Young Adults with Cleft Lip and Palate: Are They Receiving Team Services?

It is widely acknowledged that a team approach is preferred practice and contributes to optimizing the surgical, dental, speech and psychosocial outcomes for individuals with CLP. Young adulthood often marks the transition from child-centered interdisciplinary care to adult-centered care. There is a paucity in literature relating to the transition of care for young adults with CLP. The purpose of this survey research is therefore to explore the CLP team practices regarding young adults with CLP

Polymorphism of Beta2-Adrenoceptor and Regular Use of Formoterol in Asthma: Preliminary Results

Polymorphism at codon 16 of the beta2-adrenoceptor (beta2-AR) affects the responsiveness to salmeterol in asthmatics. Data concerning formoterol are more controversial in the literature. The aim of this study was to verify whether homozygous for arginine-16 (ArgArg16) and homozygous for glycine-16 (GlyGly16) genotypes differently influence the long-term responsiveness to formoterol. Twenty-nine patients with mild-to-moderate asthma, in stable clinical conditions, underwent genotyping at codon 16 of the beta2-AR by RFLP-PCR assay. The effects of a 4-week monotherapy with formoterol (12 μg BID) were tested on the peak expiratory flow (PEF) variability and the forced expiratory volume in 1 sec (FEV1) slope of the dose-response curve to salbutamol. Variability in PEF significantly increased during the 4-week treatment period in 14 patients with GlyGly16, but not in 15 patients with ArgArg16 and ArgGly16 (P=0.032). The FEV1 slope of the dose-response curve to salbutamol decreased after the 4-week treatment period in GlyGly16, but not in pooled ArgArg16 and ArgGly16 patients. This study provides preliminary evidence that tolerance to formoterol develops more frequently in asthmatics with GlyGly16 genotype. If confirmed in a larger population, this finding might be useful in choosing the bronchodilator therapy on the basis of genetic polymorphism of the beta2-AR

Impact of different exposure models and spatial resolution on the long-term effects of air pollution.

Abstract Long-term exposure to air pollution has been related to mortality in several epidemiological studies. The investigations have assessed exposure using various methods achieving different accuracy in predicting air pollutants concentrations. The comparison of the health effects estimates are therefore challenging. This paper aims to compare the effect estimates of the long-term effects of air pollutants (particulate matter with aerodynamic diameter less than 10 μm, PM10, and nitrogen dioxide, NO2) on cause-specific mortality in the Rome Longitudinal Study, using exposure estimates obtained with different models and spatial resolutions. Annual averages of NO2 and PM10 were estimated for the year 2015 in a large portion of the Rome urban area (12 × 12 km2) applying three modelling techniques available at increasing spatial resolution: 1) a chemical transport model (CTM) at 1km resolution; 2) a land-use random forest (LURF) approach at 200m resolution; 3) a micro-scale Lagrangian particle dispersion model (PMSS) taking into account the effect of buildings structure at 4 m resolution with results post processed at different buffer sizes (12, 24, 52, 100 and 200 m). All the exposures were assigned at the residential addresses of 482,259 citizens of Rome 30+ years of age who were enrolled on 2001 and followed-up till 2015. The association between annual exposures and natural-cause, cardiovascular (CVD) and respiratory (RESP) mortality were estimated using Cox proportional hazards models adjusted for individual and area-level confounders. We found different distributions of both NO2 and PM10 concentrations, across models and spatial resolutions. Natural cause and CVD mortality outcomes were all positively associated with NO2 and PM10 regardless of the model and spatial resolution when using a relative scale of the exposure such as the interquartile range (IQR): adjusted Hazard Ratios (HR), and 95% confidence intervals (CI), of natural cause mortality, per IQR increments in the two pollutants, ranged between 1.012 (1.004, 1.021) and 1.018 (1.007, 1.028) for the different NO2 estimates, and between 1.010 (1.000, 1.020) and 1.020 (1.008, 1.031) for PM10, with a tendency of larger effect for lower resolution exposures. The latter was even stronger when a fixed value of 10 μg/m3 is used to calculate HRs. Long-term effects of air pollution on mortality in Rome were consistent across different models for exposure assessment, and different spatial resolutions

IL BIAS ATTENZIONALE NELL’ANSIA SOCIALE: IL RUOLO DEGLI STIMOLI EMOZIONALI

Il disturbo d’ansia sociale è caratterizzato da una paura intensa e persistente di essere giudicati negativamente dagli altri, per il timore di svelare una personalità globalmente inadeguata. Numerosi autori hanno evidenziato che individui con ansia sociale presentano un bias attenzionale (BA) verso stimoli minacciosi. Tuttavia, sono presenti risultati contrastanti. Mentre alcuni autori non hanno osservato un BA, somministrando un compito con stimoli lessicali, altri hanno evidenziato un BA verso stimoli minacciosi con l’uso di stimoli pittorici. Lo studio si propone di confrontare con un paradigma di Emotional Spatial Cueing tre tipologie di stimoli: pittorici (immagini e volti) e lessicali. Studenti con bassa ansia sociale (N=42; BAS) e con alta ansia sociale (N=42; AAS) hanno completato l’Emotional Spatial Cueing e la Liebowitz Social Anxiety Scale. Sono stati utilizzati tre tipi di stimolo: immagini, selezionate dall’International Affective Picture System; volti, selezionati dal database di Maccari et al. (2014); parole, valutate da 20 studenti universitari, secondo un valore di emozionalità e minaccia. Un’ANOVA 2 (Gruppo: BAS, AAS) x 3 (Esperimento: Immagini, Parole, Volti) x 2 (Validità: prova valida, prova invalida) x 2 (Emozione: neutra, minacciosa) sui tempi di reazione (TR) ha evidenziato effetti significativi dell’Esperimento (F2,164=4,10; p=.018), della Validità (F1,82=289,69; p=.0001), dell’Emozione (F1,82=12,70; p=.0001) e le interazioni Esperimento x Emozione (F2,164=15,49; p=.0001) e Gruppo x Esperimento x Emozione (F2,164=3,03; p=.05). Dei confronti pianificati hanno indicato nell’Esperimento Volti una differenza tra il gruppo BAS e AAS (F1,82=7,19; p=.0001), con TR minori verso i volti neutri (531,18ms), rispetto ai volti minacciosi (537,48ms) solo nel gruppo AAS (F1,82=3,98; p=.04). Questo è il primo studio che confronta differenti tipi di stimolo in persone con ansia sociale, suggerendo una maggiore sensibilità delle persone con ansia sociale verso immagini di volti minacciosi. Questo risultato assume particolare rilevanza nell’ambito dello sviluppo di training volti alla riduzione del bias attenzionale

Modulation of Amyloid β-Induced Microglia Activation and Neuronal Cell Death by Curcumin and Analogues

: Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is not restricted to the neuronal compartment but includes important interactions with immune cells, including microglia. Protein aggregates, common pathological hallmarks of AD, bind to pattern recognition receptors on microglia and trigger an inflammatory response, which contributes to disease progression and severity. In this context, curcumin is emerging as a potential drug candidate able to affect multiple key pathways implicated in AD, including neuroinflammation. Therefore, we studied the effect of curcumin and its structurally related analogues cur6 and cur16 on amyloid-β (Aβ)-induced microglia activation and neuronal cell death, as well as their effect on the modulation of Aβ aggregation. Primary cortical microglia and neurons were exposed to two different populations of Aβ42 oligomers (Aβ42Os) where the oligomeric state had been assigned by capillary electrophoresis and ultrafiltration. When stimulated with high molecular weight Aβ42Os, microglia released proinflammatory cytokines that led to early neuronal cell death. The studied compounds exerted an anti-inflammatory effect on high molecular weight Aβ42O-stimulated microglia and possibly inhibited microglia-mediated neuronal cell toxicity. Furthermore, the tested compounds demonstrated antioligomeric activity during the process of in vitro Aβ42 aggregation. These findings could be investigated further and used for the optimization of multipotent candidate molecules for AD treatment