bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cambrian successions of the Meguma Terrane, Nova Scotia, and Harlech Dome, North Wales: dispersed fragments of a peri-Gondwanan basin?
Authors: Waldron John W.F. , Schofield David I. , White Chris E. , Barr Sandra M. 
Published: January 2011

Abstract:

The Meguma Terrane of Nova Scotia and the Harlech Dome of North Wales preserve similar sedimentary successions of Cambrian age. Both successions comprise a thick succession of early Cambrian sandstone turbidites, overlain by early to middle Cambrian alternating mud-rich and sand-rich units in which manganese is concentrated in two stratigraphic intervals. Above these, both successions comprise anoxic, organic-rich turbidites, shallowing upward into paler, more bioturbated Tremadocian mudstone with
Rhabdinopora
. Within the limited constraints of the available biostratigraphic and geochronological data, major changes in environment occurred synchronously in the two successions. Both successions show much greater similarity to each other than to adjacent successions on ‘Avalonia'. A detrital zircon analysis from the Rhinog Formation, low in the Harlech Dome succession, reveals distinct clusters of ages around 537 Ma and 2.0–2.1 Ga. A close similarity to analyses from the Meguma Terrane suggests proximity between the two terranes on the margin of Gondwana during the Cambrian Period. We suggest the term Megumia for the palaeogeographical domain that included the two successions, which was dispersed during subsequent Appalachian and Caledonian movements. These observations suggest that Megumia may have separated terranes previously regarded as parts of Avalonia.

Supplementary material:

U/Pb detrital zircon analytical data are available at
http://www.geolsoc.org.uk/SUP18431
.
Seismic interpretation of the Laga basin; constraints on the structural setting and kinematics of the Central Apennines
Authors: Bigi S. , Casero P. , Ciotoli G. 
Published: January 2011

Abstract:
The Messinian Laga basin is the largest foreland basin within the Central Apennines fold and thrust belt (Italy). This area, actively investigated in the 1980s and 1990s for hydrocarbon resources, is considered a valuable analogue for clastic reservoirs developed in confined structural settings. Furthermore, it represents a key area for understanding the evolution of the Apennines, as it links the internal, structurally uplifted Early Miocene fold and thrust belt of the western Central Apennines with the more external and recent belt to the east. Despite several papers published on this area, the only reconstruction of the substratum structure is an internal and classified industry report. During the present study, we had access to a seismic database comprising 200 km of seismic profiles that were collected between 1983 and 1990. These data allowed us to reconstruct the structural setting of the Laga basin substratum, define the lateral continuity of the main compressional structures within the basin, construct a balanced cross-section, and define the shortening values.
Design and public policy considerations for accessible e-book readers
Authors: Danielsen Chris , Taylor Anne , Majerus Wesley 
Published: January 2011

Public policy increasingly plays a role in influencing the work that we do as HCI researchers, interaction designers, and practitioners. "Public policy" is a broad term that includes both government policy and policy within non-governmental organizations, such as standards bodies. The "Interacting with Public Policy" forum focuses on topics at the intersection of human-computer interaction and public policy.

Jonathan Lazar, Editor | JLazar@towson.edu
Genome-Based Prediction of Breast Cancer Risk in the General Population: A Modeling Study Based on Meta-Analyses of Genetic Associations
Authors: van Zitteren Moniek , van der Net Jeroen B. , Kundu Suman , Freedman Andrew N. , van Duijn Cornelia M. , Janssens A. Cecile J.W. 
Published: January 2011

AbstractBackground: Genome-wide association studies identified novel breast cancer susceptibility variants that could be used to predict breast cancer in asymptomatic women. This review and modeling study aimed to investigate the current and potential predictive performance of genetic risk models.Methods: Genotypes and disease status were simulated for a population of 10,000 women. Genetic risk models were constructed from polymorphisms from meta-analysis including, in separate scenarios, all polymorphisms or statistically significant polymorphisms only. We additionally investigated the magnitude of the odds ratios (OR) for 1 to 100 hypothetical polymorphisms that would be needed to achieve similar discriminative accuracy as available prediction models [modeled range of area under the receiver operating characteristic curve (AUC) 0.70–0.80].Results: Of the 96 polymorphisms that had been investigated in meta-analyses, 41 showed significant associations. AUC was 0.68 for the genetic risk model based on all 96 polymorphisms and 0.67 for the 41 significant polymorphisms. Addition of 50 additional variants, each with risk allele frequencies of 0.30, requires per-allele ORs of 1.2 to increase this AUC to 0.70, 1.3 to increase AUC to 0.75, and 1.5 to increase AUC to 0.80. To achieve AUC of 0.80, even 100 additional variants would need per-allele ORs of 1.3 to 1.7, depending on risk allele frequencies.Conclusion: The predictive ability of genetic risk models in breast cancer has the potential to become comparable to that of current breast cancer risk models.Impact: Risk prediction based on low susceptibility variants becomes a realistic tool in prevention of nonfamilial breast cancer. Cancer Epidemiol Biomarkers Prev; 20(1); 9–22. ©2011 AACR.
Effect of Oral Snus and Medicinal Nicotine in Smokers on Toxicant Exposure and Withdrawal Symptoms: A Feasibility Study
Authors: Kotlyar Michael , Hertsgaard Louise A. , Lindgren Bruce R. , Jensen Joni A. , Carmella Steven G. , Stepanov Irina , Murphy Sharon E. , Hecht Stephen S. , Hatsukami Dorothy K. 
Published: January 2011

Abstract
Background: Smokeless, spitless tobacco products are being introduced and marketed as cigarette substitutes. Data are needed regarding how smokers interested in cessation would use these products, the levels of resultant toxicant exposure, and the feasibility of using these products as aids for tobacco cessation.
Methods: Smokers were randomized to receive Camel Snus (n = 51), Taboka (n = 52), or medicinal nicotine (n = 27) and required to quit smoking for 4 weeks. Measures of toxicant exposure and symptoms of craving and withdrawal were assessed prior to and during product use.
Results: Concentrations of exhaled carbon monoxide, urinary cotinine, urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and urinary N′-nitrosonornicotine and its glucuronide (total NNN) were significantly (P values &lt;0.05) lower at the end of treatment in each group except for total NNN in those receiving Camel Snus (P = 0.066). A significant group × time effect was observed for total NNAL concentrations (P = 0.002) with the decrease greatest in the medicinal nicotine group and smallest decrease in the Camel Snus group. No significant differences between groups were found in craving and withdrawal symptoms.
Conclusions: Enrolling smokers into a cessation study utilizing newer smokeless tobacco products is feasible. Camel Snus and Taboka use was not found to be superior to medicinal nicotine in reducing withdrawal symptoms but decreases in NNAL were smaller in users of Camel Snus.
Impact: This study demonstrates the feasibility of conducting a smoking cessation study utilizing these newer tobacco products. An appropriately powered study is needed to assess smoking cessation rates using these newer products compared with established, safer products such as medicinal nicotine. Cancer Epidemiol Biomarkers Prev; 20(1); 91–100. ©2011 AACR.
Reduced Plasma Level of CXC Chemokine Ligand 7 in Patients with Pancreatic Cancer
Authors: Matsubara Junichi , Honda Kazufumi , Ono Masaya , Tanaka Yoshinori , Kobayashi Michimoto , Jung Giman , Yanagisawa Koji , Sakuma Tomohiro , Nakamori Shoji , Sata Naohiro , Nagai Hideo , Ioka Tatsuya , Okusaka Takuji , Kosuge Tomoo , Tsuchida Akihiko , Shimahara Masashi , Yasunami Yohichi , Chiba Tsutomu , Hirohashi Setsuo , Yamada Tesshi 
Published: January 2011

Abstract
Background: Early detection is essential to improve the outcome of patients with pancreatic cancer. A noninvasive and cost-effective diagnostic test using plasma/serum biomarkers would facilitate the detection of pancreatic cancer at the early stage.
Methods: Using a novel combination of hollow fiber membrane–based low-molecular-weight protein enrichment and LC-MS-based quantitative shotgun proteomics, we compared the plasma proteome between 24 patients with pancreatic cancer and 21 healthy controls (training cohort). An identified biomarker candidate was then subjected to a large blinded independent validation (n = 237, validation cohort) using a high-density reverse-phase protein microarray.
Results: Among a total of 53,009 MS peaks, we identified a peptide derived from CXC chemokine ligand 7 (CXCL7) that was significantly reduced in pancreatic cancer patients, showing an area under curve (AUC) value of 0.84 and a P value of 0.00005 (Mann–Whitney U test). Reduction of the CXCL7 protein was consistently observed in pancreatic cancer patients including those with stage I and II disease in the validation cohort (P &lt; 0.0001). The plasma level of CXCL7 was independent from that of CA19-9 (Pearson's r = 0.289), and combination with CXCL7 significantly improved the AUC value of CA19-9 to 0.961 (P = 0.002).
Conclusions: We identified a significant decrease of the plasma CXCL7 level in patients with pancreatic cancer, and combination of CA19-9 with CXCL7 improved the discriminatory power of the former for pancreatic cancer.
Impact: The present findings may provide a new diagnostic option for pancreatic cancer and facilitate early detection of the disease. Cancer Epidemiol Biomarkers Prev; 20(1); 160–71. ©2011 AACR.
Variations in Chromosomes 9 and 6p21.3 with Risk of Non–Hodgkin Lymphoma
Authors: Wang Sophia S. , Menashe Idan , Cerhan James R. , Cozen Wendy , Severson Richard K. , Davis Scott , Hutchinson Amy , Rothman Nathaniel , Chanock Stephen J. , Bernstein Leslie , Hartge Patricia , Morton Lindsay M. 
Published: January 2011

AbstractBackground: There is growing evidence linking genetic variations to non–Hodgkin lymphoma (NHL) etiology. To complement ongoing agnostic approaches for identifying susceptibility genes, we evaluated 488 candidate gene regions and their relation to risk for NHL and NHL subtypes.Methods: We genotyped 6,679 tag single nucleotide polymorphisms (SNPs) in 947 cases and 826 population-based controls from a multicenter U.S. case–control study. Gene-level summary of associations were obtained by computing the minimum P value (“minP test”) on the basis of 10,000 permutations. We used logistic regression to evaluate the association between genotypes and haplotypes with NHL. For NHL subtypes, we conducted polytomous multivariate unconditional logistic regression (adjusted for sex, race, age). We calculated P-trends under the codominant model for each SNP.Results: Fourteen gene regions were associated with NHL (P &lt; 0.01). The most significant SNP associated with NHL maps to the SYK gene (rs2991216, P-trend = 0.00005). The three most significant gene regions were on chromosome 6p21.3 (RING1/RXRB; AIF1; BAT4). Accordingly, SNPs in RING1/RXRB (rs2855429), AIF1 (rs2857597), and BAT4 (rs3115667) were associated with NHL (P-trends ≤ 0.0002) and both diffuse large B-cell and follicular lymphomas (P-trends &lt; 0.05).Conclusions: Our results suggest potential importance for SYK on chromosome 9 with NHL etiology. Our results further implicate 6p21.3 gene variants, supporting the need for full characterization of this chromosomal region in relation to lymphomagenesis.Impact: Gene variants on chromosome 9 may represent a new region of interesting for NHL etiology. The independence of the reported variants in 6p21.3 from implicated variants (TNF/HLA) supports the need to confirm causal variants in this region Cancer Epidemiol Biomarkers Prev; 20(1); 42–9. ©2011 AACR.
The Epidemiology of Oral HPV Infection among a Multinational Sample of Healthy Men
Authors: Kreimer Aimee R. , Villa Alessandro , Nyitray Alan G. , Abrahamsen Martha , Papenfuss Mary , Smith Danelle , Hildesheim Allan , Villa Luisa L. , Lazcano-Ponce Eduardo , Giuliano Anna R. 
Published: January 2011

Abstract
Background: Oral human papillomavirus type-16 (HPV16) infection is a risk factor for oropharyngeal cancer. We examined oral HPV infection among healthy men.
Methods: Oral rinse/gargle specimens and questionnaire data were collected from 1,688 healthy men aged 18 to 74 (median = 31 years), from the United States, Mexico, and Brazil. HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59, and noncarcinogenic HPV types were detected using Roche Linear Array.
Results: Oral HPV DNA was detected in 67 of 1,680 (4.0%, 95% CI = 3.1%–5.0%) β-globin–positive specimens; carcinogenic HPVs were detected in 1.3% (95% CI = 0.8%–2.0%; n = 22) and HPV16 was the most commonly detected carcinogenic HPV type (0.6%, 95% CI = 0.2%–1.1%; n = 10). The prevalence of oral HPV infection was similar by country except for HPV55, which had notably higher prevalence in Mexico (3.0%) than Brazil (0%) or the United States (0.2%). Oral HPV prevalence nonsignificantly increased over increasing age categories (Ptrend = 0.096). The strongest predictor of oral HPV was current tobacco use, which increased the odds 2.5-fold (95% CI = 1.4–4.4). Oral sexual behaviors were not associated with oral HPV infection.
Conclusions: Oral HPV16 infection was rare in healthy men, especially at younger ages, and was positively associated with current tobacco use.
Impact: Oral HPV appears to be about 10-fold less prevalent than infection at genital sites in men (4% vs. ∼40%, respectively). It remains unclear whether this reflects reduced exposure or if the oral region is more resistant to HPV infection compared with anogenital sites. Cancer Epidemiol Biomarkers Prev; 20(1); 172–82. ©2011 AACR.
Risk of Cervical Cancer Associated with Allergies and Polymorphisms in Genes in the Chromosome 5 Cytokine Cluster
Authors: Johnson Lisa G. , Schwartz Stephen M. , Malkki Mari , Du Qin , Petersdorf Effie W. , Galloway Denise A. , Madeleine Margaret M. 
Published: January 2011

Abstract
Background: Human papillomavirus is the acknowledged cause of cervical cancer. We hypothesized that allergies, characterized by hyperimmune reaction to common allergens and which have been associated with various cancers, may be related to cervical cancer, and that genetic variation in cytokine genes related to allergies might impact cervical cancer risk.
Methods: We investigated the risk of invasive squamous cell cervical cancer (SCC) associated with self-reported allergies and with variation in allergy-related cytokine genes using data from a case–control study (561 cases, 1,258 controls) conducted in Washington State. Logistic regression models yielded odds ratios (OR) and 95% CI.
Results: Pollen allergy, the most commonly reported allergy, was associated with reduced SCC risk (OR: 0.6; 95% CI: 0.5–0.8). Of 60 tagging single-nucleotide polymorphisms covering eight genes (CSF2, IL3, IL4, IL13, CSF2RB, IL4R, IL13RA1, IL13RA2), several were related to pollen allergies among controls: IL4R rs3024647 (dominant OR: 1.5; 95% CI: 1.0–2.3; P = 0.04), CSF2RB rs16997517 (dominant OR: 2.2; 95% CI: 1.0–4.7; P = 0.04), and IL13 rs1800925 (per-allele OR: 1.7; 95% CI: 1.3–2.4; P = 0.0007). Two variants were inversely associated with SCC risk: IL4R rs3024656 (per-allele OR: 0.8; 95% CI: 0.6–1.0; P = 0.03) and CSF2RB rs16997517 (dominant OR: 0.4; 95% CI: 0.2–0.9; P = 0.04).
Conclusions: Pollen allergies were related to reduced SCC risk. CSF2RB rs16997517 was directly related to pollen allergies in controls and to reduced SCC risk.
Impact: If other studies confirm these results, the mechanism behind allergy-associated immune response associated with SCC risk may be worth exploring in the context of therapeutic or prophylactic vaccines. Cancer Epidemiol Biomarkers Prev; 20(1); 199–207. ©2011 AACR.
Development and Validation of a New, Sensitive Immunochemical Assay for O6-Methylguanine in DNA and Its Application in a Population Study
Authors: Georgiadis Panagiotis , Kaila Stella , Makedonopoulou Paraskevi , Fthenou Eleni , Chatzi Leda , Pletsa Vasiliki , Kyrtopoulos Soterios A. 
Published: January 2011

Abstract
Background: Investigations of the presence of the precarcinogenic DNA adduct O6-methylguanine (O6-meG) in humans and its association with exposure or cancer risk have been hindered by the absence of analytic methods of adequate sensitivity and throughput. We report the development, validation, and application of an ELISA-type assay for O6-meG appropriate for large-scale population studies.
Methods: In the new analytic method, restriction enzymes are used to digest DNA to fragments of size expected to contain no more than one O6-meG residue. Anti-adduct antisera are used to transfer O6-meG–containing fragments to a solid surface, where they are detected using anti-ssDNA antisera, the high ratio of normal nucleotides to adducts providing a strong signal enhancement.
Results: An assay with a limit of detection of 1.5 adducts/109 nucleotides using 10 μg of DNA, a dynamic range of approximately two orders of magnitude and satisfactory precision and accuracy characteristics was established and validated. Analysis of samples from 120 subjects from the Rhea mother–child cohort in Crete led to the detection of O6-meG in 70% of maternal and 50% of cord blood buffy coat samples at mean levels of 0.65 and 0.38 adducts/108 nucleotides, respectively.
Conclusions: The frequent observation of O6-meG in human DNA is compatible with dietary compounds (e.g. N-nitroso compounds or their precursors), or endogenous processes being responsible for the formation of this adduct.
Impact: The new assay opens the way for large-scale population studies of O6-meG as a biomarker of exposure or risk. The approach used in this assay can, in principle, be extended to any DNA adduct for which suitable antisera are available. Cancer Epidemiol Biomarkers Prev; 20(1); 82–90. ©2011 AACR.
Genetic Variation in VEGF Family Genes and Breast Cancer Risk: A Report from the Shanghai Breast Cancer Genetics Study
Authors: Beeghly-Fadiel Alicia , Shu Xiao-Ou , Lu Wei , Long Jirong , Cai Qiuyin , Xiang Yong-Bing , Zheng Ying , Zhao Zhongming , Gu Kai , Gao Yu-Tang , Zheng Wei 
Published: January 2011

Abstract
Background: In addition to mediating aspects of physiologic and pathologic angiogenesis, the VEGF family also contributes to carcinogenesis.
Methods: We comprehensively characterized genetic variation across four VEGF family genes and evaluated associations with breast cancer risk with odds ratios (OR) and 95% CIs for participants of the two-stage case–control Shanghai Breast Cancer Genetics Study (SBCGS). Stage 1 evaluated 200 single nucleotide polymorphisms (SNP) across two VEGF ligands (VEGFA and VEGFC) and two VEGF receptors (FLT1/VEGFR1 and KDR/VEGFR2) among 2,079 cases and 2,148 controls. Five SNPs with promising associations were assessed in stage 2 among 4,419 cases and 1,851 controls.
Results: Two SNPs were consistently associated with breast cancer risk across our two study stages and were significant in combined analyses. Compared with FLT1 rs9551471 major allele homozygotes (AA), reduced risks were associated with AG (OR = 0.92, 95% CI: 0.84–1.00) and GG (OR = 0.78, 95% CI: 0.64–0.95) genotypes (Ptrend = 0.005). Compared with VEGFA rs833070 major allele carriers (CC or CT), increased risk was associated with TT genotypes (OR = 1.26, 95% CI: 1.05–1.52, P = 0.016).
Conclusion: Results from our study indicate that common genetic variation in VEGFA and FLT1 (VEGFR1) may contribute to breast cancer susceptibility.
Impact: Our findings provide clues for future studies on VEGF family genes in relation to cancer susceptibility and survival. Cancer Epidemiol Biomarkers Prev; 20(1); 33–41; ©2011 AACR.
Dating the Rise of Esophageal Adenocarcinoma: Analysis of Connecticut Tumor Registry Data, 1940–2007
Authors: Abrams Julian A. , Sharaiha Reem Z. , Gonsalves Lou , Lightdale Charles J. , Neugut Alfred I. 
Published: January 2011

Abstract
Background: The timing of onset of the rise in incidence of esophageal adenocarcinoma (EAC) has not been clearly defined, and doing so may provide clues with regard to exposures associated with the changed epidemiology of this malignancy. We therefore aimed to investigate historical trends in the incidence of EAC and other upper gastrointestinal malignancies.
Methods: We did a population-based study using Connecticut Tumor Registry (1940–2007) and Surveillance, Epidemiology, and End Results (SEER; 1973–2007) data. Age-adjusted incidence rates (per 100,000 person-years) were calculated for EAC and other upper gastrointestinal malignancies.
Results: The incidence of EAC remained relatively constant until 1965–69, and then rose from 0.41 (95%CI, 0.26–0.56) to 1.31 (95%CI 1.07–1.54) in 1978–82 and 5.31 (95%CI 4.89–5.73) in 2003–07. The incidence of gastric cardia cancer began to rise in the 1950s and plateaued in the 1990s. The incidence of esophageal squamous cell carcinoma began to decrease around 1980. The trends from Connecticut Tumor Registry data closely mirrored those from SEER data.
Conclusions: The incidence of EAC began to rise in the late 1960s, predating the rise in obesity by a decade. Reduced infection rates of Helicobacter pylori, changes in microbiome, or other exposures may have contributed to the changed epidemiology of this malignancy.
Impact: Analysis of historical data of trends in EAC incidence implicate a change in environmental factors from the mid-20th century as primarily responsible for the initial rise in EAC incidence, predating the rise in obesity prevalence in the United States by over a decade. Cancer Epidemiol Biomarkers Prev; 20(1); 183–6. ©2011 AACR.
Metformin and Incident Breast Cancer among Diabetic Women: A Population-Based Case–Control Study in Denmark
Authors: Bosco Jaclyn Lee Fong , Antonsen Sussie , Sørensen Henrik Toft , Pedersen Lars , Lash Timothy L. 
Published: January 2011

AbstractBackground: Preliminary evidence suggests that metformin may decrease breast cancer risk by decreasing insulin levels and reducing cell proliferation. We evaluated the effect of metformin medication on the risk of incident breast cancer among peri- and postmenopausal women.Methods: We used Danish medical registries to conduct a nested case–control study among type 2 diabetic women 50 years or older who resided in northern Denmark from 1989 to 2008 (n = 4,323). We identified 393 diabetic cases and used risk-set sampling to select 10 diabetic controls per case (n = 3,930) matched on county of residence. Odds ratios (OR) and 95% CIs were estimated by conditional logistic regression associating metformin use with breast cancer occurrence.Results: Ninety-six cases (24%) and 1,154 controls (29%) used metformin for at least 1-year duration. Cases were slightly older on average than controls, but they were similar in distribution for parity, use of hormone replacement therapy, and history of diabetes complications. Metformin users were less likely with a diagnosis of breast cancer (OR = 0.77; 95% CI = 0.61–0.99) than nonmetformin users. Adjustment for diabetes complications, clinically diagnosed obesity, and important predictors of breast cancer did not substantially alter the association (OR = 0.81; 95% CI = 0.63–0.96).Conclusion: Our results suggest that metformin may protect against breast cancer in type 2 diabetic peri- or postmenopausal women.Impact: This study supports the growing evidence of a role for metformin in breast cancer chemoprevention. Cancer Epidemiol Biomarkers Prev; 20(1); 101–11. ©2011 AACR.