No abstract

We have designed and tested a device based on non-Newtonian fluids for the attenuation of tangential impacts energy in helmets. A shear thickening fluid based on borurated silicones has given the best results in terms of impact energy attenuation in a system that selectively mimics tangential impacts and for this reason it has been used to fill the chamber of a pad, prepared by additive manufacturing, for impact energy dissipation. The pad is composed of a case containing the fluid in which is immersed a rigid pin that is free to move in all direction and therefore is able to absorb energy during its movement inside the fluid. A motorcycle helmet, already composed of two concentrical EPS (Expanded Polystyrene) liners, has been implemented with 7 pads between the two EPS layers. The two layers have only been connected by means of the dissipating pad and are free to rotate and to dissipate energy during the rotation. The results of oblique impacts according to ECE 22.06 with 3 impact positions, shows a reduction of the Brain Injury Criterion of 14% for the helmet with the pads, compared to the standard helmet, with values well below the threshold imposed by the norm. On the contrary, the maximum of the peak rotational accelleration show a 3% increase. Nevertheless, the rotational acceleration versus time curves indicates that in all 3 orientations the time of the maximum is shifted towards longer times for the helmets with the pads, indicating that the pads retard the acceleration of the head due to the efficient rotation of the two EPS parts connected by the pads. The described system could be implemented with minimal modifications in existing protective sport and motorcycle helmets.

Fragile X syndrome (FXS), caused by lack of fragile X mental retardation protein (FMRP), is associated with a high prevalence of autism. The deficit of FMRP reported in idiopathic autism suggests a mechanistic overlap between FXS and autism. The overall goal of this study is to detect neuropathological commonalities of FMRP deficits in the brains of people with idiopathic autism and with syndromic autism caused by dup15q11.2-q13 (dup15). This study tests the hypothesis based on our preliminary data that both idiopathic and syndromic autism are associated with brain region-specific deficits of neuronal FMRP and structural changes of the affected neurons. This immunocytochemical study revealed neuronal FMRP deficits and shrinkage of deficient neurons in the cerebral cortex, subcortical structures, and cerebellum in subjects with idiopathic and dup(15)/autism. Neuronal FMRP deficit coexists with surprising infiltration of the brains of autistic children and adults with FMRP-positive astrocytes known to be typical only for the fetal and short postnatal periods. In the examined autistic subjects, these astrocytes selectively infiltrate the border between white and gray matter in the cerebral and cerebellar cortex, the molecular layer of the cortex, part of the amygdala and thalamus, central cerebellar white matter, and dentate nucleus. Astrocyte pathology results in an additional local loss of FMRP in neurons and their shrinkage. Neuronal deficit of FMRP and shrinkage of affected neurons in structures free of FMRP-positive astrocytes and regions infiltrated with FMRP-expressing astrocytes appear to reflect mechanistic, neuropathological, and functional commonalities of FMRP abnormalities in FXS and autism spectrum disorder. Autism Res 2018, 11: 1316-1331. © 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Immunocytochemistry reveals a deficit of fragile X mental retardation protein (FMRP) in neurons of cortical and subcortical brain structures but increased FMRP expression in astrocytes infiltrating gray and white matter. The detected shrinkage of FMRP-deficient neurons may provide a mechanistic explanation of reported neuronal structural and functional changes in autism. This study contributes to growing evidence of mechanistic commonalities between fragile X syndrome and autism spectrum disorder.