Estimates in Beurling--Helson type theorems. Multidimensional case

We consider the spaces $A_p(\mathbb T^m)$ of functions $f$ on the $m$ -dimensional torus $\mathbb T^m$ such that the sequence of the Fourier coefficients $\hat{f}=\{\hat{f}(k), ~k \in \mathbb Z^m\}$ belongs to $l^p(\mathbb Z^m), ~1\leq p<2$. The norm on $A_p(\mathbb T^m)$ is defined by $\|f\|_{A_p(\mathbb T^m)}=\|\hat{f}\|_{l^p(\mathbb Z^m)}$. We study the rate of growth of the norms $\|e^{i\lambda\varphi}\|_{A_p(\mathbb T^m)}$ as $|\lambda|\rightarrow \infty, ~\lambda\in\mathbb R,$ for $C^1$ -smooth real functions $\varphi$ on $\mathbb T^m$ (the one-dimensional case was investigated by the author earlier). The lower estimates that we obtain have direct analogues for the spaces $A_p(\mathbb R^m)$

Metal Ionophore Treatment Restores Dendritic Spine Density and Synaptic Protein Levels in a Mouse Model of Alzheimer's Disease

We have previously demonstrated that brief treatment of APP transgenic mice with metal ionophores (PBT2, Prana Biotechnology) rapidly and markedly improves learning and memory. To understand the potential mechanisms of action underlying this phenomenon we examined hippocampal dendritic spine density, and the levels of key proteins involved in learning and memory, in young (4 months) and old (14 months) female Tg2576 mice following brief (11 days) oral treatment with PBT2 (30 mg/kg/d). Transgenic mice exhibited deficits in spine density compared to littermate controls that were significantly rescued by PBT2 treatment in both the young (+17%, p<0.001) and old (+32%, p<0.001) animals. There was no effect of PBT2 on spine density in the control animals. In the transgenic animals, PBT2 treatment also resulted in significant increases in brain levels of CamKII (+57%, p = 0.005), spinophilin (+37%, p = 0.04), NMDAR1A (+126%, p = 0.02), NMDAR2A (+70%, p = 0.05), pro-BDNF (+19%, p = 0.02) and BDNF (+19%, p = 0.04). While PBT2-treatment did not significantly alter neurite-length in vivo, it did increase neurite outgrowth (+200%, p = 0.006) in cultured cells, and this was abolished by co-incubation with the transition metal chelator, diamsar. These data suggest that PBT2 may affect multiple aspects of snaptic health/efficacy. In Alzheimer's disease therefore, PBT2 may restore the uptake of physiological metal ions trapped within extracellular β-amyloid aggregates that then induce biochemical and anatomical changes to improve cognitive function

Perineuronal Nets Play a Role in Regulating Striatal Function in the Mouse

The striatum is the primary input nucleus of the basal ganglia, a collection of nuclei that play important roles in motor control and associative learning. We have previously reported that perineuronal nets (PNNs), aggregations of chondroitin-sulfate proteoglycans (CSPGs), form in the matrix compartment of the mouse striatum during the second postnatal week. This period overlaps with important developmental changes, including the attainment of an adult-like gait. Here, we investigate the identity of the cells encapsulated by PNNs, characterize their topographical distribution and determine their function by assessing the impact of enzymatic digestion of PNNs on two striatum-dependent behaviors: ambulation and goal-directed spatial learning. We show PNNs are more numerous caudally, and that a substantial fraction (41%) of these structures surrounds parvalbumin positive (PV+) interneurons, while approximately 51% of PV+ cells are ensheathed by PNNs. The colocalization of these structures is greatest in dorsal, lateral and caudal regions of the striatum. Bilateral digestion of striatal PNNs led to an increase in both the width and variability of hind limb gait. Intriguingly, this also resulted in an improvement in the acquisition rate of the Morris water maze. Together, these data show that PNNs are associated with specific elements of striatal circuits and play a key role in regulating the function of this important structure in the mouse

Presence Patterns and Privacy Analysis

Item does not contain fulltextBusiness applications often use such data structures as Presence Patterns for presentation of numbers of customers in service-oriented businesses including education, retailing and media. Presence Patterns contain open data derived from internal data of organizations. In this paper, we investigate different ways of defining Presence Patterns and possible privacy consequences dependent on the chosen definition. The first contribution of the paper is a definition of a family of Presence Patterns. The second contribution is a method for privacy analysis of Presence Patterns.Business Modeling and Software Design: 8th International Symposium, BMSD 2018, Vienna, Austria, July 2-4, 201

A secretagogin locus of the mammalian hypothalamus controls stress hormone release

This work was supported by the Swedish Research Council (T.Ha., T.Hö.), Hjärnfonden (T.Ha.), the Petrus and Augusta Hedlunds Foundation (T.Ha., T.Hö.), the Novo Nordisk Foundation (T.Ha., T.Hö.), Karolinska Institutet (T.Hö.), the Medical University of Vienna (T.Ha.), ANR (France, ANR-10-INBS-04-01, M.L.), the European Commission (PAINCAGE grant, T.Ha.) and the Wellcome Trust (094476/Z/10/Z, equipment grant, C.H.B. and postdoctoral research fellowship, M.F.).A hierarchical hormonal cascade along the hypothalamic-pituitary-adrenal axis orchestrates bodily responses to stress. Although corticotropin-releasing hormone (CRH), produced by parvocellular neurons of the hypothalamic paraventricular nucleus (PVN) and released into the portal circulation at the median eminence, is known to prime downstream hormone release, the molecular mechanism regulating phasic CRH release remains poorly understood. Here, we find a cohort of parvocellular cells interspersed with magnocellular PVN neurons expressing secretagogin. Single-cell transcriptome analysis combined with protein interactome profiling identifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagogin's Ca2+ sensor properties and protein interactions with the vesicular traffic and exocytosis release machineries to liberate this key hypothalamic releasing hormone. Pharmacological tools combined with RNA interference demonstrate that secretagogin's loss of function occludes adrenocorticotropic hormone release from the pituitary and lowers peripheral corticosterone levels in response to acute stress. Cumulatively, these data define a novel secretagogin neuronal locus and molecular axis underpinning stress responsiveness.PostprintPeer reviewe