On the Solved Turbulent Scales in Turbulent Plume Fires

Plume fires are characterized by a turbulent nature with a large number of different scales. LES is often used to solve the largest structures and to model the smallest ones. Grid size and time steps become decisive to place the limit between resolved and modelled turbulence. Significant information on this limit and its placement can be obtained with spectral analyses of the specific turbulent kinetic energy. While frequency analysis is relatively easy, an analysis in the wavenumber domain is more challenging. The IWC method, typically used in structures and acoustics, is used here for this purpose. IWC method allows to obtain wavenumber spectra with a better resolution than those obtained with a direct approach. Furthermore, in this paper the IWC method is also used in its reverse form to obtain frequency spectra. Although rather dense grids have been chosen, the number of nodes along the plume and their spacing is not such as to guarantee detailed wavenumber spectra with the direct approach and consequently with the reverse IWC. On the contrary, the IWC method provides wavenumber spectra in agreement with those obtained directly, but of much higher quality

Ocular Refraction at Birth and Its Development During the First Year of Life in a Large Cohort of Babies in a Single Center in Northern Italy

The purpose of this study was to investigate refraction at birth and during the first year of life in a large cohort of babies born in a single center in Northern Italy. We also aimed to analyze refractive errors in relation to the gestational age at birth. An observational ophthalmological assessment was performed within 24 h of birth on 12,427 newborns. Refraction was examined using streak retinoscopy after the administration of tropicamide (1%). Values in the range of between +0.50 ≤ D ≤ +4.00 were defined as physiological refraction at birth. Newborns with refraction values outside of the physiological range were followed up during the first year of life. Comparative analyses were conducted in a subgroup of babies with known gestational ages. The following distribution of refraction at birth was recorded: 88.03% of the babies had physiological refraction, 5.03% had moderate hyperopia, 2.14% had severe hyperopia, 3.4%, had emmetropia, 0.45%, had myopia, 0.94% had astigmatism, and 0.01% had anisometropia. By the end of the first year of life, we observed reductions in hyperopia and astigmatism, and stabilization of myopia. Preterm babies had a four-fold higher risk of congenital myopia and a three-fold higher risk of congenital emmetropia as compared to term babies. Refraction profiles obtained at birth changed during the first year of life, leading to a normalization of the refraction values. Gestational age at birth affected the incidence of refractive errors and amblyopia

Dual inhibitory action of trazodone on dorsal raphe serotonergic neurons through 5-HT1A receptor partial agonism and α1-adrenoceptor antagonism

Trazodone is an antidepressant drug with considerable affinity for 5-HT1A receptors and α1-adrenoceptors for which the drug is competitive agonist and antagonist, respectively. In this study, we used cell-attached or whole-cell patch-clamp recordings to characterize the effects of trazodone at somatodendritic 5-HT1A receptors (5-HT1AARs) and α1-adrenoceptors of serotonergic neurons in rodent dorsal raphe slices. To reveal the effects of trazodone at α1-adrenoceptors, the baseline firing of 5-HT neurons was facilitated by applying the selective α1-adrenoceptor agonist phenylephrine at various concentrations. In the absence of phenylephrine, trazodone (1-10 μM) concentration-dependently silenced neurons through activation of 5-HT1AARs. The effect was fully antagonized by the selective 5-HT1A receptor antagonist Way-100635. With 5-HT1A receptors blocked by Way-100635, trazodone (1-10 μM) concentration-dependently inhibited neuron firing facilitated by 1 μM phenylephrine. Parallel rightward shift of dose-response curves for trazodone recorded in higher phenylephrine concentrations (10-100 μM) indicated competitive antagonism at α1-adrenoceptors. Both effects of trazodone were also observed in slices from Tph2-/- mice that lack synthesis of brain serotonin, showing that the activation of 5-HT1AARs was not mediated by endogenous serotonin. In whole-cell recordings, trazodone activated 5-HT1AAR-coupled G protein-activated inwardly-rectifying (GIRK) channel conductance with weak partial agonist efficacy (~35%) compared to that of the full agonist 5-CT. Collectively our data show that trazodone, at concentrations relevant to its clinical effects, exerts weak partial agonism at 5-HT1AARs and disfacilitation of firing through α1-adrenoceptor antagonism. These two actions converge in inhibiting dorsal raphe serotonergic neuron activity, albeit with varying contribution depending on the intensity of α1-adrenoceptor stimulation