bluuebunny/crossref_metadata_2025_split huggingface dataset:
Geographies of Touch/Touched by Geography
Authors: Dixon Deborah P. , Straughan Elizabeth R. 
Published: May 2010

AbstractConsiderable attention within geography has been paid to the physiologies, knowledges and practices that give substance and import to the senses – sight, hearing, smell, taste and touch – and the manner in which these work alone, or in concert, to facilitate particular forms of relations between and amongst people, other life forms and objects. This article takes stock of the manner in which touch has entered into these debates and in particular of recent efforts to place touch, touching and being touched within non‐essentialist, human geographic analyses. In doing so it draws attention, first, to studies that have used ‘non’ or ‘more than’ representational theory to emphasise the role of pathic, or precognitive, experiences of place in the production of proximal forms of knowledge and second, to work that explores the inter‐play between the ‘interior’ psychologies of intimacy and indifference, acceptance and alienation (i.e. feelings of being in/losing/being out of touch) and the ‘exterior,’ corporeal work of texture and friction, push and feel. We conclude by calling for more critical attention to the work of touch in constructing scaled geographies and the recognition of legal and jurisdictional geographies in determining where, when and how touching takes place, the designation of touching as ‘good’ or ‘bad’ and the imposition of penalties in response to touch.
Alfred Russel Wallace, Geographer
Authors: Smith Charles H. 
Published: May 2010

AbstractAmong the great explorers and thinkers who advanced geography in the nineteenth century and helped it evolve into the subject that exists today is a man who is not always connected with the field, Alfred Russel Wallace (1823–1913). Most commonly recognized as ‘the other man’ in the history of the discovery of the principle of natural selection, Wallace’s commitment to the study of landscape and its physical, biological, and human elements was lifelong, and resulted in a wide range of contributions to biogeography, physical geography, human geography, and ethnography. In this year of the double anniversaries of Charles Darwin’s birth and the publication ofOn the Origin of Species, a short review of Wallace’s contributions is offered in an effort to characterize Wallace as ‘a geographer who happened to be interested in evolution’.
Giant Subependymoma Developed in a Patient with Aniridia: Analyses of PAX6 and Tumor‐relevant Genes
Authors: Maekawa Motoko , Fujisawa Hironori , Iwayama Yoshimi , Tamase Akira , Toyota Tomoko , Osumi Noriko , Yoshikawa Takeo 
Published: May 2010

AbstractWe observed an unusually large subependymoma in a female patient with congenital aniridia. To analyze the genetic mechanisms of tumorigenesis, we first examined the paired box 6 (PAX6) gene using both tumor tissue and peripheral lymphocytes. Tumor suppressor activity has been proposed for PAX6 in gliomas, in addition to its well‐known role in the eye development. Using genomic quantitative PCR and loss of heterozygosity analysis, we identified hemizygous deletions in the 5′‐region of PAX6. In lymphocytes, the deletion within PAX6 spanned from between exons 6 and 7 to the 5′‐upstream region of the gene, but did not reach the upstream gene, RNC1, which is reported to be associated with tumors. The subependymoma had an additional de novo deletion spanning from the intron 4 to intron 6 of PAX6, although we could not completely determine whether these two deletions are on the same chromosome or not. We also examined other potentially relevant tumor suppressor genes: PTEN, TP53 and SOX2. However, we detected no exonic mutations or deletions in these genes. Collectively, we speculate that the defect in PAX6 may have contributed to the extremely large size of the subependymoma, due to a loss of tumor suppressor activity in glial cell lineage.
A Hybrid Model of Moral Panics: Synthesizing the Theory and Practice of Moral Panic Research
Authors: Klocke Brian V. , Muschert Glenn W. 
Published: May 2010

AbstractWe seek to address criticisms of the concept of moral panics (MPs) by offering a hybrid model of MPs that synthesizes theory and practice of MPs research. A review of the literature on MPs from sociology, media studies and related fields shows a wide variety of usage and lack of conceptual clarity of the term ‘moral panic’. Yet there are few articles explaining how to analyze MPs. We present a theoretical clarification of MPs by addressing elements of scope, intensity and reception, to create distinction from other related theoretical concepts. To develop a working method for researching MPs, one must have an understanding of social conditions that give rise to, sustain and result in the success or failure of MPs, as well as possible lasting effects. We synthesize Cohen’s process‐oriented model of MPs and Goode & Ben‐Yehuda’s attribution‐oriented model of MPs, creating a critical hybrid model of MPs that integrates processes and attributes. We then utilize the hybrid model to offer practical suggestions for researching and analyzing the conditions, processes and effects of MPs, in the hopes of encouraging a more rigorous research agenda for scholars of MPs.
Cross‐species amplification of bovid microsatellites in central African duikers (genusCephalophus) and other sympatric artiodactyls
Authors: NTIE STEPHAN , SOTO‐CALDERÓN IVÁN D. , EATON MITCHELL J. , ANTHONY NICOLA M. 
Published: May 2010

AbstractThe present study set out to evaluate cross‐species amplification of 34 bovid microsatellites in six central African duikers:Cephalophus callipygus,C. monticola,C. silvicultor,C. nigrifrons,C. dorsalisandC. leucogaster. Of these loci, 16 amplified across all species and appeared polymorphic when initially tested in polyacrylamide gel electrophoresis. Twelve of these loci were subsequently assembled into three multiplex panels of four loci each. These multiplexes successfully amplified across all six duiker species in the present study and the sympatric artiodactylsTragelaphus spekeiandHyemoschus aquaticus. The only exception was the locus BM848 that did not amplify fromC. leucogaster. For species with sufficient sample sizes (C. callipygusandC. monticola), the number of alleles ranged from three to ten and four to fifteen, respectively. Three loci deviated from Hardy–Weinberg equilibrium inC. callipygusand five inC. monticola. We attribute the latter result to possibilities of local population substructuring or to an excess of homozygotes because of null alleles. These multiplex assemblies will greatly facilitate studies of individual identification, parentage analysis, population size estimation and fine‐scale analyses of population genetic structure in central African artiodactyls.
Thoracoscopic resection for intrathoracic neurogenic tumors
Authors: Odaka M , Akiba T , Nakada T , Asano H , Yabe M , Kamiya N , Hirano J , Morikawa T 
Published: May 2010

AbstractIntroduction: The thoracoscopic approach is becoming the standard for intrathoracic neurogenic tumors, though certain technical issues still need to be resolved. The purpose of this study is to evaluate the feasibility of thoracoscopic surgery for intrathoracic neurogenic tumors.Methods: We evaluated short‐term outcomes of 14 consecutive patients who underwent resection of intrathoracic neurogenic tumors between July 2005 and June 2009. Among them, three patients had tumors located at the thoracic apex, and one had a tumor with an intraspinal extension (dumbbell‐type tumor).Results: A complete thoracoscopic resection was achieved in all patients with no postoperative mortality. The dumbbell‐type tumor was resected with a combined neurosurgical–thoracoscopic approach. The postoperative course was uneventful in all patients.Conclusion: Our thoracoscopic approach was able to obtain satisfactory visualization of the field and enabled safe surgery for intrathoracic neurogenic tumors. This approach is minimally invasive and is indicated even for tumors located at the thoracic apex or those with intraspinal extensions.
An overview of the Canadian Cordilleran lithospheric mantleThis article is one of a series of papers published in this Special Issue on the theme Lithoprobe — parameters, processes, and the evolution of a continent.
Authors: Francis Don , Minarik William , Proenza Yuliana , Shi Lang 
Published: May 2010

Recent alkaline basalts have brought xenoliths of the underlying lithospheric mantle to the surface at more than 20 localities along the strike length of the Canadian Cordillera. The populations of 13 of these xenolith suites display a common mode at 39–40 wt.% MgO and 3.0–3.5.0 wt.% Al2O3, corresponding to a relatively fertile lherzolite whose composition could reflect 8%–10% melting of primitive mantle. The present oxidation state of the Cordillera lithospheric mantle obtained from olivine–spinel equilibria is ∼1 log unit below the fayalite–magnetite–quartz (FMQ) buffer, which is essentially the same as the oxidation state at the time of the melting event that stabilized the Cordilleran lithospheric mantle in the mid-Proterozoic, as constrained by the relative variation of Sc and V. Two xenolith suites near the Yukon – British Columbia border exhibit a second stronger mode, corresponding to relatively refractory spinel harzburgite with significantly higher Mg contents (45–46 wt.% MgO) and lower Al contents (0.5–1.0 wt.% Al2O3). These bi-modal mantle xenolith suites overlie a teleseismic S-wave slowness anomaly in the underlying asthenospheric mantle, and the harzburgites appear to have been produced by a more recent, localized partial melting (∼15%) of the lherzolite lithosphere. The temperatures estimated from clinopyroxene–orthopyroxene equilibria indicate that the lithospheric mantle beneath the Canadian Cordillera is significantly hotter than that beneath the adjacent Archean of the North American craton, with temperatures at the Moho on the order of 800 °C, a minimum geothermal gradient of ∼10 °C/km, and a thickness of <∼65 km.
GLOBAL METAL-ION BINDING PROTEIN FINGERPRINT: A METHOD TO IDENTIFY MOTIF-LESS METAL-ION BINDING PROTEINS
Authors: MOHAN ABHILASH , ANISHETTY SHARMILA , GAUTAM PENNATHUR 
Published: May 2010

Metal-ion binding proteins play a vital role in biological processes. Identifying putative metal-ion binding proteins is through knowledge-based methods. These involve the identification of specific motifs that characterize a specific class of metal-ion binding protein. Metal-ion binding motifs have been identified for the common metal ions. A robust global fingerprint that is useful in identifying a metal-ion binding protein from a non-metal-ion binding protein has not been devised. Such a method will help in identifying novel metal-ion binding proteins and proteins that do not possess a canonical metal-ion binding motif. We have used a set of physico-chemical parameters of metal-ion binding proteins encoded by the genes CzcA, CzcB and CzcD as a training set to supervised classifiers and have been able to identify several other metal ion binding proteins leading us to believe that metal-ion binding proteins have a global fingerprint, which cannot be pinned down to a single feature of the protein sequence.
Human Enhancer of Filamentation 1 Is a Mediator of Hypoxia-Inducible Factor-1α–Mediated Migration in Colorectal Carcinoma Cells
Authors: Kim Sun-Hee , Xia Dianren , Kim Sang-Wook , Holla Vijaykumar , Menter David G. , DuBois Raymond N. 
Published: May 2010

Abstract
Human enhancer of filamentation 1 (HEF1; also known as NEDD9 or Cas-L) is a scaffolding protein that is implicated in regulating diverse cellular processes, such as cellular attachment, motility, cell cycle progression, apoptosis, and inflammation. Here, we identify HEF1 as a novel hypoxia-inducible factor-1α (HIF-1α)–regulated gene and reveal that HEF1 mediates hypoxia-induced migration of colorectal carcinoma cells. HEF1 is highly expressed in cultured colorectal carcinoma cells exposed to hypoxia and in the hypoxic areas of human colorectal cancer (CRC) specimens. Moreover, our data show that HIF-1α mediates the effects of hypoxia on induction of HEF1 expression via binding to a hypoxia-responsive element of the HEF1 promoter. Importantly, the induction of HEF1 expression significantly enhances hypoxia-stimulated HIF-1α transcriptional activity by modulating the interaction between HIF-1α and its transcriptional cofactor p300. Inhibition of HEF1 expression also reduced the levels of hypoxia-inducible genes, including those that regulate cell motility. Cell migration was reduced dramatically following knockdown of HEF1 expression under hypoxic conditions. Thus, this positive feedback loop may contribute to adaptive responses of carcinoma cells encountering hypoxia during cancer progression. Cancer Res; 70(10); 4054–63. ©2010 AACR.
Signatures of MicroRNAs and Selected MicroRNA Target Genes in Human Melanoma
Authors: Philippidou Demetra , Schmitt Martina , Moser Dirk , Margue Christiane , Nazarov Petr V. , Muller Arnaud , Vallar Laurent , Nashan Dorothee , Behrmann Iris , Kreis Stephanie 
Published: May 2010

AbstractSmall noncoding microRNAs (miRNA) regulate the expression of target mRNAs by repressing their translation or orchestrating their sequence-specific degradation. In this study, we investigated miRNA and miRNA target gene expression patterns in melanoma to identify candidate biomarkers for early and progressive disease. Because data presently available on miRNA expression in melanoma are inconsistent thus far, we applied several different miRNA detection and profiling techniques on a panel of 10 cell lines and 20 patient samples representing nevi and primary or metastatic melanoma. Expression of selected miRNAs was inconsistent when comparing cell line–derived and patient-derived data. Moreover, as expected, some discrepancies were also detected when miRNA microarray data were correlated with qPCR-measured expression levels. Nevertheless, we identified miRNA-200c to be consistently downregulated in melanocytes, melanoma cell lines, and patient samples, whereas miRNA-205 and miRNA-23b were markedly reduced only in patient samples. In contrast, miR-146a and miR-155 were upregulated in all analyzed patients but none of the cell lines. Whole-genome microarrays were performed for analysis of selected melanoma cell lines to identify potential transcriptionally regulated miRNA target genes. Using Ingenuity pathway analysis, we identified a deregulated gene network centered around microphthalmia-associated transcription factor, a transcription factor known to play a key role in melanoma development. Our findings define miRNAs and miRNA target genes that offer candidate biomarkers in human melanoma. Cancer Res; 70(10); 4163–73. ©2010 AACR.
Schweinfurthin A Selectively Inhibits Proliferation and Rho Signaling in Glioma and Neurofibromatosis Type 1 Tumor Cells in a NF1-GRD–Dependent Manner
Authors: Turbyville Thomas J. , Gürsel Demirkan B. , Tuskan Robert G. , Walrath Jessica C. , Lipschultz Claudia A. , Lockett Stephen J. , Wiemer David F. , Beutler John A. , Reilly Karlyne M. 
Published: May 2010

Abstract
Neurofibromatosis type 1 (NF1) is the most common genetic disease affecting the nervous system. Patients typically develop many tumors over their lifetime, leading to increased morbidity and mortality. The NF1 gene, mutated in NF1, is also commonly mutated in sporadic glioblastoma multiforme (GBM). Because both NF1 and GBM are currently incurable, new therapeutic approaches are clearly needed. Natural products represent an opportunity to develop new therapies, as they have been evolutionarily selected to play targeted roles in organisms. Schweinfurthin A is a prenylated stilbene natural product that has previously shown specific inhibitory activity against brain and hematopoietic tumor lines. We show that patient-derived GBM and NF1 malignant peripheral nerve sheath tumor (MPNST) lines, as well as tumor lines derived from the Nf1−/+;Trp53−/+ (NPcis) mouse model of astrocytoma and MPNST are highly sensitive to inhibition by schweinfurthin A and its synthetic analogs. In contrast, primary mouse astrocytes are resistant to the growth inhibitory effects of schweinfurthin A, suggesting that schweinfurthin A may act specifically on tumor cells. Stable transfection of the GTPase-activating protein related domain of Nf1 into Nf1−/−;Trp53−/− astrocytoma cells confers resistance to schweinfurthin A. In addition, the profound effect of schweinfurthin A on dynamic reorganization of the actin cytoskeleton led us to discover that schweinfurthin A inhibits growth factor–stimulated Rho signaling. In summary, we have identified a class of small molecules that specifically inhibit growth of cells from both central and peripheral nervous system tumors and seem to act on NF1-deficient cells through cytoskeletal reorganization correlating to changes in Rho signaling. Mol Cancer Ther; 9(5); 1234–43. ©2010 AACR.
ENMD-1198, a New Analogue of 2-Methoxyestradiol, Displays Both Antiangiogenic and Vascular-Disrupting Properties
Authors: Pasquier Eddy , Sinnappan Snega , Munoz Marcia A. , Kavallaris Maria 
Published: May 2010

AbstractThe formation of a new vascular network by angiogenesis is a key driver in tumor growth and metastasis, making this an attractive therapeutic target. Different strategies are being developed to either prevent tumor angiogenesis or disrupt the tumor vasculature already in place. In this in vitro study, we investigated the antivascular properties of ENMD-1198, a new anticancer drug currently in clinical trials. ENMD-1198 is a new analogue of 2-methoxyestradiol, a microtubule-targeting agent that has shown promising results in the treatment of multiple myeloma and hormone-refractory prostate cancer. Using both bone marrow–derived and dermal microvascular endothelial cell lines, we analyzed the effect of ENMD-1198 on the different functions of endothelial cells involved in angiogenesis. In both cell lines, ENMD-1198 was more potent than 2-methoxyestradiol at inhibiting endothelial cell proliferation, motility, migration, and morphogenesis. In addition, ENMD-1198 induced a significant decrease in vascular endothelial growth factor receptor-2 protein expression in endothelial cells. Furthermore, videomicroscopy experiments showed that ENMD-1198 was able to completely disrupt preformed vascular structures within 2 hours. This vascular-disrupting activity was associated with extensive depolymerization of the microtubule network and accumulation of actin stress fibers and large focal adhesions in vascular endothelial cells. Collectively, our results show that this new compound displays potent antivascular properties, and this study provides important insights into the mechanism of action of this promising new anticancer drug. Mol Cancer Ther; 9(5); 1408–18. ©2010 AACR.
mRNA and microRNA Expression Profiles of the NCI-60 Integrated with Drug Activities
Authors: Liu Hongfang , D'Andrade Petula , Fulmer-Smentek Stephanie , Lorenzi Philip , Kohn Kurt W. , Weinstein John N. , Pommier Yves , Reinhold William C. 
Published: May 2010

Abstract
As part of the Spotlight on Molecular Profiling series, we present here new profiling studies of mRNA and microRNA expression for the 60 cell lines of the National Cancer Institute (NCI) Developmental Therapeutics program (DTP) drug screen (NCI-60) using the 41,000-probe Agilent Whole Human Genome Oligo Microarray and the 15,000-feature Agilent Human microRNA Microarray V2. The expression levels of ∼21,000 genes and 723 human microRNAs were measured. These profiling studies include quadruplicate technical replicates for six and eight cell lines for mRNA and microRNA, respectively, and duplicates for the remaining cell lines. The resulting data sets are freely available and searchable online in our CellMiner database. The result indicates high reproducibility for both platforms and an essential biological similarity across the various cell types. The mRNA and microRNA expression levels were integrated with our previously published 1,429-compound database of anticancer activity obtained from the NCI DTP drug screen. Large blocks of both mRNAs and microRNAs were identified with predominately unidirectional correlations to ∼1,300 drugs, including 121 drugs with known mechanisms of action. The data sets presented here will facilitate the identification of groups of mRNAs, microRNAs, and drugs that potentially affect and interact with one another. Mol Cancer Ther; 9(5); 1080–91. ©2010 AACR.
Preclinical Evaluation of Nilotinib Efficacy in an Imatinib-Resistant KIT-Driven Tumor Model
Authors: Cullinane Carleen , Natoli Anthony , Hui Yorlon , Conus Nelly , Jackson Susan , Brüggen Joseph , Manley Paul W. , McArthur Grant A. 
Published: May 2010

Abstract
The novel KIT inhibitor nilotinib is currently being evaluated for its clinical utility in the treatment of gastrointestinal stromal tumor. However, the effects of nilotinib in cells expressing commonly occurring KIT mutations remain to be fully defined. The aim of this study was therefore to investigate the efficacy of nilotinib against cells expressing imatinib-sensitive or imatinib-resistant KIT mutations and to evaluate [18F] fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging as a biomarker of nilotinib response in vivo. Nilotinib inhibited the proliferation of imatinib-responsive V560G-KIT FDC-P1 and imatinib-resistant D816V-KIT FDC-P1 cells with a GI50 of 4.9 and 630 nmol/L, respectively, whereas apoptosis studies revealed that nilotinib and imatinib were equipotent against the V560G cell line. In contrast, although 10 μmol/L nilotinib induced &gt;50% apoptosis in the D816V cells at 16 hours, 10 μmol/L imatinib had no effect on cell survival at 24 hours. Syngeneic DBA2/J mice bearing FDC-P1-KIT tumors were evaluated for response to nilotinib by FDG-PET. V560G-KIT FDC-P1 tumor FDG uptake was significantly reduced compared with baseline levels following 2 days of nilotinib treatment. In contrast, no effect of nilotinib was observed on tumor growth or FDG-PET uptake into D816V tumors despite intratumoral drug levels reaching in excess of 10 μmol/L at 4 hours after dosing. Biomarker analysis revealed the inhibition of KIT phosphorylation in V560G but not D816V tumors. These findings show the in vivo activity of nilotinib in the treatment of tumors bearing V560G-KIT but not D816V-KIT and the utility of FDG-PET imaging to assess tumor response to this agent. Mol Cancer Ther; 9(5); 1461–8. ©2010 AACR.