Ice–ocean interaction and calving front morphology at two west Greenland tidewater outlet glaciers

Warm, subtropical-originating Atlantic water (AW) has been identified as a primary driver of mass loss across the marine sectors of the Greenland Ice Sheet (GrIS), yet the specific processes by which this water mass interacts with and erodes the calving front of tidewater glaciers is frequently modelled and much speculated upon but remains largely unobserved. We present a suite of fjord salinity, temperature, turbidity versus depth casts along with glacial runoff estimation from Rink and Store glaciers, two major marine outlets draining the western sector of the GrIS during 2009 and 2010. We characterise the main water bodies present and interpret their interaction with their respective calving fronts. We identify two distinct processes of ice–ocean interaction which have distinct spatial and temporal footprints: (1) homogenous free convective melting which occurs across the calving front where AW is in direct contact with the ice mass, and (2) localised upwelling-driven melt by turbulent subglacial runoff mixing with fjord water which occurs at distinct injection points across the calving front. Throughout the study, AW at 2.8 ± 0.2 °C was consistently observed in contact with both glaciers below 450 m depth, yielding homogenous, free convective submarine melting up to ~200 m depth. Above this bottom layer, multiple interactions are identified, primarily controlled by the rate of subglacial fresh-water discharge which results in localised and discrete upwelling plumes. In the record melt year of 2010, the Store Glacier calving face was dominated by these runoff-driven plumes which led to a highly crenulated frontal geometry characterised by large embayments at the subglacial portals separated by headlands which are dominated by calving. Rink Glacier, which is significantly deeper than Store has a larger proportion of its submerged calving face exposed to AW, which results in a uniform, relatively flat overall frontal geometry

Moderate alcohol consumption lowers the risk of type 2 diabetes: a meta-analysis of prospective observational studies

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Meta-analysis of the relationship between alcohol consumption and coronary heart disease and mortality in type 2 diabetic patients

Aims/hypothesis: This systematic review examines the relationship between alcohol consumption and long-term complications of type 2 diabetes. Meta-analyses could only be performed for total mortality, mortality from CHD, and CHD incidence, because the availability of articles on other complications was too limited. Materials and methods: A PubMed search through to September 2005 was performed and the reference lists of relevant articles examined. Among the relevant articles there were six cohort studies reporting on the risk of total mortality and/or fatal and/or incident CHD in alcohol non-consumers and in at least two groups of alcohol consumers. Results: Statistical pooling showed lower risks in alcohol consumers than in non-consumers (the reference category). The relative risk (RR) of total mortality was 0.64 (95% CI 0.49-0.82) in the <6 g/day category. In the higher alcohol consumption categories (6 to <18, and ≥18 g/day), the RRs of total mortality were not significant. Risks of fatal and total CHD were significantly lower in all three categories of alcohol consumers (<6, 6 to <18 and ≥18 g/day) than in non-consumers, with RRs ranging from 0.34 to 0.75. Conclusions/interpretation: This meta-analysis shows that, as with findings in the general population, moderate alcohol consumption is associated with a lower risk of mortality and CHD in type 2 diabetic populations. © Springer-Verlag 2006.

The effect of moderate alcohol consumption on adiponectin oligomers and muscle oxidative capacity: a human intervention study

Aims/hypothesis The aim of this study was to investigate whether moderate alcohol consumption increases plasma high molecular weight (HMW) adiponectin and/or muscle oxidative capacity. Materials and methods Eleven lean (BMI 18 - 25 kg/m(2)) and eight overweight ( BMI >= 27 kg/m(2)) men consumed 100 ml whisky (similar to 32 g alcohol) or water daily for 4 weeks in a randomised, controlled, crossover trial. After each treatment period, muscle biopsies and fasting blood samples were collected. Results Adiponectin concentrations increased ( p <0.001) by 12.5% after 4 weeks of moderate alcohol consumption. Moderate alcohol consumption tended to increase HMW adiponectin by 57% ( p= 0.07) and medium molecular weight adiponectin by 12.5% ( p= 0.07), but not low molecular weight (LMW) adiponectin. Skeletal muscle citrate synthase, cytochrome c oxidase and beta-3-hydroxyacyl coenzyme A dehydrogenase (beta-HAD) activity were not changed after moderate alcohol consumption, but an interaction between alcohol consumption and BMI was observed for cytochrome c oxidase ( p= 0.072) and citrate synthase ( p= 0.102) activity. Among lean men, moderate alcohol consumption tended to increase cytochrome c oxidase ( p= 0.08) and citrate synthase activity ( p= 0.12) by 23 and 26%, respectively, but not among overweight men. In particular, plasma HMW adiponectin correlated positively with activities of skeletal muscle citrate synthase ( r= 0.64, p= 0.009), cytochrome c oxidase ( p= 0.59, p= 0.009) and beta-HAD ( r= 0.46, p= 0.056), while such correlation was not present for LMW adiponectin. Whole-body insulin sensitivity and intramyocellular triacylglycerol content were not affected by moderate alcohol consumption. Conclusions/interpretation Moderate alcohol consumption increases adiponectin concentrations, and in particular HMW adiponectin. Concentrations of HMW adiponectin in particular were positively associated with skeletal muscle oxidative capacity

Effects of body weight and alcohol consumption on insulin sensitivity

<p>Abstract</p> <p>Background</p> <p>Obesity is a risk factor for the development of insulin resistance, which can eventually lead to type-2 diabetes. Alcohol consumption is a protective factor against insulin resistance, and thus protects against the development of type-2 diabetes. The mechanism by which alcohol protects against the development of type-2 diabetes is not well known. To determine the mechanism by which alcohol improves insulin sensitivity, we fed water or alcohol to lean, control, and obese mice. The aim of this study was to determine whether alcohol consumption and body weights affect overlapping metabolic pathways and to identify specific target genes that are regulated in these pathways.</p> <p>Method</p> <p>Adipose tissue dysfunction has been associated with the development of type-2 diabetes. We assessed possible gene expression alterations in epididymal white adipose tissue (WAT). We obtained WAT from mice fed a calorie restricted (CR), low fat (LF Control) or high fat (HF) diets and either water or 20% ethanol in the drinking water. We screened the expression of genes related to the regulation of energy homeostasis and insulin regulation using a gene array composed of 384 genes.</p> <p>Results</p> <p>Obesity induced insulin resistance and calorie restriction and alcohol improved insulin sensitivity. The insulin resistance in obese mice was associated with the increased expression of inflammatory markers Cd68, Il-6 and Il-1α; in contrast, most of these genes were down-regulated in CR mice. Anti-inflammatory factors such as Il-10 and adrenergic beta receptor kinase 1 (Adrbk1) were decreased in obese mice and increased by CR and alcohol. Also, we report a direct correlation between body weight and the expression of the following genes: Kcnj11 (potassium inwardly-rectifying channel, subfamily J, member 11), Lpin2 (lipin2), and Dusp9 (dual-specificity MAP kinase phosphatase 9).</p> <p>Conclusion</p> <p>We show that alcohol consumption increased insulin sensitivity. Additionally, alterations in insulin sensitivity related with obesity were coupled with alterations in inflammatory genes. We provide evidence that alcohol may improve insulin sensitivity by up-regulating anti-inflammatory genes. Moreover, we have indentified potential gene targets in energy metabolic pathways and signal transducers that may contribute to obesity-related insulin resistance as well as calorie restriction and alcohol-induced insulin sensitivity.</p

A massive rock and ice avalanche caused the 2021 disaster at Chamoli, Indian Himalaya

On 7 Feb 2021, a catastrophic mass flow descended the Ronti Gad, Rishiganga, and Dhauliganga valleys in Chamoli, Uttarakhand, India, causing widespread devastation and severely damaging two hydropower projects. Over 200 people were killed or are missing. Our analysis of satellite imagery, seismic records, numerical model results, and eyewitness videos reveals that ~27x106 m3 of rock and glacier ice collapsed from the steep north face of Ronti Peak. The rock and ice avalanche rapidly transformed into an extraordinarily large and mobile debris flow that transported boulders &gt;20 m in diameter, and scoured the valley walls up to 220 m above the valley floor. The intersection of the hazard cascade with downvalley infrastructure resulted in a disaster, which highlights key questions about adequate monitoring and sustainable development in the Himalaya as well as other remote, high-mountain environments