The Energetic Particle Detector Rodríguez-Pacheco, J.; Wimmer-Schweingruber, R. F.; Mason, G. M. ...
Astronomy and astrophysics (Berlin),
10/2020, Letnik:
642
Journal Article
Recenzirano
After decades of observations of solar energetic particles from space-based observatories, relevant questions on particle injection, transport, and acceleration remain open. To address these ...scientific topics, accurate measurements of the particle properties in the inner heliosphere are needed. In this paper we describe the Energetic Particle Detector (EPD), an instrument suite that is part of the scientific payload aboard the Solar Orbiter mission. Solar Orbiter will approach the Sun as close as 0.28 au and will provide extra-ecliptic measurements beyond ∼30° heliographic latitude during the later stages of the mission. The EPD will measure electrons, protons, and heavy ions with high temporal resolution over a wide energy range, from suprathermal energies up to several hundreds of megaelectronvolts/nucleons. For this purpose, EPD is composed of four units: the SupraThermal Electrons and Protons (STEP), the Electron Proton Telescope (EPT), the Suprathermal Ion Spectrograph (SIS), and the High-Energy Telescope (HET) plus the Instrument Control Unit that serves as power and data interface with the spacecraft. The low-energy population of electrons and ions will be covered by STEP and EPT, while the high-energy range will be measured by HET. Elemental and isotopic ion composition measurements will be performed by SIS and HET, allowing full particle identification from a few kiloelectronvolts up to several hundreds of megaelectronvolts/nucleons. Angular information will be provided by the separate look directions from different sensor heads, on the ecliptic plane along the Parker spiral magnetic field both forward and backwards, and out of the ecliptic plane observing both northern and southern hemispheres. The unparalleled observations of EPD will provide key insights into long-open and crucial questions about the processes that govern energetic particles in the inner heliosphere.
The low incidence of embryonal rhabdomyosarcoma prevents any one person or institution from presenting any meaningful data in the form of effective treatment based on clinical experience. We realize ...that this is an antidotal case but the stakes are high when treating any malignancy of the young. Therefore, we advocate early and aggressive therapy using all modalities of treatments, and cite this case which initially seemed hopeless but to date has all the hallmarks of a cure.
The brain circuits underlying behavioral fear have been extensively studied over the last decades. Although the vast majority of experimental studies assess fear as a transient state of apprehension ...in response to a discrete threat, such phasic states of fear can shift to a sustained anxious apprehension, particularly in face of diffuse cues with unpredictable environmental contingencies. Unpredictability, in turn, is considered an important variable contributing to anxiety disorders. The networks of the extended amygdala have been suggested keys to the control of phasic and sustained states of fear, although the underlying synaptic pathways and mechanisms remain poorly understood. Here, we show that the endocannabinoid system acting in synaptic circuits of the extended amygdala can explain the fear response profile during exposure to unpredictable threat. Using fear training with predictable or unpredictable cues in mice, combined with local and cell-type-specific deficiency and rescue of cannabinoid type 1 (CB1) receptors, we found that presynaptic CB1 receptors on distinct amygdala projections to bed nucleus of the stria terminalis (BNST) are both necessary and sufficient for the shift from phasic to sustained fear in response to an unpredictable threat. These results thereby identify the causal role of a defined protein in a distinct brain pathway for the temporal development of a sustained state of anxious apprehension during unpredictability of environmental influences, reminiscent of anxiety symptoms in humans.
A consensus genetic map of chickpea (Cicer arietinum L.) was constructed by merging linkage maps from 10 different populations, using STMS (Sequence-tagged Microsatellite Sites) as bridging markers. ...These populations derived from five wide crosses (C. arietinum × Cicer reticulatum) and five narrow crosses (Desi × Kabuli types) were previously used for mapping genes for several agronomic traits such as ascochyta blight, fusarium wilt, rust resistance, seed weight, flowering time and days to flower. The integrated map obtained from wide crosses consists of 555 loci including, among other markers, 135 STMSs and 33 cross-genome markers distributed on eight linkage groups and covers 652.67 cM. The map obtained from narrow crosses comprises 99 STMSs, 3 SCARs, 1 ASAP, fusarium resistance gene, 5 morphological traits as well as RAPD and ISSR markers distributed on eight linkage groups covering 426.99 cM. Comparison between maps from wide and narrow crosses reflects a general coincidence, although some discrepancies are discussed. Medicago truncatula cross-genome markers were BLASTed against the M. truncatula pseudogenome permitting assignments of chickpea linkage groups LGI, II, III, IV, V and VI on Medicago chromosomes 2, 5, 7, 1, 3 and 4, respectively. A marker detectable on Medicago chromosome 4 were also located on LGVIII, This consensus map is an important progress to assist breeders for selecting suitable markers to be used in marker-assisted selection (MAS).
We report the finding of two copy number variants (CNVs) in a 12-year-old boy presenting both with autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD). Clinical ...features included aggressive behavior, mood instability, suicidal statements, repetitive and restrictive behavior, sensitivity to noise, learning problems and dyslexia, though no intellectual disability was present. Using array-based comparative genomic hybridization (array-CGH), we identified two CNVs, both triplex duplications of 324 kb on 3p26.3, and 284 kb on 4q13.1, respectively. One of the CNVs is located on chromosome 4q13.1 in the region of the gene encoding for adhesion G protein-coupled receptor L3 (ADGRL3, former name: latrophilin-3, LPHN3), the other on chromosome 3p26.3 in the region of the two pseudogenes AC090043.1 and RPL23AP39. The patient described in the present study showed increased symptoms under methylphenidate treatment but responded positively to 3 mg per day of the atypical neuroleptic drug aripiprazole. To our knowledge, this is the first report of a CNV in the ADGRL3 gene and its first association with ASD in humans.
Non‐technical summary Long‐lasting changes in efficacy of cell–cell communication (long‐term potentiation; LTP) at specialized sites (synapses) between neurons in the brain are thought to underlie ...forms of learning and memory. These forms of LTP can occur at excitatory synapses and inhibitory synapses, thus in‐ or decreasing the activity of neurons. We provide evidence for a novel form of LTP at inhibitory synapses (LTPi) on a subset of neurons in the amygdala of mice, a brain region involved in fear and anxiety. This LTPi enhances the release of the inhibitory neurotransmitter GABA at synapses between inhibitory interneurons and excitatory principal neurons (PNs) in a sub‐region of the amygdala. The described LTPi is heavily dependent on the production and diffusion of the volatile gas nitric oxide (NO), produced by PNs during stages of increased activity. These findings indicate that NO‐mediated long‐term regulation of inhibitory transmission in the amygdala might contribute to the learning of fear.
Long‐lasting changes of synaptic efficacy are thought to be a prerequisite for memory formation and maintenance. In the basolateral complex of the amygdala (BLA), one of the main regions for fear and extinction learning of the brain, various forms of long‐term potentiation (LTP) have been described for excitatory glutamatergic synapses. In contrast, little is known about the mechanisms of LTP at inhibitory GABAergic synapses. Here we provide evidence that (1) LTP at inhibitory GABAergic synapses (LTPi) between inhibitory interneurons and principal neurons (PNs) can be induced by theta‐burst stimulation (TBS), (2) this LTPi is prevented by AMPA‐ or NMDA‐receptor antagonists, and (3) this LTPi is abolished by the NO synthase (NOS) inhibitor l‐NAME or the NO scavenger PTIO, and thus is critically dependent on nitric oxide (NO) signalling. These findings are corroborated by immunocytochemical stainings for neuronal (n) NOS, which revealed the existence of nNOS‐positive neurons and fibres in the BLA. We conclude that LTP of GABAergic synaptic transmission to PNs is induced by activation of AMPA and NMDA receptors at glutamatergic synapses and subsequent retrograde NO signalling to enhance GABAergic transmission. This form of LTP at GABAergic synapses comprises a novel form of heterosynaptic plasticity within the BLA, apt to shape conditioned fear responses.
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