Nori 1-motives

Let EHM be Nori's category of effective homological mixed motives. In this paper, we consider the thick abelian subcategory EHM_1 generated by the i-th relative homology of pairs of varieties for i = 0,1. We show that EHM_1 is naturally equivalent to the abelian category M_1 of Deligne 1-motives with torsion; this is our main theorem. Along the way, we obtain several interesting results. Firstly, we realize M_1 as the universal abelian category obtained, using Nori's formalism, from the Betti representation of an explicit diagram of curves. Secondly, we obtain a conceptual proof of a theorem of Vologodsky on realizations of 1-motives. Thirdly, we verify a conjecture of Deligne on extensions of 1-motives in the category of mixed realizations for those extensions that are effective in Nori's sense

1-motivic sheaves and the Albanese functor

We introduce n-generated sheaves and n-motivic sheaves, describing completely for n = 0, 1 and proposing a conjecture for n > 1. We then obtain functors L\pi_0 and LAlb on DM_{eff}(k) deriving \pi_0 and Alb. The functor LAlb extends the one constructed (by the second author jointly with B.Kahn) to non-necessarily geometric motives. These functors are then used to define higher N\'eron-Severi groups and higher Albanese sheaves. The latter may be considered as an algebraic avatar of Deligne (co)homology.Comment: 54 pages, fully revised exposition with a new "structure theorem" for 1-motivic sheaves, see Theorem 1.3.10, including finitely presented (or constructible) 1-motivic sheave

Accuracy of generic mesh conformation: the future of facial morphological analysis

Three-dimensional (3D) analysis of the face is required for the assessment of changes following surgery, to monitor the progress of pathological conditions and for the evaluation of facial growth. Sophisticated methods have been applied for the evaluation of facial morphology, the most common being dense surface correspondence. The method depends on the application of a mathematical facial mask known as the generic facial mesh for the evaluation of the characteristics of facial morphology. This study evaluated the accuracy of the conformation of generic mesh to the underlying facial morphology. The study was conducted on 10 non-patient volunteers. Thirty-four 2-mm-diameter self-adhesive, non-reflective markers were placed on each face. These were readily identifiable on the captured 3D facial image, which was captured by Di3D stereophotogrammetry. The markers helped in minimising digitisation errors during the conformation process. For each case, the face was captured six times: at rest and at the maximum movements of four facial expressions. The 3D facial image of each facial expression was analysed. Euclidean distances between the 19 corresponding landmarks on the conformed mesh and on the original 3D facial model provided a measure of the accuracy of the conformation process. For all facial expressions and all corresponding landmarks, these distances were between 0.7 and 1.7 mm. The absolute mean distances ranged from 0.73 to 1.74 mm. The mean absolute error of the conformation process was 1.13 ± 0.26 mm. The conformation of the generic facial mesh is accurate enough for clinical trial proved to be accurate enough for the analysis of the captured 3D facial images

Loss of hypothermic and anti-pyretic action of paracetamol in cyclooxygenase-1 knockout mice is indicative of inhibition of cyclooxygenase-1 variant enzymes

Paracetamol (acetaminophen), is a centrally-acting antipyretic analgesic drug, which can also lower body temperature. Despite a century of clinical use, its mechanism of pharmacological action has not been completely elucidated. Previously, we demonstrated significant attenuation in the paracetamol induced hypothermia in parallel with its inhibitory action on the synthesis of brain prostaglandin E₂ (PGE₂) in cyclooxygenase-1 (COX-1) knockout mice in comparison to wild-type mice. The above reported pharmacological actions by paracetamol were completely retained in COX-2 knockout mice. We thus concluded that the mechanism of hypothermic action of paracetamol is dependent on inhibition of a COX-1 gene-derived enzyme. In the current investigation, we provide further support for this notion by demonstrating that the paracetamol-induced hypothermia is not mediated through inhibition of COX-1 as neither the COX-1 selective inhibitor, SC560, nor the COX-1/COX-2 dual inhibitor, indomethacin, induced hypothermia at pharmacologically active doses in mice. In addition, using a COX-2-dependent and PGE₂-mediated model of endotoxin-induced fever, paracetamol induced anti-pyretic and hypothermic actions in COX-1 wild-type mice. These effects were fully or partially attenuated in COX-1 knockout mice after prophylactic or therapeutic administration, respectively. Therapeutically-administered paracetamol also reduced hypothalamic PGE₂ biosynthesis in febrile COX-1 wild-type mice, but not in febrile COX-1 knockout mice. In conclusion, we provide further evidence which suggests that the hypothermic and now anti-pyretic actions of paracetamol are mediated through inhibition of a COX-1 variant enzyme

Earth-like sand fluxes on Mars

Strong and sustained winds on Mars have been considered rare, on the basis of surface meteorology measurements and global circulation models, raising the question of whether the abundant dunes and evidence for wind erosion seen on the planet are a current process. Recent studies showed sand activity, but could not determine whether entire dunes were moving—implying large sand fluxes—or whether more localized and surficial changes had occurred. Here we present measurements of the migration rate of sand ripples and dune lee fronts at the Nili Patera dune field. We show that the dunes are near steady state, with their entire volumes composed of mobile sand. The dunes have unexpectedly high sand fluxes, similar, for example, to those in Victoria Valley, Antarctica, implying that rates of landscape modification on Mars and Earth are similar

Characterization of three vasopressin receptor 2 variants: an apparent polymorphism (V266A) and two loss-of-function mutations (R181C and M311V).

Arginine vasopressin (AVP) is released from the posterior pituitary and controls water homeostasis. AVP binding to vasopressin V2 receptors (V2Rs) located on kidney collecting duct epithelial cells triggers activation of Gs proteins, leading to increased cAMP levels, trafficking of aquaporin-2 water channels, and consequent increased water permeability and antidiuresis. Typically, loss-of-function V2R mutations cause nephrogenic diabetes insipidus (NDI), whereas gain-of-function mutations cause nephrogenic syndrome of inappropriate antidiuresis (NSIAD). Here we provide further characterization of two mutant V2Rs, R181C and M311V, reported to cause complete and partial NDI respectively, together with a V266A variant, in a patient diagnosed with NSIAD. Our data in HEK293FT cells revealed that for cAMP accumulation, AVP was about 500- or 30-fold less potent at the R181C and M311V mutants than at the wild-type receptor respectively (and about 4000- and 60-fold in COS7 cells respectively). However, in contrast to wild type V2R, the R181C mutant failed to increase inositol phosphate production, while with the M311V mutant, AVP exhibited only partial agonism in addition to a 37-fold potency decrease. Similar responses were detected in a BRET assay for β-arrestin recruitment, with the R181C receptor unresponsive to AVP, and partial agonism with a 23-fold decrease in potency observed with M311V in both HEK293FT and COS7 cells. Notably, the V266A V2R appeared functionally identical to the wild-type receptor in all assays tested, including cAMP and inositol phosphate accumulation, β-arrestin interaction, and in a BRET assay of receptor ubiquitination. Each receptor was expressed at comparable levels. Hence, the M311V V2R retains greater activity than the R181C mutant, consistent with the milder phenotype of NDI associated with this mutant. Notably, the R181C mutant appears to be a Gs protein-biased receptor incapable of signaling to inositol phosphate or recruiting β-arrestin. The etiology of NSIAD in the patient with V266A V2R remains unknown

The six-functor formalism for rigid analytic motives

We offer a systematic study of rigid analytic motives over general rigid analytic spaces, and we develop their six-functor formalism. A key ingredient is an extended proper base change theorem that we are able to justify by reducing to the case of algebraic motives. In fact, more generally, we develop a powerful technique for reducing questions about rigid analytic motives to questions about algebraic motives, which is likely to be useful in other contexts as well. We pay special attention to establishing our results without noetherianity assumptions on rigid analytic spaces. This is indeed possible using Raynaud's approach to rigid analytic geometry

Acute entanglement and Photon/Phonons statistics in a balanced/unbalanced PT-symmetry systems

We study the significance of Photon/Phonons bunching and antibunching on the dynamics of the quantum entanglement in the presence of coupled PT-symmetry systems with balanced/unbalanced gain and loss. We suggest a hybrid electromechanical system to realize a strong and tunable coupling between a Coplanar-Waveguide (CPW) microwave cavity and a nanomechanical resonator (NAMR) via a superconducting Transmon qubit. The hybrid electromechanical system consists of a non-hermitian Hamiltonian with balanced/unbalanced gain and loss. The interplay between the quantum entanglement and the -symmetry systems is also thoroughly investigated. We frame a connection between Number operators, Photon/Phonons antibunching, and entanglement. It has been observed that the relative Photon/Phonons numbers play a key role in quantum entanglement dynamics. Furthermore, we study that quantum entanglement can be characterized by defining a Photon/Phonons antibunching. The Photon/Phonons antibunching is strongly dependent on the initial squeezed state and the rate of balanced/unbalanced gain and loss of the system

Auditory feedback control mechanisms do not contribute to cortical hyperactivity within the voice production network in adductor spasmodic dysphonia

Adductor spasmodic dysphonia (ADSD), the most common form of spasmodic dysphonia, is a debilitating voice disorder characterized by hyperactivity and muscle spasms in the vocal folds during speech. Prior neuroimaging studies have noted excessive brain activity during speech in ADSD participants compared to controls. Speech involves an auditory feedback control mechanism that generates motor commands aimed at eliminating disparities between desired and actual auditory signals. Thus, excessive neural activity in ADSD during speech may reflect, at least in part, increased engagement of the auditory feedback control mechanism as it attempts to correct vocal production errors detected through audition. To test this possibility, functional magnetic resonance imaging was used to identify differences between ADSD participants and age-matched controls in (i) brain activity when producing speech under different auditory feedback conditions, and (ii) resting state functional connectivity within the cortical network responsible for vocalization. The ADSD group had significantly higher activity than the control group during speech (compared to a silent baseline task) in three left-hemisphere cortical regions: ventral Rolandic (sensorimotor) cortex, anterior planum temporale, and posterior superior temporal gyrus/planum temporale. This was true for speech while auditory feedback was masked with noise as well as for speech with normal auditory feedback, indicating that the excess activity was not the result of auditory feedback control mechanisms attempting to correct for perceived voicing errors in ADSD. Furthermore, the ADSD group had significantly higher resting state functional connectivity between sensorimotor and auditory cortical regions within the left hemisphere as well as between the left and right hemispheres, consistent with the view that excessive motor activity frequently co-occurs with increased auditory cortical activity in individuals with ADSD.First author draf

Sensorimotor adaptation to auditory perturbation of speech is facilitated by noninvasive brain stimulation

Repeated exposure to disparity between the motor plan and auditory feedback during speech production results in a proportionate change in the motor system’s response called auditory-motor adaptation. Artificially raising F1 in auditory feedback results in a concomitant decrease in F1 during speech production. Transcranial direct current stimulation (tDCS) can be used to alter neuronal excitability in focal areas of the brain. The present experiment explored the effect of noninvasive brain stimulation applied to the speech premotor cortex on the timing and magnitude of adaptation responses to artificially raised F1 in auditory feedback. Participants (N = 18) completed a speaking task in which they read target words aloud. Participants' speech was processed to raise F1 by 30% and played back to them over headphones in real time. A within-subjects design compared acoustics of participants’ speech while receiving anodal (active) tDCS stimulation versus sham (control) stimulation. Participants' speech showed an increasing magnitude of adaptation of F1 over time during anodal stimulation compared to sham. These results indicate that tDCS can affect behavioral response during auditory-motor adaptation, which may have translational implications for sensorimotor training in speech disorders