bluuebunny/crossref_metadata_2025_split huggingface dataset:
Movements of wintering American marten (Martes americana): relative influences of prey activity and forest stand age
Authors: Vigeant-Langlois Charles , Desrochers André 
Published: November 2011

American marten (Martes americana (Turton, 1806)) was traditionally associated with old-growth forests, but recent evidence suggests that they are frequently found in younger forests as well. To better understand habitat requirements by this economically important furbearer, we investigated its fine-scale movement behavior in relation to local prey activity (tracks) and stand age. We georeferenced 34 marten tracks (57 km), associated prey tracks, and subnivean forays in a balsam fir forest of southern Québec, Canada. Marten movements were more tortuous in the presence of high numbers of prey tracks and near subnivean foraging sites. The latter relationships were stronger at a fine spatial scale (10 m movement steps) than at coarser scales (20 or 40 m movement steps). Marten movement tortuosity was unrelated to forest stand age after accounting for prey activity. These results support the hypothesis that the American marten does not hunt mainly in old-growth forests but appears to concentrate its foraging behaviour in areas with high prey activity.
A Novel Approach to Predict the Likelihood of Specific Ovarian Tumor Pathology Based on Serum CA-125: A Multicenter Observational Study
Authors: Van Calster Ben , Valentin Lil , Van Holsbeke Caroline , Zhang Jing , Jurkovic Davor , Lissoni Andrea Alberto , Testa Antonia Carla , Czekierdowski Artur , Fischerová Daniela , Domali Ekaterini , Van de Putte Gregg , Vergote Ignace , Van Huffel Sabine , Bourne Tom , Timmerman Dirk 
Published: November 2011

Abstract
Background: The CA-125 tumor marker has limitations when used to distinguish between benign and malignant ovarian masses. We therefore establish likelihood curves of six subgroups of ovarian pathology based on CA-125 and menopausal status.
Methods: This cross-sectional study conducted by the International Ovarian Tumor Analysis group involved 3,511 patients presenting with a persistent adnexal mass that underwent surgical intervention. CA-125 distributions for six tumor subgroups (endometriomas and abscesses, other benign tumors, borderline tumors, stage I invasive cancers, stage II–IV invasive cancers, and metastatic tumors) were estimated using kernel density estimation with stratification for menopausal status. Likelihood curves for the tumor subgroups were derived from the distributions.
Results: Endometriomas and abscesses were the only benign pathologies with median CA-125 levels above 20 U/mL (43 and 45, respectively). Borderline and invasive stage I tumors had relatively low median CA-125 levels (29 and 81 U/mL, respectively). The CA-125 distributions of stage II–IV invasive cancers and benign tumors other than endometriomas or abscesses were well separated; the distributions of the other subgroups overlapped substantially. This held for premenopausal and postmenopausal patients. Likelihood curves and reference tables comprehensibly show how subgroup likelihoods change with CA-125 and menopausal status.
Conclusions and Impact: Our results confirm the limited clinical value of CA-125 for preoperative discrimination between benign and malignant ovarian pathology. We have shown that CA-125 may be used in a different way. By using likelihood reference tables, we believe clinicians will be better able to interpret preoperative serum CA-125 results in patients with adnexal masses. Cancer Epidemiol Biomarkers Prev; 20(11); 2420–8. ©2011 AACR.
A Genome-Wide Survey over the ChIP-On-Chip Identified Androgen Receptor-Binding Genomic Regions Identifies a Novel Prostate Cancer Susceptibility Locus at 12q13.13
Authors: Feng Junjie , Sun Jielin , Kim Seong-Tae , Lu Yizhen , Wang Zhong , Zhang Zheng , Gronberg Henrik , Isaacs William B. , Zheng S. Lilly , Xu Jianfeng 
Published: November 2011

Abstract
Background: The molecular mechanisms for the genome-wide association studies (GWAS)-identified prostate cancer (PCa) risk-associated single-nucleotide polymorphisms (SNP) remain largely unexplained. One recent finding that the PCa risk SNPs are enriched in genomic regions containing androgen receptor (AR)-binding sites has suggested altered AR signaling as a potentially important mechanism.
Methods: To explore novel associations by leveraging this knowledge, we utilized a meta-analysis previously done over SNPs harbored in ChIP-on-chip identified AR-binding genomic regions using the GWAS data from the Johns Hopkins Hospital (JHH) and the Cancer Genetic Markers of Susceptibility (CGEMS) study, and subsequently evaluated the top associations in a third population from the CAncer of the Prostate in Sweden (CAPS) study.
Results: One SNP (rs4919743: G&gt;A), located at the KRT8 locus at 12q13.13 which encodes a keratin protein (K8) long used as a prostate epithelial malignancy marker and implicated in the tumorigenesis of several cancer types, was identified to be associated with PCa risk. The frequency of its minor “A” allele was consistently higher in PCa cases than in controls in all three study populations, with a combined OR of 1.22 (95% CI: 1.13–1.32) and an overall P value of 4.50 × 10−7 (Bonferroni corrected, P = 0.006).
Conclusion: We have identified a novel genetic locus that is associated with PCa risk.
Impact: This study illustrated the great potential of prior biological knowledge in facilitating the search for novel disease-associated genetic loci. This finding warrants further replication in other studies. Cancer Epidemiol Biomarkers Prev; 20(11); 2396–403. ©2011 AACR.
HPV and HPV Vaccine Education Intervention: Effects on Parents, Healthcare Staff, and School Staff
Authors: Reiter Paul L. , Stubbs Brenda , Panozzo Catherine A. , Whitesell Dianne , Brewer Noel T. 
Published: November 2011

Abstract
Background: Increasing knowledge about human papillomavirus (HPV) and HPV vaccine is a potentially important way to increase vaccination rates, yet few education interventions have addressed these topics. We report the results of an education intervention targeting three key groups who have contact with adolescent females.
Methods: We conducted HPV education intervention sessions during 2008 and 2009 in Guilford County, North Carolina. Parents (n = 376), healthcare staff (n = 118), and school staff (n = 456) attended the one-time sessions and completed self-administered surveys. Analyses used mixed regression models to examine the intervention's effects on participants' self-rated HPV knowledge, objectively assessed HPV and HPV vaccine knowledge, and beliefs about HPV vaccine.
Results: Participants had relatively low levels of objectively assessed HPV and HPV vaccine knowledge prior to the intervention. The education intervention increased self-rated HPV knowledge among all three key groups (all P &lt; 0.001), and objectively assessed knowledge about many aspects of HPV and HPV vaccine among healthcare and school staff members (all P &lt; 0.05). Following the intervention, more than 90% of school staff members believed HPV and HPV vaccine education is worthwhile for school personnel and that middle schools are an appropriate venue for this education. Most parents (97%) and school staff members (85%) indicated they would be supportive of school-based vaccination clinics.
Conclusions: Our education intervention greatly increased HPV and HPV vaccine knowledge among groups influential to the HPV vaccination behaviors of adolescent females.
Impact: Education interventions represent a simple yet potentially effective strategy for increasing HPV vaccination and garnering stronger support for school-based vaccination clinics. Cancer Epidemiol Biomarkers Prev; 20(11); 2354–61. ©2011 AACR.
International Trends in Liver Cancer Incidence Rates
Authors: Center Melissa M. , Jemal Ahmedin 
Published: November 2011

Abstract
Background: Several previous studies have documented region or country-specific liver cancer incidence trends around the world. However, no study has systematically examined the international pattern using the most recently updated incidence data from the International Agency for Research on Cancer.
Methods: We examined recent trends in liver cancer incidence rates from 1993 to 2002 by joinpoint analysis for 32 cancer registries worldwide, using Cancer Incidence in Five Continents. We also examined the male to female rate ratios for these and four additional registries, based on the 1998–2002 incidence data.
Results: Liver cancer incidence rates for both men and women statistically significantly increased from 1993 to 2002 for 8 of 32 cancer registries considered in the analysis. Increases were largely confined to economically developed countries of Western Europe, North America, and Oceania. In contrast, rates decreased in both men and women in 5 registries including 3 in Asia. Despite this, the incidence rates in Asian countries are twice as high as those in Africa and more than four times as high as rates in North America. Male to female rate ratios varied from 0.9 in sub-Saharan African and South American registries to 5.0 in France and Egypt.
Conclusions: Liver cancer incidence rates continue to increase in some low-risk parts of the world whereas they are decreasing in some of the highest risk countries in Asia. Etiologic studies are required to further elucidate factors contributing to the divergent liver cancer incidence trends worldwide.
Impact: Our description of international liver cancer incidence trends may stimulate further etiologic studies. Cancer Epidemiol Biomarkers Prev; 20(11); 2362–8. ©2011 AACR.
Joint Effects of Alcohol Consumption and Polymorphisms in Alcohol and Oxidative Stress Metabolism Genes on Risk of Head and Neck Cancer
Authors: Hakenewerth Anne M. , Millikan Robert C. , Rusyn Ivan , Herring Amy H. , North Kari E. , Barnholtz-Sloan Jill S. , Funkhouser William F. , Weissler Mark C. , Olshan Andrew F. 
Published: November 2011

Abstract
Background: Single-nucleotide polymorphisms (SNP) in alcohol metabolism genes are associated with squamous cell carcinoma of the head and neck (SCCHN) and may influence cancer risk in conjunction with alcohol. Genetic variation in the oxidative stress pathway may impact the carcinogenic effect of reactive oxygen species produced by ethanol metabolism. We hypothesized that alcohol interacts with these pathways to affect SCCHN incidence.
Methods: Interview and genotyping data for 64 SNPs were obtained from 2,552 European- and African-American subjects (1,227 cases and 1,325 controls) from the Carolina Head and Neck Cancer Epidemiology Study, a population-based case–control study of SCCHN conducted in North Carolina from 2002 to 2006. We estimated ORs and 95% confidence intervals (CI) for SNPs and haplotypes, adjusting for age, sex, race, and duration of cigarette smoking. P values were adjusted for multiple testing using Bonferroni correction.
Results: Two SNPs were associated with SCCHN risk: ADH1B rs1229984 A allele (OR = 0.7; 95% CI, 0.6–0.9) and ALDH2 rs2238151 C allele (OR = 1.2; 95% CI, 1.1–1.4). Three were associated with subsite tumors: ADH1B rs17028834 C allele (larynx, OR = 1.5; 95% CI, 1.1–2.0), SOD2 rs4342445 A allele (oral cavity, OR = 1.3; 95% CI, 1.1–1.6), and SOD2 rs5746134 T allele (hypopharynx, OR = 2.1; 95% CI, 1.2–3.7). Four SNPs in alcohol metabolism genes interacted additively with alcohol consumption: ALDH2 rs2238151, ADH1B rs1159918, ADH7 rs1154460, and CYP2E1 rs2249695. No alcohol interactions were found for oxidative stress SNPs.
Conclusions and Impact: Previously unreported associations of SNPs in ALDH2, CYP2E1, GPX2, SOD1, and SOD2 with SCCHN and subsite tumors provide evidence that alterations in alcohol and oxidative stress pathways influence SCCHN carcinogenesis and warrant further investigation. Cancer Epidemiol Biomarkers Prev; 20(11); 2438–49. ©2011 AACR.
Antitumor Activity of NVP-BKM120—A Selective Pan Class I PI3 Kinase Inhibitor Showed Differential Forms of Cell Death Based on p53 Status of Glioma Cells
Authors: Koul Dimpy , Fu Jun , Shen Ruijun , LaFortune Tiffany A. , Wang Shuzhen , Tiao Ningyi , Kim Yong-Wan , Liu Juinn-Lin , Ramnarian Deepti , Yuan Ying , Garcia-Echevrria Carlos , Maira Sauveur-Michel , Yung W.K. Alfred 
Published: November 2011

Abstract
Purpose: The aim of this study was to show preclinical efficacy and clinical development potential of NVP-BKM120, a selective pan class I phosphatidylinositol-3 kinase (PI3K) inhibitor in human glioblastoma (GBM) cells in vitro and in vivo.
Experimental Design: The effect of NVP-BKM120 on cellular growth was assessed by CellTiter-Blue assay. Flow cytometric analyses were carried out to measure the cell-cycle, apoptosis, and mitotic index. Mitotic catastrophe was detected by immunofluorescence. The efficacy of NVP-BKM120 was tested using intracranial U87 glioma model.
Results: We tested the biologic effects of a selective PI3K inhibitor NVP-BKM120 in a set of glioma cell lines. NVP-BKM120 treatment for 72 hours resulted in a dose-dependent growth inhibition and effectively blocked the PI3K/Akt signaling cascade. Although we found no obvious relationship between the cell line's sensitivity to NVP-BKM120 and the phosphatase and tensin homolog (PTEN) and epidermal growth factor receptor (EGFR) statuses, we did observe a differential sensitivity pattern with respect to p53 status, with glioma cells containing wild-type p53 more sensitive than cells with mutated or deleted p53. NVP-BKM120 showed differential forms of cell death on the basis of p53 status of the cells with p53 wild-type cells undergoing apoptotic cell death and p53 mutant/deleted cells having a mitotic catastrophe cell death. NVP-BKM120 mediates mitotic catastrophe mainly through Aurora B kinase. Knockdown of p53 in p53 wild-type U87 glioma cells displayed microtubule misalignment, multiple centrosomes, and mitotic catastrophe cell death. Parallel to the assessment of the compound in in vitro settings, in vivo efficacy studies using an intracranial U87 tumor model showed an increased median survival from 26 days (control cohort) to 38 and 48 days (treated cohorts).
Conclusion: Our present findings establish that NVP-BKM120 inhibits the PI3K signaling pathways, leading to different forms of cell death on the basis of p53 statuses. Further studies are warranted to determine if NVP-BKM120 has potential as a glioma treatment. Clin Cancer Res; 18(1); 184–95. ©2011 AACR.
Antitumor Activity of Sustained N-Myc Reduction in Rhabdomyosarcomas and Transcriptional Block by Antigene Therapy
Authors: Tonelli Roberto , McIntyre Alan , Camerin Consuelo , Walters Zoë S. , Di Leo Korinne , Selfe Joanna , Purgato Stefania , Missiaglia Edoardo , Tortori Andrea , Renshaw Jane , Astolfi Annalisa , Taylor Kathryn R. , Serravalle Salvatore , Bishop Ryan , Nanni Cristina , Valentijn Linda J. , Faccini Andrea , Leuschner Ivo , Formica Serena , Reis-Filho Jorge S. , Ambrosini Valentina , Thway Khin , Franzoni Monica , Summersgill Brenda , Marchelli Rosangela , Hrelia Patrizia , Cantelli-Forti Giorgio , Fanti Stefano , Corradini Roberto , Pession Andrea , Shipley Janet 
Published: November 2011

Abstract
Purpose: Rhabdomyosarcomas are a major cause of cancer death in children, described with MYCN amplification and, in the alveolar subtype, transcription driven by the PAX3-FOXO1 fusion protein. Our aim was to determine the prevalence of N-Myc protein expression and the potential therapeutic effects of reducing expression in rhabdomyosarcomas, including use of an antigene strategy that inhibits transcription.
Experimental Design: Protein expression was assessed by immunohistochemistry. MYCN expression was reduced in representative cell lines by RNA interference and an antigene peptide nucleic acid (PNA) oligonucleotide conjugated to a nuclear localization signal peptide. Associated gene expression changes, cell viability, and apoptosis were analyzed in vitro. As a paradigm for antigene therapy, the effects of systemic treatment of mice with rhabdomyosarcoma cell line xenografts were determined.
Results: High N-Myc levels were significantly associated with genomic amplification, presence of the PAX3/7-FOXO1 fusion genes, and proliferative capacity. Sustained reduction of N-Myc levels in all rhabdomyosarcoma cell lines that express the protein decreased cell proliferation and increased apoptosis. Positive feedback was shown to regulate PAX3-FOXO1 and N-Myc levels in the alveolar subtype that critically decrease PAX3-FOXO1 levels on reducing N-Myc. Pharmacologic systemic administration of the antigene PNA can eliminate alveolar rhabdomyosarcoma xenografts in mice, without relapse or toxicity.
Conclusion: N-Myc, with its restricted expression in non-fetal tissues, is a therapeutic target to treat rhabdomyosarcomas, and blocking gene transcription using antigene oligonucleotide strategies has therapeutic potential in the treatment of cancer and other diseases that has not been previously realized in vivo. Clin Cancer Res; 18(3); 796–807. ©2011 AACR.
m-Calpain Induction in Vascular Endothelial Cells on Human and Mouse Atheromas and Its Roles in VE-Cadherin Disorganization and Atherosclerosis
Authors: Miyazaki Takuro , Taketomi Yoshitaka , Takimoto Masafumi , Lei Xiao-Feng , Arita Shigeko , Kim-Kaneyama Joo-ri , Arata Satoru , Ohata Hisayuki , Ota Hidekazu , Murakami Makoto , Miyazaki Akira 
Published: November 2011

Background—
Although dysfunction of VE-cadherin–mediated adherence junctions in vascular endothelial cells (ECs) is thought to be one of the initial steps of atherosclerosis, little is known regarding how VE-cadherin is disrupted during atherogenic development. This study focused on the role of calpain, an intracellular cysteine protease, in the proteolytic disorganization of VE-cadherin and subsequent progression of atherosclerosis.

Methods and Results—

Increased expression of m-calpain was observed in aortic ECs in atherosclerotic lesions in humans and low-density lipoprotein receptor–deficient (
ldlr
−/−
) mice. Furthermore, proteolytic disorganization of VE-cadherin was shown in aortic ECs in
ldlr
−/−
and apolipoprotein E–deficient (
apoE
−/−
) mice. Long-term administration of calpain inhibitors into these mice attenuated atherosclerotic lesion development and proinflammatory responses, as well as VE-cadherin disorganization, without normalization of plasma lipid profiles. Furthermore, in vivo transfection of m-calpain siRNA to
ldlr
−/−
mice prevented disorganization of VE-cadherin and proatherogenic hyperpermeability in aortic ECs. Treatment of cultured ECs with oxidized LDL, lysophosphatidylcholine, or LDL pretreated with secreted phospholipase A
2
led to the induction of m-calpain but not of μ-calpain, thereby eliciting selective m-calpain overactivation. These data suggest that lysophosphatidylcholine-induced m-calpain directly cleaves a juxtamembrane region of VE-cadherin, resulting in dissociation of β-catenin from the VE-cadherin complex, disorganization of adherence junctions, and hyperpermeability in ECs.

Conclusions—
Subtype-selective induction of m-calpain in aortic ECs during atherosclerotic progression is associated with proteolytic disorganization of VE-cadherin and proatherogenic hyperpermeability in cells. Thus, a strategy to selectively inhibit m-calpain may be useful for the therapeutic treatment of patients with atherosclerosis.
An Application of Univariate and Multivariate Approaches in fMRI to Quantifying the Hemispheric Lateralization of Acoustic and Linguistic Processes
Authors: McGettigan Carolyn , Evans Samuel , Rosen Stuart , Agnew Zarinah K. , Shah Poonam , Scott Sophie K. 
Published: November 2011

Abstract
The question of hemispheric lateralization of neural processes is one that is pertinent to a range of subdisciplines of cognitive neuroscience. Language is often assumed to be left-lateralized in the human brain, but there has been a long running debate about the underlying reasons for this. We addressed this problem with fMRI by identifying the neural responses to amplitude and spectral modulations in speech and how these interact with speech intelligibility to test previous claims for hemispheric asymmetries in acoustic and linguistic processes in speech perception. We used both univariate and multivariate analyses of the data, which enabled us to both identify the networks involved in processing these acoustic and linguistic factors and to test the significance of any apparent hemispheric asymmetries. We demonstrate bilateral activation of superior temporal cortex in response to speech-derived acoustic modulations in the absence of intelligibility. However, in a contrast of amplitude-modulated and spectrally modulated conditions that differed only in their intelligibility (where one was partially intelligible and the other unintelligible), we show a left dominant pattern of activation in STS, inferior frontal cortex, and insula. Crucially, multivariate pattern analysis showed that there were significant differences between the left and the right hemispheres only in the processing of intelligible speech. This result shows that the left hemisphere dominance in linguistic processing does not arise because of low-level, speech-derived acoustic factors and that multivariate pattern analysis provides a method for unbiased testing of hemispheric asymmetries in processing.
Twenty-third Annual Margaret Mann Phillips Lecture: Pagan Philosophy and Patristics in Erasmus and His Contemporaries
Authors: Kraye Jill 
Published: November 2011

AbstractAs admirers of the classical past, Renaissance humanists were frequently faced with the problem of how to deal with those aspects of ancient culture, such as pagan philosophy, which presented serious challenges to their sincerely held Christian beliefs. In seeking to resolve this longstanding dilemma, many humanists looked to the Church Fathers, who offered them a variety of different approaches to the issue. These ranged from highlighting the compatibility of certain philosophical schools with Christian theology to rejecting the ancient philosophical heritage in part or in its entirety. This article explores the interaction between pagan philosophy and patristics in Renaissance thought, focusing in particular on the role which each played in the intellectual activity of Erasmus and those of his contemporaries who remained within the Catholic fold, and attempting to determine the extent to which the project to restore these two bodies of writing occupied common ground in the humanist program for the recovery of antiquity.
Erasmian Rhetoric of Dialogue and Declamation and the Staging of Persuasion in Antonio Brucioli's Dialogi della morale filosofia
Authors: Leushuis Reinier 
Published: November 2011

AbstractThe Dialogi della morale filosofia by Antonio Brucioli (1487–1566), a Florentine humanist exiled in Venice, contain significant reworkings of Erasmian material. In the first edition (1526) Brucioli includes a dialogue version of Erasmus' declamation Encomium matrimonii; in the second edition (1537–1538) he recasts the colloquy Coniugium. While critics have discussed Erasmus' influence on Brucioli in the context of religious renewal, this article assesses the influence of Erasmian rhetoric on Brucioli's Dialogi from a literary perspective, namely in connection with early sixteenth-century developments of the dialogue genre in Italy. It argues that several of Brucioli's dialogues reveal an early application in the Italian literary context of Erasmian dialogical and declamatory strategies that exploit the mimetic value of the spoken exchange. Brucioli successfully valorizes these strategies to create a rhetorical “staging of persuasion” for the sake of the propagation of classical moral wisdom. The final part of this article establishes a connection between Brucioli's attempts to create a praxis of speaking on moral philosophy through dialogue and Erasmus' experiments with vivid spoken exchange in the Colloquia's earliest form as Familiarum colloquiorum formulae (1522).