Alaska: Glaciers of Kenai Fjords National Park and Katmai National Park and Preserve (Chapter 12)

Much recent research points to the shrinkage of the Earth's small glaciers, however, few studies have been performed to quantify the amount of change over time. We measured glacier-extent changes in two national parks in southeastern Alaska. There are hundreds of glaciers in Kenai Fjords National Park (KEFJ) and Katmai National Park and Preserve (KATM) covering over 2373 sq km of parkland. There are two primary areas of glaciation in KEFJ - the Harding Icefield and the Grewingk-Yalik Glacier Complex, and three primary areas of glaciation in KATM - the Mt. Douglas area, the Kukak Volcano to Mt. Katmai area and the Mt. Martin area. We performed glacier mapping using satellite imagery, from the 1970s, 1980s, and from 2000. Results of the analysis show that there has been a reduction in the amount of glacier ice cover in the two parks over the study period, of approximately 22 sq km of ice, approximately - 1.6% from 1986 to 2000 (for KEFJ), and of approximately 76 sq km of glacier ice, or about -7.7% from 1986187 to 2000 (for KATM). In the future, measurements of surface elevation changes of these ice masses should be acquired; together with our extent-change measurements, the volume change of the ice masses can then be determined to estimate their contribution to sea-level rise. The work is a continuation of work done in KEFJ, but in KATM, our measurements represent the first comprehensive study of the glaciers in this remote, little-studied area

Alaska: Glaciers of Kenai Fjords National Park and Katmai and Lake Clark National Parks and Preserve

There are hundreds of glaciers in Kenai Fjords National Park (KEFJ) and Katmai National Park and Preserve (KATM) covering over 2276 sq km of park land (circa 2000). There are two primary glacierized areas in KEFJ -- the Harding Icefield and the Grewingk-Yalik Glacier Complex, and three primary glacierized areas in KATM - the Mt. Douglas area, the Kukak Volcano to Mt. Katmai area and the Mt. Martin area. Most glaciers in these parks terminate on land, though a few terminate in lakes. Only KEFJ has tidewater glaciers, which terminate in the ocean. Glacier mapping and analysis of the change in glacier extent has been accomplished on a decadal scale using satellite imagery, primarily Landsat data from the 1970s, 1980s, and from 2000. Landsat Multispectral Scanner (MSS), Thematic Mapper (TM) and Enhanced Thematic Mapper Plus (ETM+) imagery was used to map glacier extent on a park-wide basis. Classification of glacier ice using image processing software, along with extensive manual editing, was employed to create Geographic Information System (GIS) outlines of the glacier extent for each park. Many glaciers that originate in KEFJ but terminate outside the park boundaries were also mapped. Results of the analysis show that there has been a reduction in the amount of glacier ice cover in the two parks over the study period. Our measurements show a reduction of approximately 21 sq km, or -1.5% (from 1986 to 2000), and 76 sq km, or -7.7% (from 1986/87 to 2000), in KEFJ and KATM, respectively. This work represents the first comprehensive study of glaciers of KATM. Issues that complicate the mapping of glacier extent include: debris-cover (moraine and volcanic ash), shadows, clouds, fresh snow, lingering snow from the previous season, and differences in spatial resolution between the MSS and TM or ETM+ sensors. Similar glacier mapping efforts in western Canada estimate mapping errors of 3-4%. Measurements were also collected from a suite of glaciers in KEFJ and KATM detailing terminus positions and rates of recession using datasets including the 15-minute USGS quadrangle maps (1950/1951), Landsat imagery (1986/1987, 2000, 2006) and 2005 Ikonos imagery (KEFJ only)

The Randolph Glacier Inventory: a globally complete inventory of glaciers

The Randolph Glacier Inventory (RGI) is a globally complete collection of digital outlines of glaciers, excluding the ice sheets, developed to meet the needs of the Fifth Assessment of the Intergovernmental Panel on Climate Change for estimates of past and future mass balance. The RGI was created with limited resources in a short period. Priority was given to completeness of coverage, but a limited, uniform set of attributes is attached to each of the ∼198 000 glaciers in its latest version, 3.2. Satellite imagery from 1999–2010 provided most of the outlines. Their total extent is estimated as 726 800±34 000 km2. The uncertainty, about ±5%, is derived from careful single-glacier and basin-scale uncertainty estimates and comparisons with inventories that were not sources for the RGI. The main contributors to uncertainty are probably misinterpretation of seasonal snow cover and debris cover. These errors appear not to be normally distributed, and quantifying them reliably is an unsolved problem. Combined with digital elevation models, the RGI glacier outlines yield hypsometries that can be combined with atmospheric data or model outputs for analysis of the impacts of climatic change on glaciers. The RGI has already proved its value in the generation of significantly improved aggregate estimates of glacier mass changes and total volume, and thus actual and potential contributions to sea-level rise

Analysis of heritability and shared heritability based on genome-wide association studies for 13 cancer types

Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl², on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.11 page(s

Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for Thirteen Cancer Types

BACKGROUND: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. METHODS: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. RESULTS: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, hl (2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (ρ = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (ρ = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (ρ = 0.51, SE =0.18), and bladder and lung (ρ = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. CONCLUSION: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation

Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types

Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation