Reconstructing large-scale structure with neutral hydrogen surveys

Upcoming 21-cm intensity surveys will use the hyperfine transition in emission to map out neutral hydrogen in large volumes of the universe. Unfortunately, large spatial scales are completely contaminated with spectrally smooth astrophysical foregrounds which are orders of magnitude brighter than the signal. This contamination also leaks into smaller radial and angular modes to form a foreground wedge, further limiting the usefulness of 21-cm observations for different science cases, especially cross-correlations with tracers that have wide kernels in the radial direction. In this paper, we investigate reconstructing these modes within a forward modeling framework. Starting with an initial density field, a suitable bias parameterization and non-linear dynamics to model the observed 21-cm field, our reconstruction proceeds by {combining} the likelihood of a forward simulation to match the observations (under given modeling error and a data noise model) {with the Gaussian prior on initial conditions and maximizing the obtained posterior}. For redshifts z=2 and 4, we are able to reconstruct 21cm field with cross correlation, rc > 0.8 on all scales for both our optimistic and pessimistic assumptions about foreground contamination and for different levels of thermal noise. The performance deteriorates slightly at z=6. The large-scale line-of-sight modes are reconstructed almost perfectly. We demonstrate how our method also provides a technique for density field reconstruction for baryon acoustic oscillations, outperforming standard methods on all scales. We also describe how our reconstructed field can provide superb clustering redshift estimation at high redshifts, where it is otherwise extremely difficult to obtain dense spectroscopic samples, as well as open up a wealth of cross-correlation opportunities with projected fields (e.g. lensing) which are restricted to modes transverse to the line of sight

Conductor losses calculation in two-dimensional simulations of H-plane rectangular waveguides

This paper presents a novel numerical approach to simulate H-plane rectangular-waveguide microwave circuits considering a reduced quasi-2D simulation domain with benefits for computational cost and time. With the aim to evaluate the attenuation of the full height 3D component, we propose a modified expression for the waveguide top/bottom wall conductivity. Numerical 2D simulations are validated against results from full wave 3-D commercial electromagnetic simulator. After a benchmark on a simple straight waveguide model, the method has been successfully applied to an asymmetric un-balanced power splitter, where an accurate power loss prediction is mandatory. Simulation time and memory consumption can be reduced by a factor ten and seven respectively, in comparison with complete 3D geometries. Finally, we show that, also for quasi-2D E-bend waveguide, a case where the translational H-plane symmetry is broken, the error on conductor losses computation is mitigated by our approach since the method remains still valid in a first approximation

Noncommutativity and Lorentz Violation in Relativistic Heavy Ion Collisions

The experimental detection of the effects of noncommuting coordinates in electrodynamic phenomena depends on the magnitude of |\theta B|, where \theta is the noncommutativity parameter and B a background magnetic field. With the present upper bound on \theta, given by \theta_{\rm bound} \simeq 1/(10 {\rm TeV})^2, there was no large enough magnetic field in nature, including those observed in magnetars, that could give visible effects or, conversely, that could be used to further improve \theta_{\rm bound}. On the other hand, recently it has been proposed that intense enough magnetic fields should be produced at the beginning of relativistic heavy ion collisions. We discuss here lepton pair production by free photons as one kind of signature of noncommutativity and Lorentz violation that could occur at RHIC or LHC. This allows us to obtain a more stringent bound on \theta, given by 10^{-3} \theta_{\rm bound}, if such "exotic" events do not occur.Comment: Five pages, no figures

The Anxiolytic Drug Buspirone Prevents Rotenone-Induced Toxicity in a Mouse Model of Parkinson's Disease.

A pharmacological and genetic blockade of the dopamine D3 receptor (D3R) has shown to be neuroprotective in models of Parkinson's disease (PD). The anxiolytic drug buspirone, a serotonin receptor 1A agonist, also functions as a potent D3R antagonist. To test if buspirone elicited neuroprotective activities, C57BL/6 mice were subjected to rotenone treatment (10mg/kg i.p for 21 days) to induce PD-like pathology and were co-treated with increasing dosages of buspirone (1, 3, or 10 mg/kg i.p.) to determine if the drug could prevent rotenone-induced damage to the central nervous system (CNS). We found that high dosages of buspirone prevented the behavioural deficits caused by rotenone in the open field test. Molecular and histological analyses confirmed that 10 mg/kg of buspirone prevented the degeneration of TH-positive neurons. Buspirone attenuated the induction of interleukin-1β and interleukin-6 expression by rotenone, and this was paralleled by the upregulation of arginase-1, brain-derived neurotrophic factor (BDNF), and activity-dependent neuroprotective protein (ADNP) in the midbrain, striatum, prefrontal cortex, amygdala, and hippocampus. Buspirone treatment also improved mitochondrial function and antioxidant activities. Lastly, the drug prevented the disruptions in the expression of two neuroprotective peptides, pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP). These results pinpoint the neuroprotective efficacy of buspirone against rotenone toxicity, suggesting its potential use as a therapeutic agent in neurodegenerative and neuroinflammatory diseases, such as PD

Targeting the neurological comorbidities of multiple sclerosis: the beneficial effects of VIP and PACAP neuropeptides.

Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are two widely expressed neuropeptides with important immunomodulatory and neuroprotective properties in the central nervous system (CNS). Both VIP and PACAP have been implicated in several neurological diseases and have shown favourable effects in different animal models of multiple sclerosis (MS). MS is a chronic inflammatory and neurodegenerative disease of the CNS affecting over 2.5 million people worldwide. The disease is characterised by extensive neuroinflammation, demyelination and axonal loss. Currently, there is no cure for MS, with treatment options only displaying partial efficacy. Importantly, epidemiological studies in the MS population have demonstrated that there is a high incidence of neurological and psychological comorbidities such as depression, anxiety, epilepsy and stroke among afflicted people. Hence, given the widespread protective effects of the VIP/PACAP system in the CNS, this review will aim at exploring the beneficial roles of VIP and PACAP in ameliorating some of the most common neurological comorbidities associated with MS. The final scope of the review is to put more emphasis on how targeting the VIP/PACAP system may be an effective therapeutic strategy to modify MS disease course and its associated comorbidities

PACAP and VIP Mitigate Rotenone-Induced Inflammation in BV-2 Microglial Cells.

Rotenone is a commercial pesticide commonly used to model Parkinson's disease (PD) due to its ability to induce dopaminergic degeneration. Studies have confirmed that rotenone causes microglial activation, which seems to contribute to the toxic effects seen in rodent models. Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related neuropeptides that have robust neuroprotective and anti-inflammatory properties. However, their ability to regulate microglial activity in response to rotenone is not fully understood. Using rotenone as an inflammatory stimulus, we tested whether PACAP or VIP could mitigate microglial activation in BV2 microglial cells. Rotenone dose-dependently reduced cell viability and the percentage of apoptotic cells. It also increased the release of nitric oxide (NO) in culture media and the expression of microglial activation markers and pro-inflammatory markers, including CD11b, MMP-9 and IL-6, and heightened the endogenous levels of PACAP and its preferring receptor PAC1. Co-treatment with PACAP or VIP prevented rotenone-induced increase of NO, CD11b, MMP-9 and IL-6. These results indicate that both PACAP and VIP are able to prevent the pro-inflammatory effects of rotenone in BV2 cells, supporting the idea that these molecules can have therapeutic value in slowing down PD progression

IMAGE QUALITY IMPROVEMENT BY ADAPTIVE EXPOSURE CORRECTION TECHNIQUES

The proposed paper concerns the processing of images in digital format and, more specifically, particular techniques that can be advantageously used in digital still cameras for improving the quality of images acquired with a non-optimal exposure. The proposed approach analyses the CCD/CMOS sensor Bayer data or the corresponding color generated image and, after identifying specific features, it adjusts the exposure level according to a ‘camera response ’ like function. 1