Overview of HST observa7ons of Jupiter’s ultraviolet aurora during Juno orbits 3 to 7

Jupiter’s permanent ultraviolet auroral emissions have been systematically monitored from Earth orbit with the Hubble Space Telescope (HST) during an 8-month period. The Girst part of this HST large program (GO-14634) was meant to support the NASA Juno prime mission during orbits PJ03 through PJ07. The HST program will resume in Feb 2018, in time for Juno’s PJ11 perijove, right after HST’s solar and lunar avoidance periods. HST observations are designed to provide a Jovian auroral activity background for all instruments on-board Juno and for the numerous ground based and space based observatories participating to the Juno mission. In particular, several HST visits were programmed in order to obtain as many simultaneous observations with Juno-UVS as possible, sometimes in the same hemisphere, sometimes in the opposite one. In addition, the timing of some HST visits was set to take advantage of Juno’s multiple crossings of the current sheet and of the magnetic Gield lines threading the auroral emissions. These observations are obtained with the Space Telescope Imaging Spectrograph (STIS) in time-tag mode, they consist in spatially resolved movies of Jupiter’s highly dynamic aurora with timescales ranging from seconds to several days. Here, we present an overview of the present -numerous- HST results. They demonstrate that while Jupiter is always showing the same basic auroral components, it is also displaying an ever-changing auroral landscape. The complexity of the auroral morphology is such that no two observations are alike. Still, in this apparent chaos some patterns emerge. This information is giving clues on magnetospheric processes at play at the local and global scales, the latter being only accessible to remote sensing instruments such as HST

Stability of Dexamethasone in Extemporaneously Prepared Oral Suspensions

ABSTRACT Objective: To evaluate the stability of 0.5 and 1.0 mg/mL dexamethasone suspensions in a vehicle consisting of equal parts of Ora-Sweet and Ora-Plus after storage at 4°C and 25°C for up to 91 days.Methods: Suspensions of dexamethasone sodium phosphate 4 mg/mL injection solution in a 1:1 mixture of Ora-Sweet and Ora-Plus were prepared in 40-mL amber plastic bottles; final concentrations of dexamethasone were 0.5 and 1.0 mg/mL. Three bottles of each suspension were stored at 4°C (refrigerated), and 3 were stored at 25°C (room temperature). Physical characteristics, including pH, colour, odour, viscosity, precipitation, and ease of resuspension, were observed weekly for 91 days. Aliquots were removed from each bottle weekly for 91 days and stored at –84°C until analysis by a validated high-pressure liquid chromatography method. A suspension was considered stable if it maintained 90% of its initial concentration.Results: No change in pH was observed in suspensions of either concentration after storage at 4°C or 25°C for 91 days. Changes in colour and odour were slight. Viscosity was constant. Precipitates were easily resuspended, and there was no caking or clumping of material. Suspensions of both concentrations of dexamethasone maintained at least 90% of initial concentration at both temperatures throughout the 91-day period.Conclusions: Dexamethasone suspensions of both 0.5 and 1.0 mg/mL in a 1:1 mixture of Ora-Sweet and Ora-Plus were physically and chemically stable for a period of up to 91 days, with or without refrigeration. The expiry date for these products can therefore be set at 91 days.RÉSUMÉ Objectif : Évaluer la stabilité de suspensions de dexaméthasone à des concentrations de 0,5 et 1,0 mg/mL dans un excipient liquide composé à parts égales d’Ora Sweet et d’Ora Plus, après entreposage à 4 °C et 25 °C pendant une période allant jusqu’à 91 jours.Méthodes : Les suspensions de phosphate sodique de dexaméthasone à raison de 4 mg/mL de solution pour injection dans un mélange 1:1 d’Ora-Sweet et d’Ora-Plus ont été préparées dans des flacons de plastique ambré de 40 mL; les concentrations finales de dexaméthasone étaient de 0,5 et 1,0 mg/mL. Trois flacons de chaque suspension ont été entreposés à 4 °C (au réfrigérateur) et trois autres à 25°C (à la température ambiante). Les caractéristiques physiques, don le pH, la couleur, l’odeur, la viscosité, la précipitation et la facilité de remise en suspension ont été examinées à chaque semaine pendant les 91 jours. Les aliquotes ont été retirées de chaque flacon à toutes les semaines, pendant les 91 jours, et réfrigérées à –84 °C avant d’être analysées par une méthode validée de chromatographie liquide à haute pression. La suspension était considérée stable lorsqu’elle conservait 90 % de sa concentration initiale.Résultats : Aucun changement du pH n’a été observé dans l’une ou l’autre des suspensions aux deux concentrations, après leur entreposage à 4 °C ou 25 °C pendant 91 jours. Une légère altération de la couleur et de l’odeur est cependant survenue. La viscosité était stable et les précipités ont été facilement remis en suspension, sans agglomération ni agglutination de la matière. Les suspensions des deux concentrations de dexaméthasone ont conservé au moins 90 % de leur concentration initiale aux deux températures pendant la période d’étude de 91 jours.Conclusions : Les suspensions de dexaméthasone aux concentrations de 0,5 et 1 mg/mL dans un mélange 1:1 d’Ora Sweet et d’Ora Plus ont montré une stabilité physique et chimique pendant une période allant jusqu’à 91 jours, avec ou sans réfrigération. La date de péremption de ces produits peut par conséquent être établie à 91 jours

Acute spinal cord injury, part II: Contemporary pharmacotherapy

Spinal cord injury (SCI) remains a common and devastating problem of modern society. Through an understanding of underlying pathophysiologic mechanisms involved in the evolution of SCI, treatments aimed at ameliorating neural damage may be developed. The possible pharmacologic treatments for acute spinal cord injury are herein reviewed. Myriad treatment modalities, including corticosteroids, 21-amino-steroids, opioid receptor antagonists, gangliosides, thyrotropin-releasing hormone (TRH) and TRH analogs, antioxidants and free radical scavengers, calcium channel blockers, magnesium replacement therapy, sodium channel blockers, N-methyl-D-aspartate receptor antagonists, α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-kainate receptor antagonists, modulators of arachadonic acid metabolism, neurotrophic growth factors, serotonin antagonists, antibodies against inhibitors of axonal regeneration, potassium channel blockers (4-aminopyridine), paclitaxel, clenbuterol, progesterone, gabexate mesylate, activated protein C, caspase inhibitors, tacrolimus, antibodies against adhesion molecules, and other immunomodulatory therapy have been studied to date. Although most of these agents have shown promise, only one agent, methylprednisolone, has been shown to provide benefit in large clinical trials. Given these data, many individuals consider methylprednisolone to be the standard of care for the treatment of acute SCI. However, this has not been established definitively, and questions pertaining to methodology have emerged regarding the National Acute Spinal Cord Injury Study trials that provided these conclusions. Additionally, the clinical significance (in contrast to statistical significance) of recovery after methylprednisolone treatment is unclear and must be considered in light of the potential adverse effects of such treatment. This first decade of the new millennium, now touted as the Decade of the Spine, will hopefully witness the emergence of universal and efficacious pharmacologic therapy and ultimately a cure for SCI

Acute spinal cord injury, part I: Pathophysiologic mechanisms

Spinal cord injury (SCI) is a devastating and common neurologic disorder that has profound influences on modern society from physical, psychosocial, and socioeconomic perspectives. Accordingly, the present decade has been labeled the Decade of the Spine to emphasize the importance of SCI and other spinal disorders. Spinal cord injury may be divided into both primary and secondary mechanisms of injury. The primary injury, in large part, determines a given patient\u27s neurologic grade on admission and thereby is the strongest prognostic indicator. However, secondary mechanisms of injury can exacerbate damage and limit restorative processes, and hence, contribute to overall morbidity and mortality. A burgeoning body of evidence has facilitated our understanding of these secondary mechanisms of injury that are amenable to pharmacological interventions, unlike the primary injury itself. Secondary mechanisms of injury encompass an array of perturbances and include neurogenic shock, vascular insults such as hemorrhage and ischemia-reperfusion, excitotoxicity, calcium-mediated secondary injury and fluid-electrolyte disturbances, immunologic injury, apoptosis, disturbances in mitochondrion function, and other miscellaneous processes. Comprehension of secondary mechanisms of injury serves as a basis for the development and application of targeted pharmacological strategies to confer neuroprotection and restoration while mitigating ongoing neural injury. The first article in this series will comprehensively review the pathophysiology of SCI while emphasizing those mechanisms for which pharmacologic therapy has been developed, and the second article reviews the pharmacologic interventions for SCI

Cerebral vasospasm after subarachnoid hemorrhage: Putative role of inflammation

Cerebral vasospasm is a common, formidable, and potentially devastating complication in patients who have sustained subarachnoid hemorrhage (SAH). Despite intensive research efforts, cerebral vasospasm remains incompletely understood from both the pathogenic and therapeutic perspectives. At present, no consistently efficacious and ubiquitously applied preventive and therapeutic measures are available in clinical practice. Recently, convincing data have implicated a role of inflammation in the development and maintenance of cerebral vasospasm. A burgeoning (although incomplete) body of evidence suggests that various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be critical in the pathogenesis of cerebral vasospasm. Recent studies attempting to dissect the cellular and molecular basis of the inflammatory response accompanying SAH and cerebral vasospasm have provided a promising groundwork for future studies. It is plausible that the inflammatory response may indeed represent a critical common pathway in the pathogenesis of cerebral vasospasm pursuant to SAH. Investigations into the nature of the inflammatory response accompanying SAH are needed to elucidate the precise role(s) of inflammatory events in SAH-induced pathologies

Juno, Hubble and James Webb observing Jupiter’s aurora

Hubble Space Telescope (HST) observations of Jupiter’s aurora, supporting the Juno mission, started on 30 Nov 2016. So far, they successfully covered orbits PJ03 to PJ06. After PJ07 in July 2017, the HST campaign will be interrupted by a solar avoidance period, preventing any observations from late August to the end of December 2017 (PJ08 to PJ10). The campaign will resume with PJ11 and continue until the end of HST cycle 25 (PJ15). Here, we present a brief summary of the HST data that has been acquired so far. It shows a broad range of auroral morphologies, suggesting that the Juno mission is sampling di ff erent facets of Jupiter’s magnetospheric activity. One should keep in mind that HST will not last forever. We should be ready to switch to the James Webb Telescope and take advantage of the overlap between the HST and JWST missions to prepare a smooth transition. The numerous infrared observations of Jupiter’s aurora obtained from ground based telescopes during Juno and obviously with Juno-JIRAM demonstrate that we can expect much from the tremendous performances of the JWST NIRCam and NIRSpec instruments