How Many CMEs Have Flux Ropes? Deciphering the Signatures of Shocks, Flux Ropes, and Prominences in Coronagraph Observations of CMEs

We intend to provide a comprehensive answer to the question on whether all Coronal Mass Ejections (CMEs) have flux rope structure. To achieve this, we present a synthesis of the LASCO CME observations over the last sixteen years, assisted by 3D MHD simulations of the breakout model, EUV and coronagraphic observations from STEREO and SDO, and statistics from a revised LASCO CME database. We argue that the bright loop often seen as the CME leading edge is the result of pileup at the boundary of the erupting flux rope irrespective of whether a cavity or, more generally, a 3-part CME can be identified. Based on our previous work on white light shock detection and supported by the MHD simulations, we identify a new type of morphology, the `two-front' morphology. It consists of a faint front followed by diffuse emission and the bright loop-like CME leading edge. We show that the faint front is caused by density compression at a wave (or possibly shock) front driven by the CME. We also present high-detailed multi-wavelength EUV observations that clarify the relative positioning of the prominence at the bottom of a coronal cavity with clear flux rope structure. Finally, we visually check the full LASCO CME database for flux rope structures. In the process, we classify the events into two clear flux rope classes (`3-part', `Loop'), jets and outflows (no clear structure). We find that at least 40% of the observed CMEs have clear flux rope structures. We propose a new definition for flux rope CMEs (FR-CMEs) as a coherent magnetic, twist-carrying coronal structure with angular width of at least 40 deg and able to reach beyond 10 Rsun which erupts on a time scale of a few minutes to several hours. We conclude that flux ropes are a common occurrence in CMEs and pose a challenge for future studies to identify CMEs that are clearly not FR-CMEs.Comment: 26 pages, 9 figs, to be published in Solar Physics Topical Issue "Flux Rope Structure of CMEs

The Origin, Early Evolution and Predictability of Solar Eruptions

Coronal mass ejections (CMEs) were discovered in the early 1970s when space-borne coronagraphs revealed that eruptions of plasma are ejected from the Sun. Today, it is known that the Sun produces eruptive flares, filament eruptions, coronal mass ejections and failed eruptions; all thought to be due to a release of energy stored in the coronal magnetic field during its drastic reconfiguration. This review discusses the observations and physical mechanisms behind this eruptive activity, with a view to making an assessment of the current capability of forecasting these events for space weather risk and impact mitigation. Whilst a wealth of observations exist, and detailed models have been developed, there still exists a need to draw these approaches together. In particular more realistic models are encouraged in order to asses the full range of complexity of the solar atmosphere and the criteria for which an eruption is formed. From the observational side, a more detailed understanding of the role of photospheric flows and reconnection is needed in order to identify the evolutionary path that ultimately means a magnetic structure will erupt

Synaptic Reorganization in the Adult Rat's Ventral Cochlear Nucleus following Its Total Sensory Deafferentation

Ablation of a cochlea causes total sensory deafferentation of the cochlear nucleus in the brainstem, providing a model to investigate nervous degeneration and formation of new synaptic contacts in the adult brain. In a quantitative electron microscopical study on the plasticity of the central auditory system of the Wistar rat, we first determined what fraction of the total number of synaptic contact zones (SCZs) in the anteroventral cochlear nucleus (AVCN) is attributable to primary sensory innervation and how many synapses remain after total unilateral cochlear ablation. Second, we attempted to identify the potential for a deafferentation-dependent synaptogenesis. SCZs were ultrastructurally identified before and after deafferentation in tissue treated for ethanolic phosphotungstic acid (EPTA) staining. This was combined with pre-embedding immunocytochemistry for gephyrin identifying inhibitory SCZs, the growth-associated protein GAP-43, glutamate, and choline acetyltransferase. A stereological analysis of EPTA stained sections revealed 1.11±0.09 (S.E.M.)×109 SCZs per mm3 of AVCN tissue. Within 7 days of deafferentation, this number was down by 46%. Excitatory and inhibitory synapses were differentially affected on the side of deafferentation. Excitatory synapses were quickly reduced and then began to increase in number again, necessarily being complemented from sources other than cochlear neurons, while inhibitory synapses were reduced more slowly and continuously. The result was a transient rise of the relative fraction of inhibitory synapses with a decline below original levels thereafter. Synaptogenesis was inferred by the emergence of morphologically immature SCZs that were consistently associated with GAP-43 immunoreactivity. SCZs of this type were estimated to make up a fraction of close to 30% of the total synaptic population present by ten weeks after sensory deafferentation. In conclusion, there appears to be a substantial potential for network reorganization and synaptogenesis in the auditory brainstem after loss of hearing, even in the adult brain

The Wave-Driver System of the Off-Disk Coronal Wave 17 January 2010

We study the 17 January 2010 flare-CME-wave event by using STEREO/SECCHI EUVI and COR1 data. The observational study is combined with an analytic model which simulates the evolution of the coronal-wave phenomenon associated with the event. From EUV observations, the wave signature appears to be dome shaped having a component propagating on the solar surface (v~280 km s-1) as well as off-disk (v~600 km s-1) away from the Sun. The off-disk dome of the wave consists of two enhancements in intensity, which conjointly develop and can be followed up to white-light coronagraph images. Applying an analytic model, we derive that these intensity variations belong to a wave-driver system with a weakly shocked wave, initially driven by expanding loops, which are indicative of the early evolution phase of the accompanying CME. We obtain the shock standoff distance between wave and driver from observations as well as from model results. The shock standoff distance close to the Sun (<0.3 Rs above the solar surface) is found to rapidly increase with values of ~0.03-0.09 Rs which give evidence of an initial lateral (over-)expansion of the CME. The kinematical evolution of the on-disk wave could be modeled using input parameters which require a more impulsive driver (t=90 s, a=1.7 km s-2) compared to the off-disk component (t=340 s, a=1.5 km s-2).Comment: accepted for publication in Solar Physic

Tracking the Expression of Excitatory and Inhibitory Neurotransmission-Related Proteins and Neuroplasticity Markers after Noise Induced Hearing Loss

Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10th octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABAA receptor subunit α1 (GABAAα1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p<0.05): lower levels of GABAAα1 in the contralateral AC at day-16 and day-32, lower levels of GAD-67 in the ipsilateral DCN at day-4, lower levels of Calb1 in the ipsilateral DCN at day-0, lower levels of GABAAα1 in the ipsilateral AC at day-4 and day-32. GAP-43 was reduced in the ipsilateral AC for the duration of the experiment. These complex fluctuations in protein expression suggests that for at least a month following acoustic trauma the auditory system is adapting to a new pattern of sensory input

Inactivation of VCP/ter94 Suppresses Retinal Pathology Caused by Misfolded Rhodopsin in Drosophila

The most common Rhodopsin (Rh) mutation associated with autosomal dominant retinitis pigmentosa (ADRP) in North America is the substitution of proline 23 by histidine (RhP23H). Unlike the wild-type Rh, mutant RhP23H exhibits folding defects and forms intracellular aggregates. The mechanisms responsible for the recognition and clearance of misfolded RhP23H and their relevance to photoreceptor neuron (PN) degeneration are poorly understood. Folding-deficient membrane proteins are subjected to Endoplasmic Reticulum (ER) quality control, and we have recently shown that RhP23H is a substrate of the ER–associated degradation (ERAD) effector VCP/ter94, a chaperone that extracts misfolded proteins from the ER (a process called retrotranslocation) and facilitates their proteasomal degradation. Here, we used Drosophila, in which Rh1P37H (the equivalent of mammalian RhP23H) is expressed in PNs, and found that the endogenous Rh1 is required for Rh1P37H toxicity. Genetic inactivation of VCP increased the levels of misfolded Rh1P37H and further activated the Ire1/Xbp1 ER stress pathway in the Rh1P37H retina. Despite this, Rh1P37H flies with decreased VCP function displayed a potent suppression of retinal degeneration and blindness, indicating that VCP activity promotes neurodegeneration in the Rh1P37H retina. Pharmacological treatment of Rh1P37H flies with the VCP/ERAD inhibitor Eeyarestatin I or with the proteasome inhibitor MG132 also led to a strong suppression of retinal degeneration. Collectively, our findings raise the possibility that excessive retrotranslocation and/or degradation of visual pigment is a primary cause of PN degeneration

ICAR: endoscopic skull‐base surgery

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Initialization shock in decadal hindcasts due to errors in wind stress over the tropical Pacific

Low prediction skill in the tropical Pacific is a common problem in decadal prediction systems, especially for lead years 2–5 which, in many systems, is lower than in uninitialized experiments. On the other hand, the tropical Pacific is of almost worldwide climate relevance through its teleconnections with other tropical and extratropical regions and also of importance for global mean temperature. Understanding the causes of the reduced prediction skill is thus of major interest for decadal climate predictions. We look into the problem of reduced prediction skill by analyzing the Max Planck Institute Earth System Model (MPI-ESM) decadal hindcasts for the fifth phase of the Climate Model Intercomparison Project and performing a sensitivity experiment in which hindcasts are initialized from a model run forced only by surface wind stress. In both systems, sea surface temperature variability in the tropical Pacific is successfully initialized, but most skill is lost at lead years 2–5. Utilizing the sensitivity experiment enables us to pin down the reason for the reduced prediction skill in MPI-ESM to errors in wind stress used for the initialization. A spurious trend in the wind stress forcing displaces the equatorial thermocline in MPI-ESM unrealistically. When the climate model is then switched into its forecast mode, the recovery process triggers artificial El Niño and La Niña events at the surface. Our results demonstrate the importance of realistic wind stress products for the initialization of decadal prediction

Dapsone‐ and nitroso dapsone‐specific activation of T cells from hypersensitive patients expressing the risk allele HLA‐B*13:01

BACKGROUND:Research into drug hypersensitivity associated with expression of specific HLA alleles has focussed on the interaction between parent drug and the HLA with no attention given to reactive metabolites. For this reason, we have studied HLA-B*13:01-linked dapsone hypersensitivity to (1) explore whether the parent drug and/or nitroso metabolite activates T-cells and (2) determine whether HLA-B*13:01 is involved in the response. METHODS:PBMC from 6 patients were cultured with dapsone and nitroso dapsone and proliferative responses and IFN-γ release were measured. Dapsone- and nitroso dapsone-specific T-cell clones were generated and phenotype, function, HLA allele restriction and cross-reactivity assessed. Dapsone intermediates were characterized by mass spectrometry. RESULTS:PBMC from 6 patients and cloned T-cells proliferated and secreted Th1/2/22 cytokines when stimulated with dapsone (clones: n=395; 80% CD4+ CXCR3hi CCR4hi , 20% CD8+CXCR3hi CCR4hi CCR6hi CCR9hi CCR10hi ) and nitroso dapsone (clones: n=399; 78% CD4+, 22% CD8+ with same chemokine receptor profile). CD4+ and CD8+ clones were HLA-class II and class I restricted, respectively, and displayed three patterns of reactivity: compound-specific, weakly crossreactive and strongly cross reactive. Nitroso dapsone formed dimers in culture and was reduced to dapsone, providing a rationale for the crossreactivity. T-cell responses to nitroso dapsone were dependent on the formation of a cysteine-modified protein adduct, while dapsone interacted in a labile manner with antigen presenting cells. CD8+ clones displayed an HLA-B*13:01-restricted pattern of activation. CONCLUSION:These studies describe the phenotype and function of dapsone- and nitroso dapsone-responsive CD4+ and CD8+ T-cells from hypersensitive patients. Discovery of HLA-B*13:01-restricted CD8+ T-cell responses indicates that drugs and their reactive metabolites participate in HLA allele-linked forms of hypersensitivity. This article is protected by copyright. All rights reserved

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

Major histocompatibility complex class I (MHC-I) molecules play a crucial role in immunity by capturing peptides for presentation to T cells and natural killer (NK) cells. The peptide termini are tethered within the MHC-I antigen-binding groove, but it is unknown whether other presentation modes occur. Here we show that 20% of the HLA-B*57:01 peptide repertoire comprises N-terminally extended sets characterized by a common motif at position 1 (P1) to P2. Structures of HLA-B*57:01 presenting N-terminally extended peptides, including the immunodominant HIV-1 Gag epitope TW10 (TSTLQEQIGW), showed that the N terminus protrudes from the peptide-binding groove. The common escape mutant TSNLQEQIGW bound HLA-B*57:01 canonically, adopting a dramatically different conformation than the TW10 peptide. This affected recognition by killer cell immunoglobulin-like receptor (KIR) 3DL1 expressed on NK cells. We thus define a previously uncharacterized feature of the human leukocyte antigen class I (HLA-I) immunopeptidome that has implications for viral immune escape. We further suggest that recognition of the HLA-B*57:01-TW10 epitope is governed by a 'molecular tension' between the adaptive and innate immune systems