1,719 research outputs found
Cumulate causes for the low contents of sulfide-loving elements in the continental crust
Despite the economic importance of chalcophile (sulfide-loving) and siderophile (metal-loving) elements (CSEs), it is unclear how they become enriched or depleted in the continental crust, compared with the oceanic crust. This is due in part to our limited understanding of the partitioning behaviour of the CSEs. Here I compile compositional data for mid-ocean ridge basalts and subduction-related volcanic rocks. I show that the mantle-derived melts that contribute to oceanic and continental crust formation rarely avoid sulfide saturation during cooling in the crust and, on average, subduction-zone magmas fractionate sulfide at the base of the continental crust prior to ascent. Differentiation of mantle-derived melts enriches lower crustal sulfide- and silicate-bearing cumulates in some CSEs compared with the upper crust. This storage predisposes the cumulate-hosted compatible CSEs (such as Cu and Au) to be recycled back into the mantle during subduction and delamination, resulting in their low contents in the bulk continental crust and potentially contributing to the scarcity of ore deposits in the upper continental crust. By contrast, differentiation causes the upper oceanic and continental crust to become enriched in incompatible CSEs (such as W) compared with the lower oceanic and continental crust. Consequently, incompatible CSEs are predisposed to become enriched in subduction-zone magmas that contribute to continental crust formation and are less susceptible to removal from the continental crust via delamination compared with the compatible CSEs
Dietary intake of professional Australian football athletes surrounding body composition assessment
Ā© 2018 The Author(s). Background: Sports Dietitians aim to assist in improving performance by developing nutrition knowledge (NK), enhancing dietary intake and optimising body composition of athletes. In a high-pressure environment, it is important to identify factors that may compromise an athlete's nutrition status. Body composition assessments are regularly undertaken in sport to provide feedback on training adaptions; however, no research has explored the impact of these assessments on the dietary intake of professional athletes. Methods: This cross-sectional study assessed dietary intake (7-day food diary), nutrition knowledge (Nutrition for Sport Knowledge Questionnaire) and body composition (Dual-energy X-ray absorptiometry) of 46 professional male Australian football (AFL) athletes during a 2017 pre-season training week (7days) where body composition assessments were undertaken. Dietary intake was assessed against International Olympic Committee recommendations for professional athletes. Results: Overall, no athlete met dietary their recommended energy intake (15Ā±1.1 vs. 9.1Ā±1.8MJ, respectively) or carbohydrate recommendations (6-10 vs. 2.4Ā±0.9g.kg-1.day-1). Only 54% met protein recommendations. Secondary analyses demonstrated significant associations between education status and energy intake (P<0.04) and vegetable intake (P<0.03), with higher levels of education being associated with higher intakes. A moderately positive association was observed between NK scores and meeting estimated energy requirements (r=0.33, P=0.03). NK scores were also positively associated with protein (r=0.35, P=0.02), fibre (r=0.51, P=0.001) and calcium intakes (r=0.43, P=0.004). Conclusions: This research identified that the dietary intake of professional AFL athletes during a pre-season training week where body composition assessments were undertaken did not meet current recommendations. Several factors may influence the dietary intake of AFL athletes, including lower education levels, poor NK and dietary intake restriction surrounding body composition assessment. Athletes may require support to continue with performance-based nutrition plans in periods surrounding body composition assessment
Binge-watching: Video-on-demand, quality TV and mainstreaming fandom
This article explores the concept of the binge as viewing protocol associated with fan practices, industry practice and linked to ācultā and āqualityā serialised content. Viewing binge-watching as an intersection of discourses of industry, audience and text, the concept is analysed here as shaped by a range of issues that dominate the contemporary media landscape. In this, factors like technological developments, fan discourses and practices being adopted as āmainstreamā media practice, changes in the discursive construction of ātelevisionā and an emerging Video-on-Demand industry contribute to the construction of binge-watching as deliberate, self-scheduled alternative to āwatching TVā
The TH1 cell lineage-determining transcription factor T-bet suppresses TH2 gene expression by redistributing GATA3 away from TH2 genes
Lineage-determining transcription factors (LD-TFs) drive the differentiation of progenitor cells into a specific lineage. In CD4+ T cells, T-bet dictates differentiation of the TH1 lineage, whereas GATA3 drives differentiation of the alternative TH2 lineage. However, LD-TFs, including T-bet and GATA3, are frequently co-expressed but how this affects LD-TF function is not known. By expressing T-bet and GATA3 separately or together in mouse T cells, we show that T-bet sequesters GATA3 at its target sites, thereby removing GATA3 from TH2 genes. This redistribution of GATA3 is independent of GATA3 DNA binding activity and is instead mediated by the T-bet DNA binding domain, which interacts with the GATA3 DNA binding domain and changes GATA3ā²s sequence binding preference. This mechanism allows T-bet to drive the TH1 gene expression program in the presence of GATA3. We propose that redistribution of one LD-TF by another may be a common mechanism that could explain how specific cell fate choices can be made even in the presence of other transcription factors driving alternative differentiation pathways
The relative importance of factors predicting outcome for myeloma patients at different ages: results from 3894 patients in the Myeloma XI trial.
Disease factors such as tumor burden and molecular risk affect myeloma patient outcomes as well as patient factors that impact the capacity to deliver treatment. How the relative importance of these factors changes with patient age has not previously been investigated comprehensively. We analyzed data from 3894 patients of all ages uniformly treated in a large clinical trial of myeloma patients, Myeloma XI. Even with novel therapeutic approaches progression-free survival (PFS) and overall survival (OS) are affected by age with a stepwise reduction in PFS and OS with each decade increase. Renal function deteriorated with increasing age whilst the frequency of t(4;14) and del(17p) decreased and gain(1q) increased. The relative contribution of performance status, international staging score and molecular risk to progression-free and overall survival varied by age group. Molecular events have a larger effect on outcome in younger patients with their relative contribution diminishing in the elderly. Performance status is important for patient outcome at all ages suggesting that physical frailty may be a more important predictor of outcome than age itself. Significant differences in the factors driving patient outcomes at different ages are important to consider as we design disease segmentation strategies to deliver personalized treatment approaches
Early relapse after highādose melphalan autologous stem cell transplant predicts inferior survival and is associated with high disease burden and genetically highārisk disease in multiple myeloma
Predicting patient outcome in multiple myeloma remains challenging despite the availability of standard prognostic biomarkers. We investigated outcome for patients relapsing early from intensive therapy on NCRI Myeloma XI. Relapse within 12 months of autologous stem cell transplant was associated with markedly worse median progressionāfree survival 2 (PFS2) of 18 months and overall survival (OS) of 26 months, compared to median PFS2 of 85 months and OS of 91 months for later relapsing patients despite equal access to and use of subsequent therapies, highlighting the urgent need for improved outcome prediction and early intervention strategies for myeloma patients
Eddy current studies from the undulator-based positron source target wheel prototype
The efĀfiĀcienĀcy of fuĀture positron sources for the next genĀerĀaĀtion of high-enĀerĀgy parĀtiĀcle colĀlidĀers (e.g. ILC, CLIC, LHeC) can be imĀproved if the positron-proĀducĀtion tarĀget is imĀmersed in the magĀnetĀic field of adĀjaĀcent capĀture opĀtics. If the tarĀget is also roĀtatĀing due to heat deĀpoĀsiĀtion conĀsidĀerĀaĀtions then eddy curĀrents may be inĀduced and lead to adĀdiĀtionĀal heatĀing and stressĀes. In this paper we preĀsent data from a roĀtatĀing tarĀget wheel proĀtoĀtype for the baseĀline ILC positron source. The wheel has been opĀerĀatĀed at revĀoĀluĀtion rates up to 1800rpm in fields of the order of 1 Tesla. ComĀparĀisons are made beĀtween torque data obĀtained from a transĀducĀer on the tarĀget drive shaft and the reĀsults of fiĀnite-elĀeĀment simĀuĀlaĀtions. RoĀtorĀdyĀnamĀics isĀsues are preĀsentĀed and fuĀture exĀperĀiĀments on other asĀpects of the positron source tarĀget staĀtion are conĀsidĀered
A FABP4-PPARĪ³ signaling axis regulates human monocyte responses to electrophilic fatty acid nitroalkenes
Nitro-fatty acids (NO2-FA) are electrophilic lipid mediators derived from unsaturated fatty acid nitration. These
species are produced endogenously by metabolic and inflammatory reactions and mediate anti-oxidative and
anti-inflammatory responses. NO2-FA have been postulated as partial agonists of the Peroxisome Proliferator-
Activated Receptor gamma (PPARĪ³), which is predominantly expressed in adipocytes and myeloid cells. Herein,
we explored molecular and cellular events associated with PPARĪ³ activation by NO2-FA in monocytes and
macrophages. NO2-FA induced the expression of two PPARĪ³ reporter genes, Fatty Acid Binding Protein 4
(FABP4) and the scavenger receptor CD36, at early stages of monocyte differentiation into macrophages. These
responses were inhibited by the specific PPARĪ³ inhibitor GW9662. Attenuated NO2-FA effects on PPARĪ³ sig-
naling were observed once cells were differentiated into macrophages, with a significant but lower FABP4 up-
regulation, and no induction of CD36. Using in vitro and in silico approaches, we demonstrated that NO2-FA bind
to FABP4. Furthermore, the inhibition of monocyte FA binding by FABP4 diminished NO2-FA-induced upre-
gulation of reporter genes that are transcriptionally regulated by PPARĪ³, Keap1/Nrf2 and HSF1, indicating that
FABP4 inhibition mitigates NO2-FA signaling actions. Overall, our results affirm that NO2-FA activate PPARĪ³ in
monocytes and upregulate FABP4 expression, thus promoting a positive amplification loop for the downstream
signaling actions of this mediator
Study of 2 beta-decay of Mo-100 and Se-82 using the NEMO3 detector
After analysis of 5797 h of data from the detector NEMO3, new limits on neutrinoless double beta decay of Mo-100 (T-1/2 > 3.1 x 10(23) y, 90% CL) and Se-82 (T-1/2 > 1.4 x 10(23) y, 90% CL) have been obtained. The corresponding limits on the effective majorana neutrino mass are: 1.4 x 10(22) y (90% CL) for Mo-100 and T-1/2 > 1.2 x 10(22) y (90% CL) for Se-82. Corresponding bounds on the Majoron-neutrino coupling constant are < (0.5-0.9) x 10(- 4) and <(0.7-1.6) x 10(- 4). Two-neutrino 2beta-decay half-lives have been measured with a high accuracy, (T1/2Mo)-Mo-100 = [7.68 +/- 0.02(stat) +/- 0.54(syst)] x 10(18) y and (T1/2Se)-Se-82 = [10.3 +/- 0.3(stat) +/- 0.7(syst)] x 10(19) y. (C) 2004 MAIK "Nauka/Interperiodica"
Thrombotic microangiopathy in untreated myeloma patients receiving carfilzomib, cyclophosphamide and dexamethasone on the CARDAMON study
Proteasome inhibitors have been associated with thrombotic microangiopathy (TMA) ā a group of disorders characterised by occlusive microvascular thrombosis causing microangiopathic haemolytic anaemia, thrombocytopenia and endāorgan damage. To date, carfilzomibāassociated TMA has predominantly been described in relapsed/refractory myeloma patients. We report eight patients with newly diagnosed myeloma who experienced TMA events while receiving carfilzomib on the phase II CARDAMON trial. The first three occurred during maintenance singleāagent carfilzomib, two occurred at induction with carfilzomib given with cyclophosphamide and dexamethasone (KCd) and three occurred during KCd consolidation. At TMA presentation 6/8 were hypertensive; 7/8 had acute kidney injury and in three, renal impairment persisted after resolution of TMA in other respects. The mechanism of carfilzomibāassociated TMA remains unclear, though patients with known hypertension seem particularly susceptible. Given the first three cases occurred during maintenance after a longer than fiveāweek treatment break, a protocol amendment was instituted with: aggressive hypertension management, carfilzomib stepāup dosing (20 mg/m2 on day 1) at start of maintenance before dose escalation to 56 mg/m2 maximum, and adding 10 mg dexamethasone as premedication to maintenance carfilzomib infusions. No further TMA events occurred during maintenance following this amendment and the TMA incidence reduced from 4Ā·2 to 1Ā·6 per 1 000 patient cycles
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