717 research outputs found

    The Origin of Nitrogen on Jupiter and Saturn from the 15^{15}N/14^{14}N Ratio

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    The Texas Echelon cross Echelle Spectrograph (TEXES), mounted on NASA's Infrared Telescope Facility (IRTF), was used to map mid-infrared ammonia absorption features on both Jupiter and Saturn in February 2013. Ammonia is the principle reservoir of nitrogen on the giant planets, and the ratio of isotopologues (15^{15}N/14^{14}N) can reveal insights into the molecular carrier (e.g., as N2_2 or NH3_3) of nitrogen to the forming protoplanets, and hence the source reservoirs from which these worlds accreted. We targeted two spectral intervals (900 and 960 cm1^{-1}) that were relatively clear of terrestrial atmospheric contamination and contained close features of 14^{14}NH3_3 and 15^{15}NH3_3, allowing us to derive the ratio from a single spectrum without ambiguity due to radiometric calibration (the primary source of uncertainty in this study). We present the first ground-based determination of Jupiter's 15^{15}N/14^{14}N ratio (in the range from 1.4×1031.4\times10^{-3} to 2.5×1032.5\times10^{-3}), which is consistent with both previous space-based studies and with the primordial value of the protosolar nebula. On Saturn, we present the first upper limit on the 15^{15}N/14^{14}N ratio of no larger than 2.0×1032.0\times10^{-3} for the 900-cm1^{-1} channel and a less stringent requirement that the ratio be no larger than 2.8×1032.8\times10^{-3} for the 960-cm1^{-1} channel (1σ1\sigma confidence). Specifically, the data rule out strong 15^{15}N-enrichments such as those observed in Titan's atmosphere and in cometary nitrogen compounds. To the extent possible with ground-based radiometric uncertainties, the saturnian and jovian 15^{15}N/14^{14}N ratios appear indistinguishable, implying that 15^{15}N-enriched ammonia ices could not have been a substantial contributor to the bulk nitrogen inventory of either planet, favouring the accretion of primordial N2_2 from the gas phase or as low-temperature ices.Comment: 33 pages, 19 figures, manuscript accepted for publication in Icaru

    World TB Day 2016: an interview with leading experts in tuberculosis research.

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    In this interview, we talk to leading tuberculosis (TB) experts from University College London and the London School of Hygiene and Tropical Medicine about the current challenges in TB research. The video of this interview is available here: https://www.youtube.com/watch?v=75Die7MQBec&feature=youtu.be . The video can also be downloaded via Additional file 1

    Evaluation of the impact of high bandwidth energy storage systems on DC protection

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    The integration of high bandwidth energy storage systems (ESS) in compact DC electrical power systems can increase the operational capability and overall flexibility of the network. However, the impact of ESSs on the performance of existing DC protection systems is not well understood. This paper identifies the key characteristics of the ESS that determine the extent of the protection blinding effects on slower acting generator systems on the network. It shows that higher fault impedances beyond that of an evaluated critical level will dampen the response of slower acting generator systems, decreasing the speed of corresponding overcurrent protection operation. The paper demonstrates the limitations of existing protection solutions and identifies more suitable protection approaches to remove/minimize the effects of protection blinding

    Divergent expression patterns of pituitary gonadotropin subunit and GnRH receptor genes to continuous GnRH in vitro and in vivo.

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    Continuous, as opposed to pulsatile, delivery of hypothalamic gonadotropin-releasing hormone (GnRH) leads to a marked decrease in secretion of pituitary gonadotropins LH and FSH and impairment of reproductive function. Here we studied the expression profile of gonadotropin subunit and GnRH receptor genes in rat pituitary in vitro and in vivo to clarify their expression profiles in the absence and continuous presence of GnRH. Culturing of pituitary cells in GnRH-free conditions downregulated Fshb, Cga, and Gnrhr expression, whereas continuous treatment with GnRH agonists upregulated Cga expression progressively and Gnrhr and Fshb expression transiently, accompanied by a prolonged blockade of Fshb but not Gnrhr expression. In contrast, Lhb expression was relatively insensitive to loss of endogenous GnRH and continuous treatment with GnRH, probably reflecting the status of Egr1 and Nr5a1 expression. Similar patterns of responses were observed in vivo after administration of a GnRH agonist. However, continuous treatment with GnRH stimulated LH secretion in vitro and in vivo, leading to decrease in LH cell content despite high basal Lhb expression. These data suggest that blockade of Fshb expression and depletion of the LH secretory pool are two major factors accounting for weakening of the gonadotroph secretory function during continuous GnRH treatment

    Protection system for an electrical power network

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    The invention is a means of fault detection and location for dc networks. AC systems attempt to measure the inductance of the line; this is not possible in a dc system. Instead, in this invention, the inductance is estimated from the initial rate of discharge of the current from the dc bus capacitor on the converter feeding the dc network. This will reduce the duration that a fault will exist, reducing damage and improving safety, as well as improving discrimination so giving a more reliable system

    Effects of newer kidney protective agents on kidney endpoints provide implications for future clinical trials

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    Doubling of serum creatinine (equivalent to a 57% decline in the estimated glomerular filtration rate (eGFR)) is an accepted component of a composite kidney endpoint in clinical trials. Smaller declines in eGFR (40%, 50%) have been applied in several recently conducted clinical trials. Here, we assessed the effects of newer kidney protective agents on endpoints including smaller proportional declines in eGFR to compare relative event rates and the magnitude of observed treatment effects. We performed a post hoc analysis of 4401 patients in the CREDENCE, 4304 in the DAPA-CKD, 5734 in the FIDELIO-DKD, and 3668 in the SONAR trials, which assessed the effects of canagliflozin, dapagliflozin, finerenone and atrasentan in patients with chronic kidney disease. Effects of active therapies versus placebo on alternative composite kidney endpoints incorporating different eGFR decline thresholds (40%, 50%, or 57% eGFR reductions from baseline) with kidney failure or death due to kidney failure were compared. Cox-proportional hazards regression models were used to assess and compare treatment effects. During follow-up, event rates were higher for endpoints incorporating smaller versus larger eGFR decline thresholds. Compared to the treatment effects on kidney failure or death due to kidney failure, the magnitude of relative treatment effects was generally similar when considering composite endpoints incorporating smaller declines in eGFR. Hazard ratios for the four interventions ranged from 0.63 to 0.82 for the endpoint incorporating 40% eGFR decline and 0.59 to 0.76 for the endpoint incorporating 57% eGFR decline. Clinical trials incorporating a 40% eGFR decline in a composite endpoint would require approximately half the number of participants compared to a 57% eGFR decline with equivalent statistical power. Thus, in populations at high risk of CKD progression, the relative effects of newer kidney protective therapies appear generally similar across endpoints based on varying eGFR decline thresholds.</p

    Delayed functional expression of neuronal chemokine receptors following focal nerve demyelination in the rat: a mechanism for the development of chronic sensitization of peripheral nociceptors

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    <p>Abstract</p> <p>Background</p> <p>Animal and clinical studies have revealed that focal peripheral nerve axon demyelination is accompanied by nociceptive pain behavior. C-C and C-X-C chemokines and their receptors have been strongly implicated in demyelinating polyneuropathies and persistent pain syndromes. Herein, we studied the degree to which chronic nociceptive pain behavior is correlated with the neuronal expression of chemokines and their receptors following unilateral lysophosphatidylcholine (LPC)-induced focal demyelination of the sciatic nerve in rats.</p> <p>Results</p> <p>Focal nerve demyelination increased behavioral reflex responsiveness to mechanical stimuli between postoperative day (POD) 3 and POD28 in both the hindpaw ipsilateral and contralateral to the nerve injury. This behavior was accompanied by a bilateral increase in the numbers of primary sensory neurons expressing the chemokine receptors CCR2, CCR5, and CXCR4 by POD14, with no change in the pattern of CXCR3 expression. Significant increases in the numbers of neurons expressing the chemokines monocyte chemoattractant protein-1 (MCP-1/CCL2), Regulated on Activation, Normal T Expressed and Secreted (RANTES/CCL5) and interferon γ-inducing protein-10 (IP-10/CXCL10) were also evident following nerve injury, although neuronal expression pattern of stromal cell derived factor-1α (SDF1/CXCL12) did not change. Functional studies demonstrated that acutely dissociated sensory neurons derived from LPC-injured animals responded with increased [Ca<sup>2+</sup>]<sub>i </sub>following exposure to MCP-1, IP-10, SDF1 and RANTES on POD 14 and 28, but these responses were largely absent by POD35. On days 14 and 28, rats received either saline or a CCR2 receptor antagonist isomer (CCR2 RA-<b>[R]</b>) or its inactive enantiomer (CCR2 RA-<b>[S]</b>) by intraperitoneal (i.p.) injection. CCR2 RA-[<b>R</b>] treatment of nerve-injured rats produced stereospecific bilateral reversal of tactile hyperalgesia.</p> <p>Conclusion</p> <p>These results suggest that the presence of chemokine signaling by both injured and adjacent, uninjured sensory neurons is correlated with the maintenance phase of a persistent pain state, suggesting that chemokine receptor antagonists may be an important therapeutic intervention for chronic pain.</p
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