The Use of Poro-Elastic Finite Elements to Model the Structural Damping Effect of Fibrous Acoustical Treatments

Recently, new models for limp, fibrous sound absorbing materials have been proposed and verified. It has also been shown that these models may be used to optimize the sound absorption and barrier performance of layered acoustical systems. During that work, it was noticed that layers of fibrous materials can, under some circumstances, provide significant damping when they are applied to panel structures. It has since been shown that that structural damping effect may be predicted analytically by using a modal expansion procedure. The latter approach, however, can only conveniently be applied in circumstances when the vibrating structure has a simple shape and boundary conditions. Thus, in the work reported here it was of interest to demonstrate that the damping effect created by fibrous materials could also be predicted by using a finite element procedure. Successful application of the finite element method would then allow the damping effect of fibrous materials on arbitrarily shaped vibrating bodies to be studied. The poro-elastic finite element model that was used here to model the fibrous material has been described extensively elsewhere. That model has now been incorporated into a software package known as SAFE (Structural Acoustic Finite Element), an analysis module of the finite/boundary element package, COMET/Acoustics. The SAFE package was used to make the calculations reported here. The detailed objectives of the present work were first to duplicate analytical structural damping predictions by using a finite element approach, and thus to verify the earlier predictions. Secondly, it was desired to gain experience with modeling limp, fibrous materials by using SAFE. Finally, it was of interest to begin to optimize the acoustical behavior of acoustical materials by using numerical tools, and to examine the impact of these materials on the structural vibration of automotive panels, for example

Transat—A Method for Detecting the Conserved Helices of Functional RNA Structures, Including Transient, Pseudo-Knotted and Alternative Structures

The prediction of functional RNA structures has attracted increased interest, as it allows us to study the potential functional roles of many genes. RNA structure prediction methods, however, assume that there is a unique functional RNA structure and also do not predict functional features required for in vivo folding. In order to understand how functional RNA structures form in vivo, we require sophisticated experiments or reliable prediction methods. So far, there exist only a few, experimentally validated transient RNA structures. On the computational side, there exist several computer programs which aim to predict the co-transcriptional folding pathway in vivo, but these make a range of simplifying assumptions and do not capture all features known to influence RNA folding in vivo. We want to investigate if evolutionarily related RNA genes fold in a similar way in vivo. To this end, we have developed a new computational method, Transat, which detects conserved helices of high statistical significance. We introduce the method, present a comprehensive performance evaluation and show that Transat is able to predict the structural features of known reference structures including pseudo-knotted ones as well as those of known alternative structural configurations. Transat can also identify unstructured sub-sequences bound by other molecules and provides evidence for new helices which may define folding pathways, supporting the notion that homologous RNA sequence not only assume a similar reference RNA structure, but also fold similarly. Finally, we show that the structural features predicted by Transat differ from those assuming thermodynamic equilibrium. Unlike the existing methods for predicting folding pathways, our method works in a comparative way. This has the disadvantage of not being able to predict features as function of time, but has the considerable advantage of highlighting conserved features and of not requiring a detailed knowledge of the cellular environment

Numerical Modeling of the Damping Effect of Fibrous Acoustical Treatments

The damping effect that is observed when a fibrous acoustical treatment is applied to a thin metal panel typical of automotive structures has been modeled by using three independent techniques. In the first two methods the fibrous treatment was modeled by using the limp frame formulation proposed by Bolton et al., while the third method makes use of a general poro-elastic model based on the Biot theory. All three methods have been found to provide consistent predictions that are in excellent agreement with one another. An examination of the numerical results shows that the structural damping effect results primarily from the suppression of the nearfield acoustical motion within the fibrous treatment, that motion being closely coupled with the vibration of the base panel. The observed damping effect is similar in magnitude to that provided by constrained layer dampers having the same mass per unit area as the fibrous layer

Glucocorticoid receptor blockade normalizes hippocampal alterations and cognitive impairment in streptozotocin-induced type 1 diabetes mice

Type 1 diabetes is a common metabolic disorder accompanied by an increased secretion of glucocorticoids and cognitive deficits. Chronic excess of glucocorticoids per se can evoke similar neuropathological signals linked to its major target in the brain, the hippocampus. This deleterious action exerted by excess adrenal stress hormone is mediated by glucocorticoid receptors (GRs). The aim of the present study was to assess whether excessive stimulation of GR is causal to compromised neuronal viability and cognitive performance associated with the hippocampal function of the diabetic mice. For this purpose, mice had type 1 diabetes induced by streptozotocin (STZ) administration (170 mg/kg, i.p.). After 11 days, these STZ-diabetic mice showed increased glucocorticoid secretion and hippocampal alterations characterized by: (1) increased glial fibrillary acidic protein-positive astrocytes as a marker reacting to neurodegeneration, (2) increased c-Jun expression marking neuronal activation, (3) reduced Ki-67 immunostaining indicating decreased cell proliferation. At the same time, mild cognitive deficits became obvious in the novel object-placement recognition task. After 6 days of diabetes the GR antagonist mifepristone (RU486) was administered twice daily for 4 days (200 mg/kg, p.o.). Blockade of GR during early type 1 diabetes attenuated the morphological signs of hippocampal aberrations and rescued the diabetic mice from the cognitive deficits. We conclude that hippocampal disruption and cognitive impairment at the early stage of diabetes are caused by excessive GR activation due to hypercorticism. These signs of neurodegeneration can be prevented and/or reversed by GR blockade with mifepristone. © 2009 Nature Publishing Group All rights reserved.Fil: Revsin, Yanina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Rekers, Niels V.. Leiden University Medical Center; Países BajosFil: Louwe, Mieke C.. Leiden University Medical Center; Países BajosFil: Saravia, Flavia Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: de Nicola, Alejandro Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Ron De Kloet, E. Leiden University Medical Center; Países BajosFil: Oitzl, Melly S.. Leiden University Medical Center; Países Bajo