A Dynamical Study of the Non-Star Forming Translucent Molecular Cloud MBM16: Evidence for Shear Driven Turbulence in the Interstellar Medium

We present the results of a velocity correlation study of the high latitude cloud MBM16 using a fully sampled $^{12}$CO map, supplemented by new $^{13}$CO data. We find a correlation length of 0.4 pc. This is similar in size to the formaldehyde clumps described in our previous study. We associate this correlated motion with coherent structures within the turbulent flow. Such structures are generated by free shear flows. Their presence in this non-star forming cloud indicates that kinetic energy is being supplied to the internal turbulence by an external shear flow. Such large scale driving over long times is a possible solution to the dissipation problem for molecular cloud turbulence.Comment: Uses AAS aasms4.sty macros. Accepted for publication in Ap

Dynamics of Coherent States in Regular and Chaotic Regimes of the Non-integrable Dicke Model

The quantum dynamics of initial coherent states is studied in the Dicke model and correlated with the dynamics, regular or chaotic, of their classical limit. Analytical expressions for the survival probability, i.e. the probability of finding the system in its initial state at time $t$, are provided in the regular regions of the model. The results for regular regimes are compared with those of the chaotic ones. It is found that initial coherent states in regular regions have a much longer equilibration time than those located in chaotic regions. The properties of the distributions for the initial coherent states in the Hamiltonian eigenbasis are also studied. It is found that for regular states the components with no negligible contribution are organized in sequences of energy levels distributed according to Gaussian functions. In the case of chaotic coherent states, the energy components do not have a simple structure and the number of participating energy levels is larger than in the regular cases.Comment: Contribution to the proceedings of the Escuela Latinoamericana de F\'isica (ELAF) Marcos Moshinsky 2017. (9 pages, 4 figures

Model Based Analysis of Shimmy in a Racing Bicycle

In this paper we are presenting a model of a racing bicycle, developed in Modelica language within the Dymola environment. The main purpose is to investigate the dynamic response of the bicycle and its modes of vibration, referring in particular to shimmy. This phenomenon occurs at high speeds and consists of sudden oscillations of the front assembly around the steering axis. Lateral accelerations on the horizontal tube of the frame can reach 5-10 g with a frequency that varies between 5-10 Hz. Even if it is quite uncommon, shimmy is a topic of great relevance, because it may be extremely dangerous for the rider. Thanks to this model, we can show that the main elements which contribute to the rise of the oscillations are the lateral compliance of the frame and the tyres’ deformation

Endothelial cells, endoplasmic reticulum stress and oxysterols

Oxysterols are bioactive lipids that act as regulators of lipid metabolism, inflammation, cell viability and are involved in several diseases, including atherosclerosis. Mounting evidence linked the atherosclerosis to endothelium dysfunction; in fact, the endothelium regulates the vascular system with roles in processes such as hemostasis, cell cholesterol, hormone trafficking, signal transduction and inflammation. Several papers shed light the ability of oxysterols to induce apoptosis in different cell lines including endothelial cells. Apoptotic endothelial cell and endothelial denudation may constitute a critical step in the transition to plaque erosion and vessel thrombosis, so preventing the endothelial damaged has garnered considerable attention as a novel means of treating atherosclerosis. Endoplasmic reticulum (ER) is the site where the proteins are synthetized and folded and is necessary for most cellular activity; perturbations of ER homeostasis leads to a condition known as endoplasmic reticulum stress. This condition evokes the unfolded protein response (UPR) an adaptive pathway that aims to restore ER homeostasis. Mounting evidence suggests that chronic activation of UPR leads to cell dysfunction and death and recently has been implicated in pathogenesis of endothelial dysfunction. Autophagy is an essential catabolic mechanism that delivers misfolded proteins and damaged organelles to the lysosome for degradation, maintaining basal levels of autophagic activity it is critical for cell survival. Several evidence suggests that persistent ER stress often results in stimulation of autophagic activities, likely as a compensatory mechanism to relieve ER stress and consequently cell death. In this review, we summarize evidence for the effect of oxysterols on endothelial cells, especially focusing on oxysterols-mediated induction of endoplasmic reticulum stress

Assessment of the Triage System in a Pediatric Emergency Department. A pilot study on critical code

Introduction. In Italy, triage involves assigning a priority color code to patients arriving at the hospital Emergency Department: red (very critical), yellow (moderately critical), green (not very critical), and white (not critical). Methods. This study was aimed at assessing the triage system in the Emergency Department of ?Giannina Gaslini? Children? s Hospital in Genoa, Italy. The authors examined 130 triage forms assigning a yellow code in 2003, in order to determine whether they had been correctly filled in with regard to the detection of vital parameters, identification of main symptoms and color code assignment. Results. Results showed that vital signs were recorded in 94% of patients, main symptoms were identified in 97%, and a yel- low code was assigned according to hospital guidelines in 84%. The percentage of underestimation (3.2%) was higher than that reported in the literature (2%). Conclusions. The study shows the need to improve compliance with the guidelines and to evaluate green and white codes

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

Gitelman syndrome associated with chondrocalcinosis and severe neuropathy: a novel heterozygous mutation in SLC12A3 gene

Gitelman syndrome (GS) is an inherited salt-wasting tubulopathy characterized by hypocalciuria, hypokalemia, hypomagnesemia and metabolic alkalosis, due to inactivating mutations in the SLC12A3 gene. Symptoms may be systemic, neurological, cardiovascular, ophthalmological or musculoskeletal. We describe a 70 year-old patient affected by recurrent arthralgias, hypoesthesia and hyposthenia in all 4 limbs and severe hypokalemia, complicated by atrial flutter. Moreover, our patient reported eating large amounts of licorice, and was treated with medium-high dosages of furosemide, thus making diagnosis very challenging. Genetic analysis demonstrated a novel heterozygous mutation in the SLC12A3 gene; therefore, we diagnosed GS and started potassium and magnesium replacement. GS combined with chondrocalcinosis and neurological involvement is quite common, but this is the first case of an EMG-proven severe neuropathy associated with GS. Herein, we underline the close correlation between hypomagnesemia, chondrocalcinosis and neurological involvement. Moreover, we report a new heterozygous mutation in exon 23 (2738G>A), supporting evidence of a large genetic heterogeneity in this late-onset congenital tubulopathy