Climate data system supports FIRE

The NASA Climate Data System (NCDS) at Goddard Space Flight Center is serving as the FIRE Central Archive, providing a centralized data holding and data cataloging service for the FIRE project. NCDS members are carrying out their responsibilities by holding all reduced observations and data analysis products submitted by individual principal investigators in the agreed upon format, by holding all satellite data sets required for FIRE, by providing copies of any of these data sets to FIRE investigators, and by producing and updating a catalog with information about the FIRE holdings. FIRE researchers were requested to provide their reduced data sets in the Standard Data Format (SDF) to the FIRE Central Archive. This standard format is proving to be of value. An improved SDF document is now available. The document provides an example from an actual FIRE SDF data set and clearly states the guidelines for formatting data in SDF. NCDS has received SDF tapes from a number of investigators. These tapes were analyzed and comments provided to the producers. One product which is now available is William J. Syrett's sodar data product from the Stratocumulus Intensive Field Observation. Sample plots from all SDF tapes submitted to the archive will be available to FSET members. Related cloud products are also available through NCDS. Entries describing the FIRE data sets are being provided for the NCDS on-line catalog. Detailed information for the Extended Time Observations is available in the general FIRE catalog entry. Separate catalog entries are being written for the Cirrus Intensive Field Observation (IFO) and for the Marine Stratocumulus IFO. Short descriptions of each FIRE data set will be installed into the NCDS Summary Catalog

La "cohérence cardiaque": une technique cardio-respiratoire efficace pour la gestion du stress et de l'anxiété en périnatalité : travail de Bachelor

Background : Le stress et l'anxiété en période périnatale sont impliqués dans la survenue de pathologies physiques et psychiques chez les mères, de pathologies de la grossesse, de problématiques de développement foetal et d'adaptation néonatale, ainsi que de perturbations de l'établissement du lien mère-enfant. Cela impacte le système de soins, et fait de la prévention du stress un problème de santé publique, pour lequel il est nécessaire de proposer des interventions. La "cohérence cardiaque" est une méthode de gestion du stress et de l'anxiété efficace, utilisée dans les services de psychiatrie et de réadaptation cardiaque depuis une dizaine d'années. Dans le domaine de l'obstétrique, infiniment peu d'études ont testé cette technique, dont il serait pertinent d'interroger la validité. Objectifs : Le but de cette revue de la littérature est de déterminer la validité de la méthode cardio-respiratoire de cohérence cardiaque pour la réduction du stress et de l'anxiété des femmes en période périnatale. Méthode : La recherche se base sur les articles des dix dernières années, issus des bases de données Pubmed et Cochrane. Elle présente les résultats analysés de cinq études pilotes portant sur l'utilisation de méthodes de respiration contrôlée couplée au biofeedback, apparentées à la cohérence cardiaque, dont l'objet est la réduction du stress et de l'anxiété. Les études ont été analysées, puis l'ensemble synthétisé pour en extraire les résultats. Résultats : La pratique de la "cohérence cardiaque" diminue significativement les scores de stress et d'anxiété. Les résultats sont controversés quant à l'impact sur les mesures biologiques telles que fréquence cardiaque, pression artérielle, taux ce cortisol salivaire, HRV ou issues obstétricales. Conclusion : En raison de l'incidence fortement délétère du stress et de l'anxiété dans la période périnatale, il est nécessaire de proposer aux femmes des moyens thérapeutiques efficaces. La "cohérence cardiaque" apparaît comme un moyen simple, peu onéreux et d'une innocuité totale, que les professionnels de santé peuvent proposer aux mères après un minimum de formation. Toutefois, des recherches complémentaires paraissent nécessaires pour en apprécier tous les bénéfices

Management of Barrett’s Esophagus: Practice-Oriented Answers to Clinical Questions

Barrett's esophagus is the most important complication of gastro-esophageal reflux disease and the only known precursor of esophageal adenocarcinoma. The diagnosis and treatment of Barrett's esophagus are clinically challenging as it requires a high level of knowledge and competence in upper gastrointestinal endoscopy. For instance, endoscopists should know when and how to perform biopsies when Barrett's esophagus is suspected. Furthermore, the correct identification and treatment of dysplastic Barrett's esophagus is crucial to prevent progression to cancer as well as it is the endoscopic surveillance of treated patients. Herein, we report practice-oriented answers to clinical questions that clinicians should be aware of when approaching patients with Barrett's esophagus

Impairments in neurogenesis are not tightly linked to depressive behavior in a transgenic mouse model of Alzheimer\u27s disease.

Alzheimer\u27s disease (AD), the most common cause of dementia, is also associated with depression. Although the precise mechanisms that lead to depression in AD are unknown, the impairments in adult hippocampal neurogenesis observed in AD may play a role. Adult-born neurons play a critical role in regulating both cognition and mood, and reduced hippocampal neurogenesis is associated with depression in other neurological disorders. To assess the relationship between Alzheimer\u27s disease, neurogenesis, and depression, we studied human amyloid precursor protein (hAPP) transgenic mice, a well-characterized model of AD. We report that reductions in hippocampal neurogenesis are evident early in disease progression in hAPP mice, but a mild depressive phenotype manifests only in later stages of disease. We found that hAPP mice exhibited a reduction in BrdU-positive cells in the subgranular zone of the dentate gyrus in the hippocampus, as well as a reduction in doublecortin-expressing cells, relative to nontransgenic controls at 5-7 months of age. These alterations in neurogenesis appeared to worsen with age, as the magnitude of reduction in doublecortin-expressing cells was greater in hAPP mice at 13-15 months of age. Only 13-15 month old hAPP mice exhibited depressive behavior in the tail suspension test. However, mice at both age groups exhibited deficits in spatial memory, which was observed in the Morris water maze test for hippocampus-dependent memory. These findings indicate that neurogenesis impairments are accompanied by cognitive deficits, but are not tightly linked to depressive behavior in hAPP mice

ΔFosB Regulates Gene Expression and Cognitive Dysfunction in a Mouse Model of Alzheimer\u27s Disease.

Alzheimer\u27s disease (AD) is characterized by cognitive decline and 5- to 10-fold increased seizure incidence. How seizures contribute to cognitive decline in AD or other disorders is unclear. We show that spontaneous seizures increase expression of ΔFosB, a highly stable Fos-family transcription factor, in the hippocampus of an AD mouse model. ΔFosB suppressed expression of the immediate early gene c-Fos, which is critical for plasticity and cognition, by binding its promoter and triggering histone deacetylation. Acute histone deacetylase (HDAC) inhibition or inhibition of ΔFosB activity restored c-Fos induction and improved cognition in AD mice. Administration of seizure-inducing agents to nontransgenic mice also resulted in ΔFosB-mediated suppression of c-Fos, suggesting that this mechanism is not confined to AD mice. These results explain observations that c-Fos expression increases after acute neuronal activity but decreases with chronic activity. Moreover, these results indicate a general mechanism by which seizures contribute to persistent cognitive deficits, even during seizure-free periods

Gut permeability and osteoarthritis, towards a mechanistic understanding of the pathogenesis: a systematic review

Osteoarthritis (OA) is the most common condition affecting human joints. Along with mechanical and genetic factors, low-grade inflammation is increasingly supported as a causal factor in the development of OA. Gut microbiota and intestinal permeability, via the disruption of tight junction competency, are proposed to explain a gut-joint axis through the interaction with the host immune system. Since previous studies and methods have underestimated the role of the gut-joint axis in OA and have only focussed on the characterisation of microbiota phenotypes, this systematic review aims to appraise the current evidence concerning the influence of gut permeability in the pathogenesis of OA. We propose that the tight junction disruption may be due to an increase in zonulin activity as already demonstrated for many other chronic inflammatory disorders. After years of unreliable quantification, one study optimised the methodology, showing a positive validated correlation between plasma lipopolysaccharide (LPS), obesity, joint inflammation, and OA severity. Chemokines show a prominent role in pain development. Our systematic review confirms preliminary evidence supporting a gut-joint axis in OA pathogenesis and progression. Being modifiable by several factors, the gut microbiota is a promising target for treatment. We propose a pathogenetic model in which dysbiosis is correlated to the bipartite graph of tight junctions and bacterially-produced products, aiming to direct future studies in the search of other bacterial products and tight junction disassembly regulators.KEY MESSAGESPrevious studies and methods have underestimated the impact of the gut-joint axis in osteoarthritis and have focussed on the characterisation of microbiota phenotypes rather than clear molecular mediators of disease.Gut dysbiosis is related to higher levels of bacterial toxins that elicit cartilage and synovium inflammatory pathways.Future research may benefit from focussing on both tight junctions and bacterially-produced products

SAM68 is a physiological regulator of SMN2 splicing in spinal muscular atrophy

Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by loss of motor neurons in patients with null mutations in the SMN1 gene. The almost identical SMN2 gene is unable to compensate for this deficiency because of the skipping of exon 7 during pre-messenger RNA (mRNA) processing. Although several splicing factors can modulate SMN2 splicing in vitro, the physiological regulators of this disease-causing event are unknown. We found that knockout of the splicing factor SAM68 partially rescued body weight and viability of SMAΔ7 mice. Ablation of SAM68 function promoted SMN2 splicing and expression in SMAΔ7 mice, correlating with amelioration of SMA-related defects in motor neurons and skeletal muscles. Mechanistically, SAM68 binds to SMN2 pre-mRNA, favoring recruitment of the splicing repressor hnRNP A1 and interfering with that of U2AF65 at the 3' splice site of exon 7. These findings identify SAM68 as the first physiological regulator of SMN2 splicing in an SMA mouse model