Splitting of the middle layer of LPW SAFNWC/MSG satellite product in order to improve the monitoring of pre-convective environments

International audienceSeven of the infrared channels from the Spinning Enhanced Visible and Infrared Imagery (SEVIRI) instrument, on board the Meteosat Second Generation (MSG), are used to retrieve Layer Precipitable Water (LPW) and Stability Analysis Imagery (SAI) in the SAFNWC framework. Both products are retrieved using a statistical retrieval based on neural networks; they are routinely generated every fifteen minutes at a satellite horizontal resolution of 3 km in NADIR only in cloud-free areas. Many factors are involved in the development of severe weather and these parameters are only some of the indicators. However, due to the high resolution of these products, the use of them in conjunction with satellite and radar images can help to identify mesoscale features related to convection. The MSG moisture and parcel instability time trend fields are especially useful during the period previous to convection. Once the outbreak of convection occurs, the products calculated in the clear air pixels surrounding the convective system can give us hints to anticipate its evolution. SAFNWC LPW and SAI were analyzed for a severe weather event during August 2004. A thunderstorm over Teruel (Spain) produced intense precipitation and hail; a tornado developed while this thunderstorm was moving towards SE. The pre-convective parcel potential buoyancy and moisture SAFNWC products changed in a way that was consistent with the observed intense convective activity. In previous studies, the atmospheric moisture in medium levels, which has been proven to be relevant in some cases, was represented by only one level parameter (ML: middle layer LPW). However, it was observed that this layer is too thick to do an adequate analysis of moisture available for convection. Hence, an improvement on the LPW algorithm has been carried out by splitting the middle layer into two new sub-layers (approximately separated at 700 hPa) and training two new neural networks. The impact of monitoring moisture in the new sub-layers separately in this severe weather event has been tested, and the improvements achieved have been evaluated

N-transfer through aspen litter and feather moss layers after fertilization with ammonium nitrate and urea

When fertilizer is broadcast in boreal forest stands, the applied nutrients must pass through a thick layer of either feather moss or leaf litter which covers the forest floor. In a growth chamber experiment we tested the transfer of N through living feather moss or aspen litter when fertilized with urea ((NH2)2CO) or NH4NO3 at a rate of 100 kg ha−1 and under different watering regimes. When these organic substrates were frequently watered to excess they allowed the highest transfer of nutrients through, although 72% of the applied fertilizer was captured in the substrates. In a field experiment we also fertilized moss and aspen litter with urea ((NH2)2CO) or NH4NO3 at a more operationally relevant rate of 330 kg ha−1. We captured the NO3− or NH4+ by ion exchange resin at the substrate–mineral soil interface. In contrast to the growth chamber experiment, this fertilizer rate killed the moss and there was no detectable increase in nutrient levels in the aspen litter or feather moss layers. Instead, the urea was more likely transferred into the mineral soil; mineral soil of the urea treatment had 1.6 times as much extractable N compared to the NH4NO3 treatment. This difference between the growth chamber and field studies was attributed to observed fertilizer- damage to the living moss and possibly damage to the litter microflora due to the higher rate of fertilization in the field. In addition, the early and substantial rainfall after fertilization in the field experiment produced conditions for rapid leaching of N through the organic layers into the mineral soil. In the field, only 8% of the urea-N that was applied was captured by the ion exchange resin, while 34% was captured in for the NH4NO3 fertilization. Thus, the conditions for rapid leaching in the field moved much of the N in the form of urea through the organic layers and into the mineral soil before it was hydrolyzed

Proper motions of the HH1 jet

We describe a new method for determining proper motions of extended objects, and a pipeline developed for the application of this method. We then apply this method to an analysis of four epochs of [S~II] HST images of the HH~1 jet (covering a period of $\sim 20$~yr). We determine the proper motions of the knots along the jet, and make a reconstruction of the past ejection velocity time-variability (assuming ballistic knot motions). This reconstruction shows an "acceleration" of the ejection velocities of the jet knots, with higher velocities at more recent times. This acceleration will result in an eventual merging of the knots in $\sim 450$~yr and at a distance of $\sim 80"$ from the outflow source, close to the present-day position of HH~1.Comment: 12 pages, 8 figure

Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy.

The underlying genetic defect in most cases of dilated cardiomyopathy (DCM), a common inherited heart disease, remains unknown. Intriguingly, many patients carry single missense variants of uncertain pathogenicity targeting the giant protein titin, a fundamental sarcomere component. To explore the deleterious potential of these variants, we first solved the wild-type and mutant crystal structures of I21, the titin domain targeted by pathogenic variant p.C3575S. Although both structures are remarkably similar, the reduced hydrophobicity of deeply buried position 3575 strongly destabilizes the mutant domain, a scenario supported by molecular dynamics simulations and by biochemical assays that show no disulfide involving C3575. Prompted by these observations, we have found that thousands of similar hydrophobicity-reducing variants associate specifically with DCM. Hence, our results imply that titin domain destabilization causes DCM, a conceptual framework that not only informs pathogenicity assessment of gene variants but also points to therapeutic strategies counterbalancing protein destabilization.S

The 2HWC HAWC Observatory Gamma Ray Catalog

We present the first catalog of TeV gamma-ray sources realized with the recently completed High Altitude Water Cherenkov Observatory (HAWC). It is the most sensitive wide field-of-view TeV telescope currently in operation, with a 1-year survey sensitivity of ~5-10% of the flux of the Crab Nebula. With an instantaneous field of view >1.5 sr and >90% duty cycle, it continuously surveys and monitors the sky for gamma ray energies between hundreds GeV and tens of TeV. HAWC is located in Mexico at a latitude of 19 degree North and was completed in March 2015. Here, we present the 2HWC catalog, which is the result of the first source search realized with the complete HAWC detector. Realized with 507 days of data and represents the most sensitive TeV survey to date for such a large fraction of the sky. A total of 39 sources were detected, with an expected contamination of 0.5 due to background fluctuation. Out of these sources, 16 are more than one degree away from any previously reported TeV source. The source list, including the position measurement, spectrum measurement, and uncertainties, is reported. Seven of the detected sources may be associated with pulsar wind nebulae, two with supernova remnants, two with blazars, and the remaining 23 have no firm identification yet.Comment: Submitted 2017/02/09 to the Astrophysical Journa

Re-thinking the Etiological Framework of Neurodegeneration

Neurodegenerative diseases are among the leading causes of disability and death worldwide. The disease-related socioeconomic burden is expected to increase with the steadily increasing life expectancy. In spite of decades of clinical and basic research, most strategies designed to manage degenerative brain diseases are palliative. This is not surprising as neurodegeneration progresses "silently" for decades before symptoms are noticed. Importantly, conceptual models with heuristic value used to study neurodegeneration have been constructed retrospectively, based on signs and symptoms already present in affected patients;a circumstance that may confound causes and consequences. Hence, innovative, paradigm-shifting views of the etiology of these diseases are necessary to enable their timely prevention and treatment. Here, we outline four alternative views, not mutually exclusive, on different etiological paths toward neurodegeneration. First, we propose neurodegeneration as being a secondary outcome of a primary cardiovascular cause with vascular pathology disrupting the vital homeostatic interactions between the vasculature and the brain, resulting in cognitive impairment, dementia, and cerebrovascular events such as stroke. Second, we suggest that the persistence of senescent cells in neuronal circuits may favor, together with systemic metabolic diseases, neurodegeneration to occur. Third, we argue that neurodegeneration may start in response to altered body and brain trophic interactions established via the hardwire that connects peripheral targets with central neuronal structures or by means of extracellular vesicle (E\-mediated communication. Lastly, we elaborate on how lifespan body dysbiosis may be linked to the origin of neurodegeneration. We highlight the existence of bacterial products that modulate the gut-brain axis causing neuroinflammation and neuronal dysfunction. As a concluding section, we end by recommending research avenues to investigate these etiological paths in the future. We think that this requires an integrated, interdisciplinary conceptual research approach based on the investigation of the multimodal aspects of physiology and pathophysiology. It involves utilizing proper conceptual models, experimental animal units, and identifying currently unused opportunities derived from human data. Overall, the proposed etiological paths and experimental recommendations will be important guidelines for future cross-discipline research to overcome the translational roadblock and to develop causative treatments for neurodegenerative diseases