Virtual acoustic rendering by state wave synthesis

International audienceIn the context of the class of virtual acoustic simulation techniques that rely on traveling wave rendering as dictated by path-tracing methods (e.g, image-source, ray-tracing, beam-tracing) we introduce State Wave Synthesis (SWS), a novel framework for the efficient rendering of sound traveling waves as exchanged between multiple directional sound sources and multiple directional sound receivers in time-varying conditions.The proposed virtual acoustic rendering framework represents sound-emitting and sound-receiving objects as multiple-input, multiple-output dynamical systems. Each input or output corresponds to a sound traveling wave received or emitted by the object from/to different orientations or at/from different positions of the object. To allow for multiple arriving/departing waves from/to different orientations and/or positions of an object in dynamic conditions, we introduce a discrete-time state-space system formulation that allows the inputs or the outputs of a system to mutate dynamically. The SWS framework treats virtual source or receiver objects as time-varying dynamical systems in state-space modal form, each allowing for an unlimited number of sound traveling wave inputs and outputs.To model the sound emission and/or reception behavior of an object, data may be collected from measurements. These measurements, which may comprise real or virtual impulse or frequency responses from a real physical object or a numerical physical model of an object, are jointly processed to design a multiple-input, multiple-output state-space model with mutable inputs and/or outputs. This mutable state-space model enables the simulation of direction- and/or position-dependent, frequency-dependent sound wave emission or reception of the object. At run-time, each of the mutable state-space object models may present any number of inputs or outputs, with each input or output associated to a received/emitted sound traveling wave from/to specific arrival/departure position or orientation. In a first formulation, the sound wave form, the traveling of sound waves between object models is simulated by means of delay lines of time-varying length. In a second formulation, the state wave form, the traveling of sound waves between object models is simulated by way of propagating the state variables of source objects along delay lines of time-varying length. SWS allows the accurate simulation of frequency-dependent source directivity and receiver directivity in time-varying conditions without any time-domain or frequency-domain explicit convolution processing. In addition, the framework enables time-varying, obstacle-induced frequency-dependent attenuation of traveling waves without any dedicated digital filters. SWS facilitates the implementation of efficient virtual acoustic rendering engines either as software or in dedicated hardware, allowing realizations in which the number of delay lines is independent of the number of traveling wave paths being simulated. Moreover, the method enables a straightforward dynamic coupling between virtual acoustic objects and their physics-based simulation counterparts as performed by computer for animation, virtual reality, video-games, music synthesis, or other applications.In this presentation we will introduce the foundations of SWS and employ a real acoustic violin and a real human head as illustrative examples for a source object and a receiver object respectively. In light of available implementation possibilities, we will examine the basic memory requirements and computational cost of the rendering framework and suggest how to conveniently include minimum-phase diffusive elements to procure additional diffuse field contributions if necessary. Finally, we will expose limitations and discuss future opportunities for development

Temporal changes in cardiac oxidative stress, inflammation and remodeling induced by exercise in hypertension: Role for local angiotensin II reduction

Exercise training reduces renin-angiotensin system (RAS) activation, decreases plasma and tissue oxidative stress and inflammation in hypertension. However, the temporal nature of these phenomena in response to exercise is unknown. We sought to determine in spontaneously hypertensive rats (SHR) and age-matched WKY controls the weekly effects of training on blood pressure (BP), plasma and left ventricle (LV) Ang II and Ang-(1–7) content (HPLC), LV oxidative stress (DHE staining), gene and protein expression (qPCR and WB) of pro-inflammatory cytokines, antioxidant enzymes and their consequence on hypertension-induced cardiac remodeling. SHR and WKY were submitted to aerobic training (T) or maintained sedentary (S) for 8 weeks; measurements were made at weeks 0, 1, 2, 4 and 8. Hypertension-induced cardiac hypertrophy was accompanied by acute plasma Ang II increase with amplified responses during the late phase of LV hypertrophy. Similar pattern was observed for oxidative stress markers, TNF alpha and interleukin-1β, associated with cardiomyocytes’ diameter enlargement and collagen deposition. SHR-T exhibited prompt and marked decrease in LV Ang II content (T1 vs T4 in WKY-T), normalized oxidative stress (T2), augmented antioxidant defense (T4) and reduced both collagen deposition and inflammatory profile (T8), without changing cardiomyocytes’ diameter and LV hypertrophy. These changes were accompanied by decreased plasma Ang II content (T2-T4) and reduced BP (T8). SHR-T and WKY-T showed parallel increases in LV and plasma Ang-(1–7) content. Our data indicate that early training-induced downregulation of LV ACE-AngII-AT1 receptor axis is a crucial mechanism to reduce oxidative/pro-inflammatory profile and improve antioxidant defense in SHR-T, showing in addition this effect precedes plasma RAS deactivation

Neuroinflammation and Neurotransmission Mechanisms Involved in Neuropsychiatric Disorders

Some classical psychiatric disorders, such as schizophrenia, autism, major depression, bipolar and obsessive‐compulsive disorders, have been related to neuroinflammatory process, immunological abnormalities, and neurotransmission impairment beyond genetic mutations. Neuroinflammation is mostly regulated by glial cells, which respond to physiological and pathological stimuli by anti‐ and pro‐inflammatory cytokine and chemokine signaling; moreover, recent studies have indicated that glial cells also respond to the neurotransmitters. Neurotransmitters regulate many biological processes, such as cell proliferation and synaptogenesis, which contribute to the formation of functional circuits. Alterations in the neurotransmission can lead to many pathological changes that occur in brain disorders. For example, studies have shown that neuroinflammation can alter the metabolism of glutamate as well as the function of its transporters, resulting in cognitive, behavioral, and psychiatric impairments. Cytokines as IL‐1β and IL‐6 appear to have an important influence in the dopaminergic and serotoninergic neurons. These data together suggest that glial cells via cytokines and abnormal regulation of neurotransmitters can influence psychiatric disorders. The present knowledge about this issue does not allow answering whether neuroinflammation is the cause or the consequence of neurotransmission imbalance and emphasizes the importance to improve in vivo imaging methods and models to elucidate this enigma

What determines auditory similarity? The effect of stimulus group and methodology.

Two experiments on the internal representation of auditory stimuli compared the pairwise and grouping methodologies as means of deriving similarity judgements. A total of 45 undergraduate students participated in each experiment, judging the similarity of short auditory stimuli, using one of the methodologies. The experiments support and extend Bonebright's (1996) findings, using a further 60 stimuli. Results from both methodologies highlight the importance of category information and acoustic features, such as root mean square (RMS) power and pitch, in similarity judgements. Results showed that the grouping task is a viable alternative to the pairwise task with N > 20 sounds whilst highlighting subtle differences, such as cluster tightness, between the different task results. The grouping task is more likely to yield category information as underlying similarity judgements

Curcumin requires tumor necrosis Factor α signaling to alleviate cognitive impairment elicited by Lipopolysaccharide

A decline in cognitive ability is a typical feature of the normal aging process, and of neurodegenerative disorders such as Alzheimer’s, Parkinson’s and Huntington’s diseases. Although their etiologies differ, all of these disorders involve local activation of innate immune pathways and associated inflammatory cytokines. However, clinical trials of anti-inflammatory agents in neurodegenerative disorders have been disappointing, and it is therefore necessary to better understand the complex roles of the inflammatory process in neurological dysfunction. The dietary phytochemical curcumin can exert anti-inflammatory, antioxidant and neuroprotective actions. Here we provide evidence that curcumin ameliorates cognitive deficits associated with activation of the innate immune response by mechanisms requiring functional tumor necrosis factor α receptor 2 (TNFR2) signaling. In vivo, the ability of curcumin to counteract hippocampusdependent spatial memory deficits, to stimulate neuroprotective mechanisms such as upregulation of BDNF, to decrease glutaminase levels, and to modulate N-methyl- D –aspartate receptor levels was absent in mice lacking functional TNFRs. Curcumin treatment protected cultured neurons against glutamate-induced excitotoxicity by a mechanism requiring TNFR2 activation. Our results suggest the possibility that therapeutic approaches against cognitive decline designed to selectively enhance TNFR2 signaling are likely to be more beneficial than the use of anti-inflammatory drugs per se.Intramural Research Program of the National Institute on Aging of the National Institutes of HealthFundação de Amparo à Pesquisa do Estado de São Paulo-FAPES

Detection and genetic characterization of domestic cat hepadnavirus in cats with cavitary effusions

: After the identification of the novel domestic cat hepadnavirus (DCH) in 2018, its potential pathogenetic role in feline hepatic diseases has been suggested. Following the detection of DCH in a cat's serum and peritoneal effusion, the aim of this study was to retrospectively investigate the presence of DCH in cats with and without cavitary effusions along with DCH presence in effusions. Stored serum and effusion samples from cats with and without effusions admitted to the Veterinary Teaching Hospital of Lodi (Italy) in 2020-2022 were included based on results of hematobiochemical parameters. Effusions were classified based on cytological and physicochemical findings. The likelihood of liver damage was estimated based on clinical and laboratory findings. Samples were tested for DCH presence by quantitative PCR (qPCR). Positive samples were subjected to whole genome sequencing and phylogenetic analysis. DCH was detected in both serum and peritoneal effusion samples of 2/72 (2.8%) enrolled cats, included in the group with effusions (2/33; 6.1%), with one cat showing inflammatory and the other non-inflammatory effusion. Both DCH-positive cats belonged to the group with a likelihood of liver damage (2/22, 9.1%). Phylogeny showed that the DCH sequences from this study clustered with the prototypic Australian strain but were not included in the clade with other Italian DCH sequences. Results suggest the circulation of different DCH variants in Italy and show the presence of DCH in effusion samples from DCH-positive cats, mirroring the presence of HBV in body fluids from HBV-infected humans. Further studies are still recommended to define the pathogenic role of DCH in cats

Idealized digital models for conical reed instruments, with focus on the internal pressure waveform

International audienceTwo models for the generation of self-oscillations of reed conical woodwinds are presented. They use the fewest parameters (of either the resonator or the ex-citer), whose influence can be quickly explored. The formulation extends iterated maps obtained for loss-less cylindrical pipes without reed dynamics. It uses spherical wave variables in idealized resonators, with one parameter more than for cylinders: the missing length of the cone. The mouthpiece volume equals that of the missing part of the cone, and is implemented as either a cylindrical pipe (first model) or a lumped element (second model). Only the first model adds a length parameter for the mouthpiece and leads to the solving of an implicit equation. For the second model, any shape of nonlinear characteristic can be directly considered. The complex characteristics impedance for spherical waves requires sampling times smaller than a round trip in the resonator. The convergence of the two models is shown when the length of the cylindrical mouthpiece tends to zero. The waveform is in semi-quantitative agreement with experiment. It is concluded that the oscillations of the positive episode of the mouthpiece pressure are related to the length of the missing part, not to the reed dynamics

Development of a high-throughput ex-vivo burn wound model using porcine skin, and its application to evaluate new approaches to control wound infection

Biofilm formation in wounds is considered a major barrier to successful treatment, and has been associated with the transition of wounds to a chronic non-healing state. Here, we present a novel laboratory model of wound biofilm formation using ex-vivo porcine skin and a custom burn wound array device. The model supports high-throughput studies of biofilm formation and is compatible with a range of established methods for monitoring bacterial growth, biofilm formation, and gene expression. We demonstrate the use of this model by evaluating the potential for bacteriophage to control biofilm formation by Staphylococcus aureus, and for population density dependant expression of S. aureus virulence factors (regulated by the Accessory Gene Regulator, agr) to signal clinically relevant wound infection. Enumeration of colony forming units and metabolic activity using the XTT assay, confirmed growth of bacteria in wounds and showed a significant reduction in viable cells after phage treatment. Confocal laser scanning microscopy confirmed the growth of biofilms in wounds, and showed phage treatment could significantly reduce the formation of these communities. Evaluation of agr activity by qRT-PCR showed an increase in activity during growth in wound models for most strains. Activation of a prototype infection-responsive dressing designed to provide a visual signal of wound infection, was related to increased agr activity. In all assays, excellent reproducibility was observed between replicates using this mode

HGF Mediates the Anti-inflammatory Effects of PRP on Injured Tendons

Platelet-rich plasma (PRP) containing hepatocyte growth factor (HGF) and other growth factors are widely used in orthopaedic/sports medicine to repair injured tendons. While PRP treatment is reported to decrease pain in patients with tendon injury, the mechanism of this effect is not clear. Tendon pain is often associated with tendon inflammation, and HGF is known to protect tissues from inflammatory damages. Therefore, we hypothesized that HGF in PRP causes the anti-inflammatory effects. To test this hypothesis, we performed in vitro experiments on rabbit tendon cells and in vivo experiments on a mouse Achilles tendon injury model. We found that addition of PRP or HGF decreased gene expression of COX-1, COX-2, and mPGES-1, induced by the treatment of tendon cells in vitro with IL-1β. Further, the treatment of tendon cell cultures with HGF antibodies reduced the suppressive effects of PRP or HGF on IL-1β-induced COX-1, COX-2, and mPGES-1 gene expressions. Treatment with PRP or HGF almost completely blocked the cellular production of PGE2 and the expression of COX proteins. Finally, injection of PRP or HGF into wounded mouse Achilles tendons in vivo decreased PGE2 production in the tendinous tissues. Injection of platelet-poor plasma (PPP) however, did not reduce PGE2 levels in the wounded tendons, but the injection of HGF antibody inhibited the effects of PRP and HGF. Further, injection of PRP or HGF also decreased COX-1 and COX-2 proteins. These results indicate that PRP exerts anti-inflammatory effects on injured tendons through HGF. This study provides basic scientific evidence to support the use of PRP to treat injured tendons because PRP can reduce inflammation and thereby reduce the associated pain caused by high levels of PGE2. © 2013 Zhang et al