Real-time massive convolution for audio applications on GPU

[EN] Massive convolution is the basic operation in multichannel acoustic signal processing. This field has experienced a major development in recent years. One reason for this has been the increase in the number of sound sources used in playback applications available to users. Another reason is the growing need to incorporate new effects and to improve the hearing experience. Massive convolution requires high computing capacity. GPUs offer the possibility of parallelizing these operations. This allows us to obtain the processing result in much shorter time and to free up CPU resources. One important aspect lies in the possibility of overlapping the transfer of data from CPU to GPU and vice versa with the computation, in order to carry out real-time applications. Thus, a synthesis of 3D sound scenes could be achieved with only a peer-to-peer music streaming environment using a simple GPU in your computer, while the CPU in the computer is being used for other tasks. Nowadays, these effects are obtained in theaters or funfairs at a very high cost, requiring a large quantity of resources. Thus, our work focuses on two mains points: to describe an efficient massive convolution implementation and to incorporate this task to real-time multichannel-sound applications. © 2011 Springer Science+Business Media, LLC.This work was partially supported by the Spanish Ministerio de Ciencia e Innovacion (Projects TIN2008-06570-C04-02 and TEC2009-13741), Universidad Politecnica de Valencia through PAID-05-09 and Generalitat Valenciana through project PROMETEO/2009/2013Belloch Rodríguez, JA.; Gonzalez, A.; Martínez Zaldívar, FJ.; Vidal Maciá, AM. (2011). Real-time massive convolution for audio applications on GPU. Journal of Supercomputing. 58(3):449-457. https://doi.org/10.1007/s11227-011-0610-8S449457583Spors S, Rabenstein R, Herbordt W (2007) Active listening room compensation for massive multichannel sound reproduction system using wave-domain adaptive filtering. J Acoust Soc Am 122:354–369Huang Y, Benesty J, Chen J (2008) Generalized crosstalk cancellation and equalization using multiple loudspeakers for 3D sound reproduction at the ears of multiple listeners. In: IEEE int conference on acoustics, speech and signal processing, Las Vegas, USA, pp 405–408Cowan B, Kapralos B (2008) Spatial sound for video games and virtual environments utilizing real-time GPU-based convolution. In: Proceedings of the ACM FuturePlay 2008 international conference on the future of game design and technology, Toronto, Ontario, Canada, November 3–5Belloch JA, Vidal AM, Martinez-Zaldivar FJ, Gonzalez A (2010) Multichannel acoustic signal processing on GPU. In: Proceedings of the 10th international conference on computational and mathematical methods in science and engineering, vol 1. Almeria, Spain, June 26–30, pp 181–187Cowan B, Kapralos B (2009) GPU-based one-dimensional convolution for real-time spatial sound generation. Sch J 3(5)Soliman SS, Mandyam DS, Srinath MD (1997) Continuous and discrete signals and systems. Prentice Hall, New YorkOppenheim AV, Willsky AS, Hamid Nawab S (1996) Signals and systems. Prentice Hall, New YorkopenGL: http://www.opengl.org/MKL library: http://software.intel.com/en-us/intel-mkl/MKL library: http://software.intel.com/en-us/intel-ipp/CUFFT library: http://developer.download.nvidia.com/compute/cuda/3_1/toolkit/docs/CUFFT_Library_3.1.pdfCUDA Toolkit 3.1: http://developer.nvidia.com/object/cuda_3_1_downloads.htmlCUDA Toolkit 3.2: http://developer.nvidia.com/object/cuda_3_1_downloads.htmlDatasheet of AC’97 SoundMAX Codec: http://www.xilinx.com/products/boards/ml505/datasheets/87560554AD1981B_c.pd

Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation

<p>Abstract</p> <p>Background</p> <p>Long-term acetate supplementation reduces neuroglial activation and cholinergic cell loss in a rat model of lipopolysaccharide-induced neuroinflammation. Additionally, a single dose of glyceryl triacetate, used to induce acetate supplementation, increases histone H3 and H4 acetylation and inhibits histone deacetylase activity and histone deacetylase-2 expression in normal rat brain. Here, we propose that the therapeutic effect of acetate in reducing neuroglial activation is due to a reversal of lipopolysaccharide-induced changes in histone acetylation and pro-inflammatory cytokine expression.</p> <p>Methods</p> <p>In this study, we examined the effect of a 28-day-dosing regimen of glyceryl triacetate, to induce acetate supplementation, on brain histone acetylation and interleukin-1β expression in a rat model of lipopolysaccharide-induced neuroinflammation. The effect was analyzed using Western blot analysis, quantitative real-time polymerase chain reaction and enzymic histone deacetylase and histone acetyltransferase assays. Statistical analysis was performed using one-way analysis of variance, parametric or nonparametric when appropriate, followed by Tukey's or Dunn's post-hoc test, respectively.</p> <p>Results</p> <p>We found that long-term acetate supplementation increased the proportion of brain histone H3 acetylated at lysine 9 (H3K9), histone H4 acetylated at lysine 8 and histone H4 acetylated at lysine 16. However, unlike a single dose of glyceryl triacetate, long-term treatment increased histone acetyltransferase activity and had no effect on histone deacetylase activity, with variable effects on brain histone deacetylase class I and II expression. In agreement with this hypothesis, neuroinflammation reduced the proportion of brain H3K9 acetylation by 50%, which was effectively reversed with acetate supplementation. Further, in rats subjected to lipopolysaccharide-induced neuroinflammation, the pro-inflammatory cytokine interleukin-1β protein and mRNA levels were increased by 1.3- and 10-fold, respectively, and acetate supplementation reduced this expression to control levels.</p> <p>Conclusion</p> <p>Based on these results, we conclude that dietary acetate supplementation attenuates neuroglial activation by effectively reducing pro-inflammatory cytokine expression by a mechanism that may involve a distinct site-specific pattern of histone acetylation and histone deacetylase expression in the brain.</p

Increased aortic stiffness and blood pressure in non-classic Pompe disease

Vascular abnormalities and glycogen accumulation in vascular smooth muscle fibres have been described in Pompe disease. Using carotid-femoral pulse wave velocity (cfPWV), the gold standard methodology for determining aortic stiffness, we studied whether aortic stiffness is increased in patients with Pompe disease. Eighty-four adult Pompe patients and 179 age- and gender-matched volunteers participated in this cross-sectional case-controlled study. Intima media thickness and the distensibility of the right common carotid artery were measured using a Duplex scanner. Aortic augmentation index, central pulse pressure, aortic reflexion time and cfPWV were assessed using the SphygmoCor® system. CfPWV was higher in patients than in volunteers (8.8 versus 7.4 m/s, p < 0.001). This difference was still present after adjustment for age, gender, mean arterial blood pressure (MAP), heart rate and diabetes mellitus (p = 0.001), and was shown by subgroup analysis to apply to the 40-59 years age group (p = 0.004) and 60+ years age group (p = 0.01), but not to younger age groups (p = 0.99). Except for a shorter aortic reflexion time (p = 0.02), indirect indicators of arterial stiffness did not differ between patients and volunteers. Relative to volunteers (20 %), more Pompe patients had a history of hypertension (36 %, p = 0.005), and the MAP was higher than in volunteers (100 versus 92 mmHg, p < 0.001). This study shows that patients with non-classic Pompe disease have increased aortic stiffness and blood pressure. Whether this is due to glycogen accumulation requires further investigation. To reduce the potential risk of cardiovascular diseases, we recommend that blood pressure and other common cardiovascular risk factors are monitored regularly

Blinding and sham control methods in trials of physical, psychological, and self-management interventions for pain (article II): a meta-analysis relating methods to trial results

Sham interventions in randomised clinical trials (RCTs) of physical, psychological, and self-management (PPS) therapies for pain are highly variable in design and thought to contribute to poor internal validity. It has, however, not been formally tested whether the extent to which sham controls resemble the treatment under investigation consistently affects trial outcomes, such as effect sizes, differential attrition, participant expectancy, and blinding effectiveness. Placebo or sham-controlled RCTs of PPS interventions of clinical pain populations were searched in twelve databases. The similarity of control interventions to the experimental treatment was rated across 25 features. Meta-regression analyses assessed putative links between employed control interventions, observed effect sizes in pain-related outcomes, attrition, and blinding success. The sample included 198 unique control interventions, dominated by manual therapy and chronic musculoskeletal pain research. Meta-analyses indicated small to moderate benefit of active treatments over control interventions, across subgroups of manual therapies, exercise, and rehabilitation, and psychological intervention trials. Multiple meta-regression modelling demonstrated that similarity between sham control and tested interventions predicted variability in pain-related outcomes, attrition, and blinding effectiveness. Influential were differences relating to the extent of intervention exposure, participant experience, and treatment environments. The results support the supposed link between blinding methods and effect sizes, based on a large and systematically sourced overview of methods. Challenges to effective blinding are, however, complex, and often difficult to discern from trial reports. Nonetheless, these insights have the potential to change trial design, conduct, and reporting and will inform guideline development

Osteopetrosis

Osteopetrosis ("marble bone disease") is a descriptive term that refers to a group of rare, heritable disorders of the skeleton characterized by increased bone density on radiographs. The overall incidence of these conditions is difficult to estimate but autosomal recessive osteopetrosis (ARO) has an incidence of 1 in 250,000 births, and autosomal dominant osteopetrosis (ADO) has an incidence of 1 in 20,000 births. Osteopetrotic conditions vary greatly in their presentation and severity, ranging from neonatal onset with life-threatening complications such as bone marrow failure (e.g. classic or "malignant" ARO), to the incidental finding of osteopetrosis on radiographs (e.g. osteopoikilosis). Classic ARO is characterised by fractures, short stature, compressive neuropathies, hypocalcaemia with attendant tetanic seizures, and life-threatening pancytopaenia. The presence of primary neurodegeneration, mental retardation, skin and immune system involvement, or renal tubular acidosis may point to rarer osteopetrosis variants, whereas onset of primarily skeletal manifestations such as fractures and osteomyelitis in late childhood or adolescence is typical of ADO. Osteopetrosis is caused by failure of osteoclast development or function and mutations in at least 10 genes have been identified as causative in humans, accounting for 70% of all cases. These conditions can be inherited as autosomal recessive, dominant or X-linked traits with the most severe forms being autosomal recessive. Diagnosis is largely based on clinical and radiographic evaluation, confirmed by gene testing where applicable, and paves the way to understanding natural history, specific treatment where available, counselling regarding recurrence risks, and prenatal diagnosis in severe forms. Treatment of osteopetrotic conditions is largely symptomatic, although haematopoietic stem cell transplantation is employed for the most severe forms associated with bone marrow failure and currently offers the best chance of longer-term survival in this group. The severe infantile forms of osteopetrosis are associated with diminished life expectancy, with most untreated children dying in the first decade as a complication of bone marrow suppression. Life expectancy in the adult onset forms is normal. It is anticipated that further understanding of the molecular pathogenesis of these conditions will reveal new targets for pharmacotherapy

Large-scale analyses of common and rare variants identify 12 new loci associated with atrial fibrillation

Atrial fibrillation affects more than 33 million people worldwide and increases the risk of stroke, heart failure, and death. Fourteen genetic loci have been associated with atrial fibrillation in European and Asian ancestry groups. To further define the genetic basis of atrial fibrillation, we performed large-scale, trans-ancestry meta-analyses of common and rare variant association studies. The genome-wide association studies (GWAS) included 17,931 individuals with atrial fibrillation and 115,142 referents; the exome-wide association studies (ExWAS) and rare variant association studies (RVAS) involved 22,346 cases and 132,086 referents. We identified 12 new genetic loci that exceeded genome-wide significance, implicating genes involved in cardiac electrical and structural remodeling. Our results nearly double the number of known genetic loci for atrial fibrillation, provide insights into the molecular basis of atrial fibrillation, and may facilitate the identification of new potential targets for drug discovery