Sensitive response of the Greenland Ice Sheet to surface melt drainage over a soft bed

This is the accepted manuscript. The final version is available from Nature Communications at http://www.nature.com/ncomms/2014/140929/ncomms6052/full/ncomms6052.html.The dynamic response of the Greenland Ice Sheet (GrIS) depends on feedbacks between surface meltwater delivery to the subglacial environment and ice flow. Recent work has highlighted an important role of hydrological processes in regulating the ice flow, but models have so far overlooked the mechanical effect of soft basal sediment. Here we use a three-dimensional model to investigate hydrological controls on a GrIS soft-bedded region. Our results demonstrate that weakening and strengthening of subglacial sediment, associated with the seasonal delivery of surface meltwater to the bed, modulates ice flow consistent with observations. We propose that sedimentary control on ice flow is a viable alternative to existing models of evolving hydrological systems, and find a strong link between the annual flow stability, and the frequency of high meltwater discharge events. Consequently, the observed GrIS resilience to enhanced melt could be compromised if runoff variability increases further with future climate warming.RCU

Ice flow dynamics and surface meltwater flux at a land-terminating sector of the Greenland ice sheet

AbstractWe present satellite-derived velocity patterns for the two contrasting melt seasons of 2009–10 across Russell Glacier catchment, a western, land-terminating sector of the Greenland ice sheet which encompasses the K(angerlussuaq)-transect. Results highlight great spatial heterogeneity in flow, indicating that structural controls such as bedrock geometry govern ice discharge into individual outlet troughs. Results also reveal strong seasonal flow variability extending 57 km up-glacier to 1200 m elevation, with the largest acceleration (100% over 11 days) occurring within 10 km of the margin coincident with spring melt. By late July 2010, 2 weeks before peak melt and runoff, 48 % of the 2400 km2 catchment had slowed to less than the winter mean. This observation supports the hypothesis that the subglacial hydrological system evolves from an inefficient distributed to an efficient drainage system, regulating flow dynamics. Despite this, the cumulative surface flux over the record melt year of 2010 was still greater compared with the perturbation over the average melt year of 2009. This study supports the proposition that local surface meltwater runoff couples to basal hydrology driving ice-sheet dynamics, and although the effect is nonlinear, our observations indicate that greater meltwater runoff yields increased net flux over this sector of the ice sheet.</jats:p

Ice tectonic deformation during the rapid in situ drainage of a supraglacial lake on the Greenland Ice Sheet.

We present detailed records of lake discharge, ice motion and passive seismicity capturing the behaviour and processes preceding, during and following the rapid drainage of a 4 km&lt;sup&gt;2&lt;/sup&gt; supraglacial lake through 1.1-km-thick ice on the western margin of the Greenland Ice Sheet. Peak discharge of 3300 m&lt;sup&gt;3&lt;/sup&gt; s&lt;sup&gt;−1&lt;/sup&gt; coincident with maximal rates of vertical uplift indicates that surface water accessed the ice–bed interface causing widespread hydraulic separation and enhanced basal motion. The differential motion of four global positioning system (GPS) receivers located around the lake record the opening and closure of the fractures through which the lake drained. We hypothesise that the majority of discharge occurred through a 3-km-long fracture with a peak width averaged across its wetted length of 0.4 m. We argue that the fracture's kilometre-scale length allowed rapid discharge to be achieved by combining reasonable water velocities with sub-metre fracture widths. These observations add to the currently limited knowledge of in situ supraglacial lake drainage events, which rapidly deliver large volumes of water to the ice–bed interface

Seismic evidence for complex sedimentary control of Greenland Ice Sheet flow

The land-terminating margin of the Greenland Ice Sheet has slowed down in recent decades, although the causes and implications for future ice flow are unclear. Explained originally by a self-regulating mechanism where basal slip reduces as drainage evolves from low to high efficiency, recent numerical modeling invokes a sedimentary control of ice sheet flow as an alternative hypothesis. Although both hypotheses can explain the recent slowdown, their respective forecasts of a long-term deceleration versus an acceleration of ice flow are contradictory. We present amplitude-versus-angle seismic data as the first observational test of the alternative hypothesis. We document transient modifications of basal sediment strengths by rapid subglacial drainages of supraglacial lakes, the primary current control on summer ice sheet flow according to our numerical model. Our observations agree with simulations of initial postdrainage sediment weakening and ice flow accelerations, and subsequent sediment restrengthening and ice flow decelerations, and thus confirm the alternative hypothesis. Although simulated melt season acceleration of ice flow due to weakening of subglacial sediments does not currently outweigh winter slowdown forced by self-regulation, they could dominate over the longer term. Subglacial sediments beneath the Greenland Ice Sheet must therefore be mapped and characterized, and a sedimentary control of ice flow must be evaluated against competing self-regulation mechanismspublishersversionPeer reviewe

Proceedings of Patient Reported Outcome Measure’s (PROMs) Conference Oxford 2017: Advances in Patient Reported Outcomes Research

A33-Effects of Out-of-Pocket (OOP) Payments and Financial Distress on Quality of Life (QoL) of People with Parkinson’s (PwP) and their Carer

Genome-wide meta-analyses reveal novel loci for verbal short-term memory and learning

Understanding the genomic basis of memory processes may help in combating neurodegenerative disorders. Hence, we examined the associations of common genetic variants with verbal short-term memory and verbal learning in adults without dementia or stroke (N = 53,637). We identified novel loci in the intronic region of CDH18, and at 13q21 and 3p21.1, as well as an expected signal in the APOE/APOC1/TOMM40 region. These results replicated in an independent sample. Functional and bioinformatic analyses supported many of these loci and further implicated POC1. We showed that polygenic score for verbal learning associated with brain activation in right parieto-occipital region during working memory task. Finally, we showed genetic correlations of these memory traits with several neurocognitive and health outcomes. Our findings suggest a role of several genomic loci in verbal memory processes.Peer reviewe

Oral Abstracts 7: RA ClinicalO37. Long-Term Outcomes of Early RA Patients Initiated with Adalimumab Plus Methotrexate Compared with Methotrexate Alone Following a Targeted Treatment Approach

Background: This analysis assessed, on a group level, whether there is a long-term advantage for early RA patients treated with adalimumab (ADA) + MTX vs those initially treated with placebo (PBO) + MTX who either responded to therapy or added ADA following inadequate response (IR). Methods: OPTIMA was a 78- week, randomized, controlled trial of ADA + MTX vs PBO + MTX in MTX-naïve early (<1 year) RA patients. Therapy was adjusted at week 26: ADA + MTX-responders (R) who achieved DAS28 (CRP) <3.2 at weeks 22 and 26 (Period 1, P1) were re-randomized to withdraw or continue ADA and PBO + MTX-R continued randomized therapy for 52 weeks (P2); IR-patients received open-label (OL) ADA + MTX during P2. This post hoc analysis evaluated the proportion of patients at week 78 with DAS28 (CRP) <3.2, HAQ-DI <0.5, and/or ΔmTSS ≤0.5 by initial treatment. To account for patients who withdrew ADA during P2, an equivalent proportion of R was imputed from ADA + MTX-R patients. Results: At week 26, significantly more patients had low disease activity, normal function, and/or no radiographic progression with ADA + MTX vs PBO + MTX (Table 1). Differences in clinical and functional outcomes disappeared following additional treatment, when PBO + MTX-IR (n = 348/460) switched to OL ADA + MTX. Addition of OL ADA slowed radiographic progression, but more patients who received ADA + MTX from baseline had no radiographic progression at week 78 than patients who received initial PBO + MTX. Conclusions: Early RA patients treated with PBO + MTX achieved comparable long-term clinical and functional outcomes on a group level as those who began ADA + MTX, but only when therapy was optimized by the addition of ADA in PBO + MTX-IR. Still, ADA + MTX therapy conferred a radiographic benefit although the difference did not appear to translate to an additional functional benefit. Disclosures: P.E., AbbVie, Merck, Pfizer, UCB, Roche, BMS—Provided Expert Advice, Undertaken Trials, AbbVie—AbbVie sponsored the study, contributed to its design, and participated in the collection, analysis, and interpretation of the data, and in the writing, reviewing, and approval of the final version. R.F., AbbVie, Pfizer, Merck, Roche, UCB, Celgene, Amgen, AstraZeneca, BMS, Janssen, Lilly, Novartis—Research Grants, Consultation Fees. S.F., AbbVie—Employee, Stocks. A.K., AbbVie, Amgen, AstraZeneca, BMS, Celgene, Centocor-Janssen, Pfizer, Roche, UCB—Research Grants, Consultation Fees. H.K., AbbVie—Employee, Stocks. S.R., AbbVie—Employee, Stocks. J.S., AbbVie, Amgen, AstraZeneca, BMS, Celgene, Centocor-Janssen, GlaxoSmithKline, Lilly, Pfizer (Wyeth), MSD (Schering-Plough), Novo-Nordisk, Roche, Sandoz, UCB—Research Grants, Consultation Fees. R.V., AbbVie, BMS, GlaxoSmithKline, Human Genome Sciences, Merck, Pfizer, Roche, UCB Pharma—Consultation Fees, Research Support. Table 1.Week 78 clinical, functional, and radiographic outcomes in patients who received continued ADA + MTX vs those who continued PBO + MTX or added open-label ADA following an inadequate response ADA + MTX, n/N (%)a PBO + MTX, n/N (%)b Outcome Week 26 Week 52 Week 78 Week 26 Week 52 Week 78 DAS28 (CRP) <3.2 246/466 (53) 304/465 (65) 303/465 (65) 139/460 (30)*** 284/460 (62) 300/460 (65) HAQ-DI <0.5 211/466 (45) 220/466 (47) 224/466 (48) 150/460 (33)*** 203/460 (44) 208/460 (45) ΔmTSS ≤0.5 402/462 (87) 379/445 (86) 382/443 (86) 330/459 (72)*** 318/440 (72)*** 318/440 (72)*** DAS28 (CRP) <3.2 + ΔmTSS ≤0.5 216/462 (47) 260/443 (59) 266/443 (60) 112/459 (24)*** 196/440 (45) 211/440 (48)*** DAS28 (CRP) <3.2 + HAQ-DI <0.5 + ΔmTSS ≤0.5 146/462 (32) 168/443 (38) 174/443 (39) 82/459 (18)*** 120/440 (27)*** 135/440 (31)** aIncludes patients from the ADA Continuation (n = 105) and OL ADA Carry On (n = 259) arms, as well as the proportional equivalent number of responders from the ADA Withdrawal arm (n = 102). bIncludes patients from the MTX Continuation (n = 112) and Rescue ADA (n = 348) arms. Last observation carried forward: DAS28 (CRP) and HAQ-DI; Multiple imputations: ΔmTSS. ***P < 0.001 and **iP < 0.01, respectively, for differences between initial treatments from chi-squar