Mass Loss of Glaciers and Ice Caps Across Greenland Since the Little Ice Age

Abstract Glaciers and ice caps (GICs) are important contributors of meltwater runoff and to global sea level rise. However, knowledge of GIC mass changes is largely restricted to the last few decades. Here we show the extent of 5327 Greenland GICs during Little Ice Age (LIA) termination (1900) and reveal that they have fragmented into 5467 glaciers in 2001, losing at least 587 km3 from their ablation areas, equating to 499 Gt at a rate of 4.34 Gt yr−1. We estimate that the long-term mean mass balance in glacier ablation areas has been at least −0.18 to −0.22 m w.e. yr−1 and note the rate between 2000 and 2019 has been three times that. Glaciers with ice-marginal lakes formed since the LIA termination have had the fastest changing mass balance. Considerable spatial variability in glacier changes suggest compounding regional and local factors present challenges for understanding glacier evolution. Key Points Total volume loss of at least 587 km3 since the Little Ice Age (LIA) termination, equating to 499 Gt and to 1.38 mm sea level equivalent Glacier mass balance from 2000 to 2019 is three times more negative than since the LIA but five times more negative in the North region Lake-terminating glaciers have experienced the greatest change in rate of mass loss Plain Language Summary Glaciers and ice caps of Greenland peripheral to the ice sheet are important contributors of meltwater to the oceans and to global sea-level rise. In this study we map the extent of 5467 glaciers during the Little Ice Age (LIA) termination c. 1900 and calculate that they have lost at least 587 km3. The rate of mass change of these glaciers between 2000 and 2019 was three times more negative than the long-term average (of 4.34 Gt yr−1) since the LIA. Lake-terminating glaciers now lose mass the fastest compared with land- or marine-terminating glaciers. Considerable spatial variability in glacier responses suggests local factors are important and makes glacier evolution complex

Associations of estimated glomerular filtration rate and albuminuria with mortality and renal failure by sex: a meta-analysis

OBJECTIVE: To assess for the presence of a sex interaction in the associations of estimated glomerular filtration rate and albuminuria with all-cause mortality, cardiovascular mortality, and end stage renal disease.DESIGN: Random effects meta-analysis using pooled individual participant data.SETTING: 46 cohorts from Europe, North and South America, Asia, and Australasia.PARTICIPANTS: 2,051,158 participants (54% women) from general population cohorts (n=1,861,052), high risk cohorts (n=151,494), and chronic kidney disease cohorts (n=38,612). Eligible cohorts (except chronic kidney disease cohorts) had at least 1000 participants, outcomes of either mortality or end stage renal disease of ? 50 events, and baseline measurements of estimated glomerular filtration rate according to the Chronic Kidney Disease Epidemiology Collaboration equation (mL/min/1.73 m(2)) and urinary albumin-creatinine ratio (mg/g).RESULTS: Risks of all-cause mortality and cardiovascular mortality were higher in men at all levels of estimated glomerular filtration rate and albumin-creatinine ratio. While higher risk was associated with lower estimated glomerular filtration rate and higher albumin-creatinine ratio in both sexes, the slope of the risk relationship for all-cause mortality and for cardiovascular mortality were steeper in women than in men. Compared with an estimated glomerular filtration rate of 95, the adjusted hazard ratio for all-cause mortality at estimated glomerular filtration rate 45 was 1.32 (95% CI 1.08 to 1.61) in women and 1.22 (1.00 to 1.48) in men (P(interaction)<0.01). Compared with a urinary albumin-creatinine ratio of 5, the adjusted hazard ratio for all-cause mortality at urinary albumin-creatinine ratio 30 was 1.69 (1.54 to 1.84) in women and 1.43 (1.31 to 1.57) in men (P(interaction)<0.01). Conversely, there was no evidence of a sex difference in associations of estimated glomerular filtration rate and urinary albumin-creatinine ratio with end stage renal disease risk.CONCLUSIONS: Both sexes face increased risk of all-cause mortality, cardiovascular mortality, and end stage renal disease with lower estimated glomerular filtration rates and higher albuminuria. These findings were robust across a large global consortium

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation; analyses timings and patterns of tumour evolution; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity; and evaluates a range of more-specialized features of cancer genomes