RESUMO
The decrease in reactance of perforated plates at high sound pressure amplitudes is of interest for the design of Helmholtz resonator liners. It is associated with the loss of end correction due to flow separation at the orifices. In practical applications, complex acoustic signals impinge on perforations. The loss of end correction due to multiple stimuli of unrelated frequency and phase has not been considered yet. This study assesses and presents an empirical approximation for the reduction of end correction of perforated plates at primary frequencies when flow separation is induced by an additional secondary unrelated high amplitude stimulus.
Assuntos
Acústica , SomRESUMO
High sound pressure levels cause impedance changes in orifices and perforated plates due to vortex shedding and jet formation at the orifices. The effects of an additional high amplitude stimulus, unrelated in terms of frequency and phase, on the impedance of perforated plates received little attention. This work experimentally studies the impedance changes of perforated plates at various primary frequencies when an additional unrelated high-level single tone actuation is applied. It is shown that the impedance, the primary sound field faces, is altered dependent on the particle velocity induced in the orifices by the secondary actuation. Dimensionless quantities correlating the change of impedance with the secondary excitation are identified from the measurements and an empirical model for the change of resistance at quasi-steady flow conditions is derived. The results show that for low amplitude primary sound fields, the change of impedance is completely dependent on the secondary sound field. In case of a high amplitude primary sound field, the impedance is dependent on the particle velocities induced by both sound fields, whereas the larger induced particle velocity is the main contributor to the impedance changes. For unsteady flow conditions, a dependency on the frequency of the secondary actuation is found.
RESUMO
In familial and sporadic forms of Parkinson's disease (PD), alpha-synuclein pathology is present in the brain stem nuclei and olfactory bulb (OB) long before Lewy bodies are detected in the substantia nigra. The OB is an active region of adult neurogenesis, where newly generated neurons physiologically integrate. While accumulation of wild-type alpha-synuclein is one of the pathogenic hallmarks of non-genetic forms of PD, the A30P alpha-synuclein mutation results in an earlier disease onset and a severe clinical phenotype. Here, we study the regulation of adult neurogenesis in the subventricular zone (SVZ)/OB system in a tetracycline-suppressive (tet-off) transgenic model of synucleinopathies, expressing human mutant A30P alpha-synuclein under the control of the calcium/calmodulin-dependent protein kinase II alpha (CaMK) promoter. In A30P transgenic mice alpha-synuclein was abundant at the site of integration in the glomerular cell layer of the OB. Without changes in proliferation in the SVZ, significantly fewer newly generated neurons were observed in the OB granule cell and glomerular layers of A30P transgenic mice than in controls, most probably due to increased cell death. By tetracycline-dependent abrogation of A30P alpha-synuclein expression, OB neurogenesis and programmed cell death was restored to control levels. Our results indicate that, using A30P conditional (tet-off) mice, A30P alpha-synuclein has a negative impact on olfactory neurogenesis and suppression of A30P alpha-synuclein enhances survival of newly generated neurons. This finding suggests that interfering with alpha-synuclein pathology can rescue newly generated neurons, possibly leading to new targets for therapeutic interventions in synucleinopathies.
