96 research outputs found
The Impact of Biofuel Mandates and Switchgrass Production on Hay Markets
The Renewable Fuel Standard mandate in the Energy Independence and Security Act of 2007 requires 16 billion gallons out of 36 billion gallons of ethanol be produced from cellulosic feedstocks in 2022, but the mandate was apparently enacted without critical assessments of the agricultural impacts of attempting to achieve energy independence. The feedstock production will likely compete with lands currently used for producing other traditional crops of which hay is likely to be affected the most since it has comparatively lower net returns. Thus ruminant production will consequently be affected greatly. This study uses ordinary least squares (OLS) to estimate and predict Oklahoma hay price which is used as objective value in linear programming (LP) model that determines the profitability options between hay and switchgrass production. The OLS results show that Oklahoma hay price is fairly stable, and hay is shipped across adjoining states. The LP results show that switchgrass production would be more profitable than hay and that switchgrass for biofuel production likely will bid land away from hay if biofuel production becomes fully operational.biofuel mandates, switchgrass production, hay production, hay markets., Agricultural and Food Policy, Environmental Economics and Policy, Production Economics, Research and Development/Tech Change/Emerging Technologies, Resource /Energy Economics and Policy,
Impact of United States Corn-Based Ethanol Production on Land Use
This study measures the impact of corn-based ethanol production in the United States on land use in other countries, or indirect land use. Indirect land use is a change from non-cropland to cropland (e.g. deforestation) that may occur in response to increasing scarcity of cropland. As farmers worldwide respond to higher crop prices in order to maintain the global food supply and demand balance, pristine lands are cleared and converted to new cropland to replace the crops for feed and food that were diverted elsewhere to biofuel production. The results show that increasing ethanol production in the US has a positive and significant relation to U.S corn price. However, U.S. corn price does not have a significant impact on changes in corn acreage in Brazil and other countries such as Canada, Japan and China. Although many authors have hypothesized that increased ethanol production in the U.S. will increase corn prices, which will result in increased change in land use in other countries, these results suggest that the effect is minimal at best. This is important because although production of ethanol for fuel is often criticized for negatively impacting the environment because of indirect land use, this study was unable to prove the existence of indirect land use.ethanol, indirect land use, Agricultural and Food Policy, Demand and Price Analysis, Land Economics/Use, Marketing,
Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.
GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the 'iCOGS' genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against >100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84-0.87; P=1.7 × 10(-43)) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology
Breast cancer risk variants at 6q25 display different phenotype associations and regulate ESR1, RMND1 and CCDC170.
We analyzed 3,872 common genetic variants across the ESR1 locus (encoding estrogen receptor α) in 118,816 subjects from three international consortia. We found evidence for at least five independent causal variants, each associated with different phenotype sets, including estrogen receptor (ER(+) or ER(-)) and human ERBB2 (HER2(+) or HER2(-)) tumor subtypes, mammographic density and tumor grade. The best candidate causal variants for ER(-) tumors lie in four separate enhancer elements, and their risk alleles reduce expression of ESR1, RMND1 and CCDC170, whereas the risk alleles of the strongest candidates for the remaining independent causal variant disrupt a silencer element and putatively increase ESR1 and RMND1 expression.This is the author accepted manuscript. The final version is available from Nature Publishing Group via http://dx.doi.org/10.1038/ng.352
Book Reviews
Eliot Wigginton. Sometimes a Shining Moment: The Foxfire Experience-- Twenty Years in a High School Classroom. Garden City, New York: Anchor Press/ Doubleday, 1985. Pp. xiv, 438. Cloth, 8.95. Review by Jayme A. Sokolow of the National Endowment for the Humanities.
Lois W. Banner. American Beauty. Chicago and London: University of Chicago Press, 1983. Pp. ix, 369. Paper, 25.00. Review by Raymond C. Bailey of Northern Virginia Community College.
Clarence L. Mohr. On the Threshold of Freedom: Masters and Slaves in Civil War Georgia. Athens and London: The University of Georgia Press, 1986. Pp. xxi, 397. Cloth, 15.95. Review by Darlene E. Fisher of New Trier Township High School, Winnetka, Il.
Barry D. Karl. The Uneasy State: The United States from 1915 to 1945. Chicago and London: University of Chicago Press, 1983. Pp. x, 257. Paper, 11.95. Review by David L. Nass of Southwest State University, Mn.
Michael P. Sullivan. The Vietnam War: A Study in the Making of American Policy. Lexington: The University Press of Kentucky, 1985. Pp. 198. Cloth, 27.50; Paper, 49.50; Paper, 16.95. Review by Calvin H. Allen, Jr of The School of the Ozarks.
Henry C. Boren. The Ancient World: An Historical Perspective. Englewood Cliffs, New Jersey: Prentice-Hall, Inc., 1986. Pp. xx, 407. Paper, 35.00; Paper, 22.95. Review by Linda Frey of the University of Montana.
Jonathan Powis. Aristocracy. New York: Basil Blackwell, 1984. Pp. ix, 110. Cloth, 8.95. Review by Robert W. Brown of Pembroke State University.
A. J. Youngson. The Prince and the Pretender: A Study in the Writing of History. Dover, New Hampshire: Croom Helm, Ltd., 1985. Pp. 270. Cloth, $29.00. Review Michael J. Salevouris of Webster University
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Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.
GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the 'iCOGS' genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against >100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84-0.87; P=1.7 × 10(-43)) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology
Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans
Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio
PALB2, CHEK2 and ATM rare variants and cancer risk : data from COGS
AbstractBackground: The rarity of mutations in PALB2, CHEK2 and ATM make it difficult to estimate precisely associated cancer risks. Population-based family studies have provided evidence that at least some of these mutations are associated with breast cancer risk as high as those associated with rare BRCA2 mutations. We aimed to estimate the relative risks associated with specific rare variants in PALB2, CHEK2 and ATM via a multicentre case-control study.Methods: We genotyped 10 rare mutations using the custom iCOGS array: PALB2 c.1592delT, c.2816T>G and c.3113G>A, CHEK2 c.349A>G, c.538C>T, c.715G>A, c.1036C>T, c.1312G>T, and c.1343T>G and ATM c.7271T>G. We assessed associations with breast cancer risk (42 671 cases and 42 164 controls), as well as prostate (22 301 cases and 22 320 controls) and ovarian (14 542 cases and 23 491 controls) cancer risk, for each variant.Results: For European women, strong evidence of association with breast cancer risk was observed for PALB2 c.1592delT OR 3.44 (95% CI 1.39 to 8.52, p = 7.1 × 10⁻⁵), PALB2 c.3113G>A OR 4.21 (95% CI 1.84 to 9.60, p = 6.9 × 10⁻⁸) and ATM c.7271T>G OR 11.0 (95% CI 1.42 to 85.7, p = 0.0012). We also found evidence of association with breast cancer risk for three variants in CHEK2, c.349A>G OR 2.26 (95% CI 1.29 to 3.95), c.1036C>T OR 5.06 (95% CI 1.09 to 23.5) and c.538C>T OR 1.33 (95% CI 1.05 to 1.67) (p ≤ 0.017). Evidence for prostate cancer risk was observed for CHEK2 c.1343T>G OR 3.03 (95% CI 1.53 to 6.03, p = 0.0006) for African men and CHEK2 c.1312G>T OR 2.21 (95% CI 1.06 to 4.63, p = 0.030) for European men. No evidence of association with ovarian cancer was found for any of these variants.Conclusions: This report adds to accumulating evidence that at least some variants in these genes are associated with an increased risk of breast cancer that is clinically important.Abstract
Background: The rarity of mutations in PALB2, CHEK2 and ATM make it difficult to estimate precisely associated cancer risks. Population-based family studies have provided evidence that at least some of these mutations are associated with breast cancer risk as high as those associated with rare BRCA2 mutations. We aimed to estimate the relative risks associated with specific rare variants in PALB2, CHEK2 and ATM via a multicentre case-control study.
Methods: We genotyped 10 rare mutations using the custom iCOGS array: PALB2 c.1592delT, c.2816T>G and c.3113G>A, CHEK2 c.349A>G, c.538C>T, c.715G>A, c.1036C>T, c.1312G>T, and c.1343T>G and ATM c.7271T>G. We assessed associations with breast cancer risk (42 671 cases and 42 164 controls), as well as prostate (22 301 cases and 22 320 controls) and ovarian (14 542 cases and 23 491 controls) cancer risk, for each variant.
Results: For European women, strong evidence of association with breast cancer risk was observed for PALB2 c.1592delT OR 3.44 (95% CI 1.39 to 8.52, p = 7.1 × 10⁻⁵), PALB2 c.3113G>A OR 4.21 (95% CI 1.84 to 9.60, p = 6.9 × 10⁻⁸) and ATM c.7271T>G OR 11.0 (95% CI 1.42 to 85.7, p = 0.0012). We also found evidence of association with breast cancer risk for three variants in CHEK2, c.349A>G OR 2.26 (95% CI 1.29 to 3.95), c.1036C>T OR 5.06 (95% CI 1.09 to 23.5) and c.538C>T OR 1.33 (95% CI 1.05 to 1.67) (p ≤ 0.017). Evidence for prostate cancer risk was observed for CHEK2 c.1343T>G OR 3.03 (95% CI 1.53 to 6.03, p = 0.0006) for African men and CHEK2 c.1312G>T OR 2.21 (95% CI 1.06 to 4.63, p = 0.030) for European men. No evidence of association with ovarian cancer was found for any of these variants.
Conclusions: This report adds to accumulating evidence that at least some variants in these genes are associated with an increased risk of breast cancer that is clinically important
Publisher Correction: Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.
This corrects the article DOI: 10.1038/ncomms5999
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