A note on the time evolution of generalized coherent states

I consider the time evolution of generalized coherent states based on non-standard fiducial vectors, and show that only for a restricted class of fiducial vectors does the associated classical motion determine the quantum evolution of the states. I discuss some consequences of this for path integral representations.Comment: 9 pages. RevTe

Decrypt the groove: Audio features of groove and their importance for auditory-motor interactions

When we listen to music we often experience a state that can be described as ”˜in the groove’. This state is characterized by the wish or even the urge to move our body to the musical pulse (Janata et al., 2012; Madison, 2006). A previous study showed that high-groove music modulates the excitability of the motor system, whereas no effect of low-groove music was found (Stupacher et al., 2013). But which musical qualities contribute to the feeling of groove? To answer this question, we extracted audio features of 80 song clips with similar instrumentation and correlated them with subjective groove ratings. Song clips and groove ratings of 19 participants were taken from Janata et al. (2012). The following features were extracted with Matlab’s MIR toolbox (Lartillot & Toiviainen, 2007): RMS energy, spectral flux, sub-band flux, pulse clarity (”˜MaxAutocor’ and ”˜Attack’), and event density. Additionally we used the Genesis Loudness toolbox to compute measures of loudness using the loudness model of Glasberg and Moore (2002).Results showed that groove ratings correlated positively (all ps < .01) with following audio features: RMS energy (r = .37), RMS variability (r = .57), pulse clarity ”˜attack’ (r = .38), spectral flux (r = .34), sub-band flux of band 1 (0-50 Hz, r = .29), and band 2 (50-100 Hz, r = .29). Additionally, groove ratings correlated positively (all ps < .05) with band 3 (100-200 Hz, r = .23), band 5 (400-800 Hz, r = .23), and band 6 (800-1600 Hz, r = .24). The mean loudness of song clips did not affect groove ratings.Since energy in low frequency bands (Burger et al., 2012; Van Dyck et al., 2013), percussiveness (similar to pulse clarity ”˜attack’), and spectral flux (Burger et al., 2012) have previously been shown to affect motor movements, our results indicate that the experience of groove is a phenomenon predominantly based on auditory-motor interactions (cf. Janata et al., 2012; Stupacher et al., 2013).ReferencesBurger, B., Thompson, M. R., Luck, G., Saarikallio, S., & Toiviainen, P. (2012). Music moves us: Beat related musical features influence regularity of music-induced movement. In Proceedings of the 12th International Conference in Music Perception and Cognition and the 8th Triennial Conference of the European Society for the Cognitive Sciences for Music, Thessaloniki, Greece.Glasberg, B. R., & Moore, B. C. J. (2002). A model of loudness applicable to time-varying sounds. Journal Audio Engineering Society, 50, 331–342.Janata, P., Tomic, S. T., & Haberman, J. M. (2012). Sensorimotor coupling in music and the psychology of the groove. Journal of Experimental Psychology. General, 141, 54–75.Lartillot, O., & Toiviainen, P. (2007). A matlab toolbox for musical feature extraction from audio. In Proc. of the 10th Int. Conference on Digital Audio Effects (DAFx-07), Bordeaux, France.Madison, G. (2006). Experiencing groove induced by music: Consistency and phenomenology. Music Perception, 24, 201–208.Stupacher, J., Hove, M. J., Novembre, G., Schütz-Bosbach, S., &Keller, P. E. (2013). Musical groove modulates motor cortex excitability: a TMS investigation. Brain and Cognition, 82, 127–136.Van Dyck, E., Moelants, D., Demey, M., Deweppe, A., Coussement, P., & Leman, M. (2013). The impact of the bass drum on human dance movement. Music Perception, 30, 349–359

Sensorimotor Synchronization With Auditory and Visual Modalities: Behavioral and Neural Differences

It has long been known that the auditory system is better suited to guide temporally precise behaviors like sensorimotor synchronization (SMS) than the visual system. Although this phenomenon has been studied for many years, the underlying neural and computational mechanisms remain unclear. Growing consensus suggests the existence of multiple, interacting, context-dependent systems, and that reduced precision in visuo-motor timing might be due to the way experimental tasks have been conceived. Indeed, the appropriateness of the stimulus for a given task greatly influences timing performance. In this review, we examine timing differences for sensorimotor synchronization and error correction with auditory and visual sequences, to inspect the underlying neural mechanisms that contribute to modality differences in timing. The disparity between auditory and visual timing likely relates to differences in the processing specialization between auditory and visual modalities (temporal vs. spatial). We propose this difference could offer potential explanation for the differing temporal abilities between modalities. We also offer suggestions as to how these sensory systems interface with motor and timing systems

Reversing Blood Flows Act through klf2a to Ensure Normal Valvulogenesis in the Developing Heart

Heart valve anomalies are some of the most common congenital heart defects, yet neither the genetic nor the epigenetic forces guiding heart valve development are well understood. When functioning normally, mature heart valves prevent intracardiac retrograde blood flow; before valves develop, there is considerable regurgitation, resulting in reversing (or oscillatory) flows between the atrium and ventricle. As reversing flows are particularly strong stimuli to endothelial cells in culture, an attractive hypothesis is that heart valves form as a developmental response to retrograde blood flows through the maturing heart. Here, we exploit the relationship between oscillatory flow and heart rate to manipulate the amount of retrograde flow in the atrioventricular (AV) canal before and during valvulogenesis, and find that this leads to arrested valve growth. Using this manipulation, we determined that klf2a is normally expressed in the valve precursors in response to reversing flows, and is dramatically reduced by treatments that decrease such flows. Experimentally knocking down the expression of this shear-responsive gene with morpholine antisense oligonucleotides (MOs) results in dysfunctional valves. Thus, klf2a expression appears to be necessary for normal valve formation. This, together with its dependence on intracardiac hemodynamic forces, makes klf2a expression an early and reliable indicator of proper valve development. Together, these results demonstrate a critical role for reversing flows during valvulogenesis and show how relatively subtle perturbations of normal hemodynamic patterns can lead to both major alterations in gene expression and severe valve dysgenesis

Enantiomer-specific pharmacokinetics of D,L-3-hydroxybutyrate:Implications for the treatment of multiple acyl-CoA dehydrogenase deficiency

D,L-3-hydroxybutyrate (D,L-3-HB, a ketone body) treatment has been described in several inborn errors of metabolism, including multiple acyl-CoA dehydrogenase deficiency (MADD; glutaric aciduria type II). We aimed to improve the understanding of enantiomer-specific pharmacokinetics of D,L-3-HB. Using UPLC-MS/MS, we analyzed D-3-HB and L-3-HB concentrations in blood samples from three MADD patients, and blood and tissue samples from healthy rats, upon D,L-3-HB salt administration (patients: 736-1123 mg/kg/day; rats: 1579-6317 mg/kg/day of salt-free D,L-3-HB). D,L-3-HB administration caused substantially higher L-3-HB concentrations than D-3-HB. In MADD patients, both enantiomers peaked at 30 to 60 minutes, and approached baseline after 3 hours. In rats, D,L-3-HB administration significantly increased Cmax and AUC of D-3-HB in a dose-dependent manner (controls vs ascending dose groups for Cmax: 0.10 vs 0.30-0.35-0.50 mmol/L, and AUC: 14 vs 58-71-106 minutes*mmol/L), whereas for L-3-HB the increases were significant compared to controls, but not dose proportional (Cmax: 0.01 vs 1.88-1.92-1.98 mmol/L, and AUC: 1 vs 380-454-479 minutes*mmol/L). L-3-HB concentrations increased extensively in brain, heart, liver, and muscle, whereas the most profound rise in D-3-HB was observed in heart and liver. Our study provides important knowledge on the absorption and distribution upon oral D,L-3-HB. The enantiomer-specific pharmacokinetics implies differential metabolic fates of D-3-HB and L-3-HB

Mutations in C16orf57 and normal-length telomeres unify a subset of patients with dyskeratosis congenita, poikiloderma with neutropenia and Rothmund–Thomson syndrome

Dyskeratosis congenita (DC) is an inherited poikiloderma which in addition to the skin abnormalities is typically associated with nail dystrophy, leucoplakia, bone marrow failure, cancer predisposition and other features. Approximately 50% of DC patients remain genetically uncharacterized. All the DC genes identified to date are important in telomere maintenance. To determine the genetic basis of the remaining cases of DC, we undertook linkage analysis in 20 families and identified a common candidate gene region on chromosome 16 in a subset of these. This region included the C16orf57 gene recently identified to be mutated in poikiloderma with neutropenia (PN), an inherited poikiloderma displaying significant clinical overlap with DC. Analysis of the C16orf57 gene in our uncharacterized DC patients revealed homozygous mutations in 6 of 132 families. In addition, three of six families previously classified as Rothmund–Thomson syndrome (RTS—a poikiloderma that is sometimes confused with PN) were also found to have homozygous C16orf57 mutations. Given the role of the previous DC genes in telomere maintenance, telomere length was analysed in these patients and found to be comparable to age-matched controls. These findings suggest that mutations in C16orf57 unify a distinct set of families which clinically can be categorized as DC, PN or RTS. This study also highlights the multi-system nature (wider than just poikiloderma and neutropenia) of the clinical features of affected individuals (and therefore house-keeping function of C16orf57), a possible role for C16orf57 in apoptosis, as well as a distinct difference from previously characterized DC patients because telomere length was normal

Digital Signal Processing

Contains an introduction and reports on fourteen research projects.National Science Foundation FellowshipNational Science Foundation (Grant ECS84-07285)U.S. Navy - Office of Naval Research (Contract N00014-81-K-0742)Sanders Associates, Inc.U.S. Air Force - Office of Scientific Research (Contract F19628-85-K-0028)Advanced Television Research ProgramAmoco Foundation FellowshipHertz Foundation Fellowshi

Clinical and biochemical characterization of four patients with mutations in ECHS1

Short-chain enoyl-CoA hydratase (SCEH, encoded by ECHS1) catalyzes hydration of 2-trans-enoyl-CoAs to 3(S)-hydroxy-acyl-CoAs. SCEH has a broad substrate specificity and is believed to play an important role in mitochondrial fatty acid oxidation and in the metabolism of branched-chain amino acids. Recently, the first patients with SCEH deficiency have been reported revealing only a defect in valine catabolism. We investigated the role of SCEH in fatty acid and branched-chain amino acid metabolism in four newly identified patients. In addition, because of the Leigh-like presentation, we studied enzymes involved in bioenergetics. Metabolite, enzymatic, protein and genetic analyses were performed in four patients, including two siblings. Palmitate loading studies in fibroblasts were performed to study mitochondrial β-oxidation. In addition, enoyl-CoA hydratase activity was measured with crotonyl-CoA, methacrylyl-CoA, tiglyl-CoA and 3-methylcrotonyl-CoA both in fibroblasts and liver to further study the role of SCEH in different metabolic pathways. Analyses of pyruvate dehydrogenase and respiratory chain complexes were performed in multiple tissues of two patients. All patients were either homozygous or compound heterozygous for mutations in the ECHS1 gene, had markedly reduced SCEH enzymatic activity and protein level in fibroblasts. All patients presented with lactic acidosis. The first two patients presented with vacuolating leukoencephalopathy and basal ganglia abnormalities. The third patient showed a slow neurodegenerative condition with global brain atrophy and the fourth patient showed Leigh-like lesions with a single episode of metabolic acidosis. Clinical picture and metabolite analysis were not consistent with a mitochondrial fatty acid oxidation disorder, which was supported by the normal palmitate loading test in fibroblasts. Patient fibroblasts displayed deficient hydratase activity with different substrates tested. Pyruvate dehydrogenase activity was markedly reduced in particular in muscle from the most severely affected patients, which was caused by reduced expression of E2 protein, whereas E2 mRNA was increased. Despite its activity towards substrates from different metabolic pathways, SCEH appears to be only crucial in valine metabolism, but not in isoleucine metabolism, and only of limited importance for mitochondrial fatty acid oxidation. In severely affected patients SCEH deficiency can cause a secondary pyruvate dehydrogenase deficiency contributing to the clinical presentatio

Digital Signal Processing

Contains an introduction and reports on twenty research projects.National Science Foundation (Grant ECS 84-07285)U.S. Navy - Office of Naval Research (Contract N00014-81-K-0742)National Science Foundation FellowshipSanders Associates, Inc.U.S. Air Force - Office of Scientific Research (Contract F19628-85-K-0028)Canada, Bell Northern Research ScholarshipCanada, Fonds pour la Formation de Chercheurs et l'Aide a la Recherche Postgraduate FellowshipCanada, Natural Science and Engineering Research Council Postgraduate FellowshipU.S. Navy - Office of Naval Research (Contract N00014-81-K-0472)Fanny and John Hertz Foundation FellowshipCenter for Advanced Television StudiesAmoco Foundation FellowshipU.S. Air Force - Office of Scientific Research (Contract F19628-85-K-0028

Progress report no. 4

Statement of responsibility on title-page reads: editors: M.J. Driscoll, D.D. Lanning, I. Kaplan, A.T. Supple ; contributors: A. Alvim, G.J. Brown, J.K. Chan, T.P. Choong, M.J. Driscoll, G. A. Ducat, I.A. Forbes, M.V. Gregory, S.Y. Ho, C.M. Hove, O. K. Kadiroglu, R.J. Kennerley, D.D. Lanning, J.L. Lazewatsky, L. Lederman, A.S. Leveckis, V.A. Miethe, P. A. Scheinert, A.M. Thompson, N.E. Todreas, C.P. Tzanos, and P.J. WoodIncludes bibliographical referencesProgress report; June 30, 1973U.S. Atomic Energy Commission contract: AT(11-1)225