Measurements of Ice Shelf Water beneath the front of the Ross Ice Shelf using gliders

Measurements made by an underwater glider deployed near the Ross Ice Shelf were used to identify the presence of Ice Shelf Water (ISW), which is defined as seawater with its potential temperature lower than its surface freezing point temperature. Properties logged by the glider included in situ temperature, electrical conductivity, pressure, GPS location at surfacings and time. For most of the first 30 recorded dives of its deployment, evidence suggests the glider was prevented from surfacing due to being under the ice shelf. For dives under the ice shelf, farthest from the ice shelf front, ISW layers of varying thicknesses and depth locations were observed; between 2 m thick (centred at 231 m depth) to >93 m thick (centred at >360 m). For dives under the ice shelf, close to the ice shelf front, either no ISW was observed or ISW layers were centred at shallower depths (116–127 m). Thicker ISW layers (e.g. up to 250 m thickness centred at 421 m) were observed for some glider dives in open water in front of the Ross Ice Shelf. No in situ supercooling (water colder than the pressure-dependent freezing point temperature) was observed

Between the devil and the deep blue sea:the role of the Amundsen Sea continental shelf in exchanges between ocean and ice shelves

The Amundsen Sea is a key region of Antarctica where ocean, atmosphere, sea ice and ice sheet interact. For much of Antarctica, the relatively warm ocean water in the open Southern Ocean (a few degrees above freezing) is unable to reach the continental shelf in large volumes under current climate conditions. In the Amundsen Sea, however, warm water penetrates onto the continental shelf and provides heat that can melt the underside of the floating ice shelves. Here we discuss how the role of the ocean has come under increased scrutiny in recent years, because ocean heat fluxes have been implicated in the thinning of the ice shelves. We present observations from the Amundsen Sea in 2014 and discuss their implications, highlighting aspects where our understanding is still incomplete

A genome-wide cross-phenotype meta-analysis of the association of blood pressure with migraine

Blood pressure (BP) was inconsistently associated with migraine and the mechanisms of BP-lowering medications in migraine prophylaxis are unknown. Leveraging large-scale summary statistics for migraine (Ncases/Ncontrols = 59,674/316,078) and BP (N = 757,601), we find positive genetic correlations of migraine with diastolic BP (DBP, rg = 0.11, P = 3.56 × 10−06) and systolic BP (SBP, rg = 0.06, P = 0.01), but not pulse pressure (PP, rg = −0.01, P = 0.75). Cross-trait meta-analysis reveals 14 shared loci (P ≤ 5 × 10−08), nine of which replicate (P < 0.05) in the UK Biobank. Five shared loci (ITGB5, SMG6, ADRA2B, ANKDD1B, and KIAA0040) are reinforced in gene-level analysis and highlight potential mechanisms involving vascular development, endothelial function and calcium homeostasis. Mendelian randomization reveals stronger instrumental estimates of DBP (OR [95% CI] = 1.20 [1.15–1.25]/10 mmHg; P = 5.57 × 10−25) on migraine than SBP (1.05 [1.03–1.07]/10 mmHg; P = 2.60 × 10−07) and a corresponding opposite effect for PP (0.92 [0.88–0.95]/10 mmHg; P = 3.65 × 10−07). These findings support a critical role of DBP in migraine susceptibility and shared biology underlying BP and migraine

Cerebral small vessel disease genomics and its implications across the lifespan

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. Here, we identify 27 genome-wide loci for WMH-volume in a cohort of 50,970 older individuals, accounting for modification/confounding by hypertension. Aggregated WMH risk variants were associated with altered white matter integrity (p = 2.5×10-7) in brain images from 1,738 young healthy adults, providing insight into the lifetime impact of SVD genetic risk. Mendelian randomization suggested causal association of increasing WMH-volume with stroke, Alzheimer-type dementia, and of increasing blood pressure (BP) with larger WMH-volume, notably also in persons without clinical hypertension. Transcriptome-wide colocalization analyses showed association of WMH-volume with expression of 39 genes, of which four encode known drug targets. Finally, we provide insight into BP-independent biological pathways underlying SVD and suggest potential for genetic stratification of high-risk individuals and for genetically-informed prioritization of drug targets for prevention trials

Prediction of disability-free survival in healthy older people

AbstractProlonging survival in good health is a fundamental societal goal. However, the leading determinants of disability-free survival in healthy older people have not been well established. Data from ASPREE, a bi-national placebo-controlled trial of aspirin with 4.7 years median follow-up, was analysed. At enrolment, participants were healthy and without prior cardiovascular events, dementia or persistent physical disability. Disability-free survival outcome was defined as absence of dementia, persistent disability or death. Selection of potential predictors from amongst 25 biomedical, psychosocial and lifestyle variables including recognized geriatric risk factors, utilizing a machine-learning approach. Separate models were developed for men and women. The selected predictors were evaluated in a multivariable Cox proportional hazards model and validated internally by bootstrapping. We included 19,114 Australian and US participants aged ≥65 years (median 74 years, IQR 71.6–77.7). Common predictors of a worse prognosis in both sexes included higher age, lower Modified Mini-Mental State Examination score, lower gait speed, lower grip strength and abnormal (low or elevated) body mass index. Additional risk factors for men included current smoking, and abnormal eGFR. In women, diabetes and depression were additional predictors. The biased-corrected areas under the receiver operating characteristic curves for the final prognostic models at 5 years were 0.72 for men and 0.75 for women. Final models showed good calibration between the observed and predicted risks. We developed a prediction model in which age, cognitive function and gait speed were the strongest predictors of disability-free survival in healthy older people.Trial registrationClinicaltrials.gov (NCT01038583)</jats:p