A reconstruction of warm-water inflow to Upernavik Isstrøm since 1925 CE and its relation to glacier retreat

International audienceThe mass loss from the Greenland Ice Sheet has increased over the past 2 decades. Marine-terminating glaciers contribute significantly to this mass loss due to increased melting and ice discharge. Periods of rapid retreat of these tidewater glaciers have been linked to the concurrent inflow of warm Atlantic-sourced waters. However, little is known about the variability of these Atlantic-derived waters within the fjords, due to a lack of multi-annual in situ measurements. Thus, to better understand the potential role of ocean warming on glacier retreat, reconstructions that characterize the variability of Atlantic water inflow to the fjords are required. Here, we investigate foraminiferal assemblages in a sediment core from Upernavik Fjord, West Greenland, in which the major ice stream Upernavik Isstrøm terminates. We conclude that the foraminiferal assemblage is predominantly controlled by changes in bottom water composition and provide a reconstruction of Atlantic water inflow to Upernavik Fjord, spanning the period 1925–2012. This reconstruction reveals peak Atlantic water influx during the 1930s and again after 2000, a pattern that is comparable to the Atlantic Multidecadal Oscillation (AMO). The comparison of these results to historical observations of front positions of Upernavik Isstrøm reveals that inflow of warm Atlantic-derived waters likely contributed to high retreat rates in the 1930s and after 2000. However, moderate retreat rates of Upernavik Isstrøm also prevailed in the 1960s and 1970s, showing that glacier retreat continued despite a reduced Atlantic water inflow, albeit at a lower rate. Considering the link between bottom water variability and the AMO in Upernavik Fjord, and the fact that a persistent negative phase of the AMO is expected for the next decade, Atlantic water inflow into the fjord may decrease in the coming decade, potentially minimizing or stabilizing the retreat of Upernavik Isstrøm during this time interval.climate chang

Non-Replication of Genome-Wide Based Associations between Common Variants in INSIG2 and PFKP and Obesity in Studies of 18,014 Danes

(rs17782313) as genetic risk factors. = 2,158) from Steno Diabetes Center. rs17782313 were observed. rs7566605 may influence the level of BMI in combination with the level of physical activity

Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge

Glucose levels 2 h after an oral glucose challenge are a clinical measure of glucose tolerance used in the diagnosis of type 2 diabetes. We report a meta-analysis of nine genome-wide association studies (n = 15,234 nondiabetic individuals) and a follow-up of 29 independent loci (n = 6,958–30,620). We identify variants at the GIPR locus associated with 2-h glucose level (rs10423928, β (s.e.m.) = 0.09 (0.01) mmol/l per A allele, P = 2.0 × 10−15). The GIPR A-allele carriers also showed decreased insulin secretion (n = 22,492; insulinogenic index, P = 1.0 × 10−17; ratio of insulin to glucose area under the curve, P = 1.3 × 10−16) and diminished incretin effect (n = 804; P = 4.3 × 10−4). We also identified variants at ADCY5 (rs2877716, P = 4.2 × 10−16), VPS13C (rs17271305, P = 4.1 × 10−8), GCKR (rs1260326, P = 7.1 × 10−11) and TCF7L2 (rs7903146, P = 4.2 × 10−10) associated with 2-h glucose. Of the three newly implicated loci (GIPR, ADCY5 and VPS13C), only ADCY5 was found to be associated with type 2 diabetes in collaborating studies (n = 35,869 cases, 89,798 controls, OR = 1.12, 95% CI 1.09–1.15, P = 4.8 × 10−18)

Studies of the common DIO2 Thr92Ala polymorphism and metabolic phenotypes in 7342 Danish white subjects

International audienceCONTEXT: The type 2 iodothyronine deiodinase (D2) catalyzes the conversion of T(4) to the active form of thyroid hormone, which is a critical regulator of thermogenesis and glucose metabolism. A Thr92Ala polymorphism in the gene encoding D2 (DIO2) has been reported to associate with insulin resistance. OBJECTIVE: The aim of the present study was to assess the impact of the DIO2 Thr92Ala variant on type 2 diabetes (T2D), obesity, and related quantitative metabolic traits including measures of insulin resistance. Because DIO2 is activated through a beta-adrenergic receptor-dependent pathway, we further hypothesized that variation in the ADRB genes interacts with DIO2 Thr92Ala variant to influence metabolic traits. DESIGN AND PATIENTS: The DIO2 polymorphism was genotyped in a total of 7342 white subjects including 1405 T2D patients. RESULTS: We detected no significant association of the DIO2 Thr92Ala polymorphism with T2D or obesity. We observed nominal significant associations of genotype with increased area under the serum insulin curve during an oral glucose tolerance test (P = 0.03) and elevated fasting plasma glucose (P = 0.02) in homozygous Ala92 allele carriers, the latter strengthened by epistasis with the ADRB2 Gly16Arg variant in a double recessive model (P = 0.004). However, after permutation procedure, performed to correct for multiple hypothesis testing, the associations did not reach study-wide significance. CONCLUSIONS: The DIO2 Thr92Ala variant does not confer an increased risk of T2D, obesity, or insulin resistance

Limited Colocalization of Microbleeds and Microstructural Changes after Severe Traumatic Brain Injury

Severe traumatic brain injury (TBI) produces shearing forces on long-range axons and brain vessels, causing axonal and vascular injury. To examine whether microbleeds and axonal injury co-localize after TBI, we performed whole-brain susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI) in 14 patients during the subacute phase after severe TBI. SWI was used to determine the number and volumes of microbleeds in five brain regions: the fronto-temporal lobe, parieto-occipital lobe, mid-sagittal region (cingular cortex, parasagittal white matter and corpus callosum), deep nuclei (basal ganglia and thalamus), and brainstem. Averaged fractional anisotropy (FA) and mean diffusivity (MD) were measured to assess microstructural changes in the normal appearing white matter due to axonal injury in the same five regions. Regional expressions of microbleeds and microstructure was used in a partial least squares model to predict the impairment of consciousness in the subacute stage after TBI as measured with the Coma Recovery Scale-Revised (CRS-R). Only in the midsagittal region, expression of microbleeds correlated with regional changes in microstructure as revealed by DTI. Microbleeds and microstructural DTI-based metrics of deep but not superficial brain regions were able to predict individual CRS-R. Our results suggest that microbleeds are not strictly related to axonal pathology in other that the midsagittal region. While each measure alone was predictive, the combination of both metrics scaled best with individual CRS-R. Structural alterations in deep brain structures are relevant in terms of determining the severity of impaired consciousness in the acute stage after TBI