32, P<0.01). School placement correlated with discrepancy in the Intrapersonal/Emotional subscale (r=0.19, P<0.05), and the child's age at testing correlated with discrepancy of the Total measure (r=0.15, P<0.01). This study demonstrates that parent perspectives alone are insufficient to measure their child's QOL. The CHEQOL-25 is a practical tool, with complementary parent and child versions, which can be used to determine health-related quality of life in children with epilepsy.
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Epilepsia/psicología , Relaciones Padres-Hijo , Padres/psicología , Calidad de Vida , Adolescente , Niño , Femenino , Humanos , MasculinoRESUMEN
We investigated the manifestation of Rabi oscillation in the coherent dynamics of excitons in self-assembled semiconductor quantum dots. The Rabi oscillation phenomenon was directly observed as a function of the input pulse area. Furthermore, by performing wave packet interferometry in the nonlinear excitation regime, we discover a new type of quantum interference phenomenon, resulting from the interplay between Rabi oscillation and quantum interference.
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AIMS: Although bipolar sensing is recommended and desirable in patients with dual chamber pacemakers (DDD) and intermittent atrial fibrillation (AF) it is a clinical reality that some patients who are given unipolar atrial leads without a prior history of AF may develop intermittent AF during follow-up. It was therefore the purpose of this prospective study to compare the electrogram amplitudes of AF potentials with sinus rhythm P-wave potentials as a relevant factor for appropriate mode switching in dual chamber pacing with unipolar atrial sensing. METHODS AND RESULTS: Forty-two patients with dual chamber pacemakers, unipolar atrial leads and intermittent AF were studied. Aside from measuring the P-wave potential, it was possible in 14 patients (4 women, 10 men; mean age: 61.8 (+/- 13.3) years) additionally to document spontaneous AF electrogram potentials using pacemaker telemetry. A prospective survey study was performed including a 6 month follow-up period with an outpatient clinic visit every 2-3 weeks. The mean P-wave electrogram amplitude was 3.4 (+/- 1.8) mV (range: 1.4-7.4) compared with the mean amplitude during AF of 2.04 (+/- 1.26) mV (range: 0.8-5.2 mV) indicating a significant attenuation of 40% during AF (P < 0.0001). A linear correlation regression analysis revealed that there was a significant correlation between the P-wave and the AF amplitude (P < 0.0001), with a correlation coefficient of r = 0.867. CONCLUSION: Once it is known that a substantial reduction exists in electrogram amplitude, compared with the P wave electrogram potential, an estimate can be made of whether AF potentials will be sensed, if the programming of atrial sensitivity is congruent with the P-wave characteristics and the presence or absence of myopotential triggering.
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Fibrilación Atrial/fisiopatología , Estimulación Cardíaca Artificial/métodos , Marcapaso Artificial , Fibrilación Atrial/terapia , Electrocardiografía , Electrofisiología , Diseño de Equipo , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios ProspectivosRESUMEN
The molecular characterization of GHRH and the GHRH receptor provides a framework for understanding the hypothalamic regulation of pituitary somatotroph function. The signaling events discerned from our investigation of GHRH receptor structure and function form the basis of a model for GHRH action, which is shown in Fig. 20. GHRH interaction with its seven transmembrane domain Gs-coupled receptor on the somatotroph (step 1) leads to the release of growth hormone from secretory granules (step 2), which is likely to involve a G protein-mediated interaction with ion channels, and to a stimulation of intracellular cAMP accumulation (step 3) (Mayo, 1992; Lin et al., 1992; Gaylinn et al., 1993). In several cell types tested, elevated cAMP leads to the phosphorylation and activation of the transcription factor CREB by protein kinase A (Gonzalez and Montminy, 1989; Sheng et al., 1991), and one target gene for CREB action is the pituitary-specific transcription factor Pit-1 or GHF-1 (step 4) (Bodner et al., 1988; Ingraham et al., 1988; McCormick et al., 1990). Pit-1 is a prototypic POU domain protein that is required for the appropriate regulation of the growth hormone gene in somatotroph cells, thus providing a pathway by which a GHRH signal can lead to increased growth hormone synthesis in the pituitary (step 5). In addition, Pit-1 is likely to directly regulate the synthesis of the GHRH receptor (step 6), in that the receptor is not expressed in the pituitary of dw/dw mice that lack functional Pit-1 (Lin et al., 1992), and a cotransfected Pit-1 expression construct can activate the GHRH receptor promoter in transiently transfected CV1 cells (Lin et al., 1993). It remains to be determined whether additional direct regulation of the GHRH receptor gene in response to the cAMP signaling pathway occurs (step 7). The inhibitory peptide somatostatin presumably interacts with this same signaling pathway through G protein-mediated suppression of the cAMP pathway (Tallent and Reisine, 1992; Bell and Reisine, 1993). In agreement with the importance of this signaling system for normal growth, a transgene encoding a nonphosphorylatable mutant CREB protein, which blocks the function of the endogenous CREB protein, is able to cause somatotroph hypoplasia and dwarfism in mice when its expression is targeted to pituitary somatotrophs (Struthers et al., 1991). Several steps in the signaling pathway leading to growth hormone secretion are subject to disruption, resulting in growth hormone deficiency.(ABSTRACT TRUNCATED AT 400 WORDS)