bluuebunny/crossref_metadata_2025_split huggingface dataset:
Propranolol, post-traumatic stress disorder and narrative identity
Authors: Bell J 
Published: October 2008

Funding:Research funded by Canadian Institutes of Health Research, NNF 80045, States of Mind: Emerging Issues in Neuroethics. While there are those who object to the prospective use of propranolol to prevent or treat post-traumatic stress disorder (PTSD), most obstreperous among them the President’s Council on Bioethics, the use of propranolol can be justified for patients with severe PTSD. Propranolol, if effective, will alter the quality of certain memories in the brain. But this is not a serious threat to the self understood in terms of narrative identity. A narrative identity framework acknowledges that memory is always being subtly altered or modified. For severe cases of PTSD propranolol may help victims who don’t respond to any other therapy or therapy combination regain their authentic self-narrative and engage once more in life activities. For those whose symptoms are not so severe the potential risks and side-effects of the drug may outweigh the benefits. Patients and family members should be allowed to decide, in consultation with their physician, whether this drug is appropriate in their case.
Cytogenetic analyses of intergeneric hybrids between barley and nine species of Elymus
Authors: Kim N.-S. , Fedak G. , Han F. , Cao W. 
Published: October 2008

Wild species in the Triticeae tribe are very valuable resources for agronomic improvement in cereal crop species. Intergeneric hybrids were produced between several barley cultivars and perennial species in the genera Elymus , Thinopyrum , and Pseudoroegneria . Caryopsis formation and subsequent plantlet regeneration from embryo culture were variable depending on the hybrid combinations. Chromosome numbers and hybrid identity were confirmed by GISH analysis on the somatic cells of the hybrids. While the hybrids showed very robust vegetative growth and exceeded the parental spikes in size, their floral morphologies resembled that of the wild species. Meiotic chromosome analysis revealed that the bivalent formation frequency per cell ranged from 0.06 in Hordeum vulgare ‘Betzes’ × Elymus curvatus to 3.0 in Elymus humidus × H. vulgare ‘Manley’. By GISH analysis on the meiocytes of the hybrid E. humidus × ‘Manley’, the frequency of autosyndetic bivalents exceeded the allosyndetic bivalent formation, which gave an insight into the genome constitution of E. humidus as an autoallohexploid species. Regardless of the low allosyndetic chromosome pairing between barley and E. humidus, this combination may be useful for further input, since E. humidus is known to carry many valuable genes for biotic and abiotic stress tolerance.
Communicating environmental geoscience; Australian communication pathways
Authors: Simpson Colin J. 
Published: October 2008

Abstract
Effectively communicating the role of geoscience in environmental, sustainable development, and sustainable resource management issues is not a straightforward process; it requires different approaches that depend upon the audience being addressed. These audiences are broadly differentiated into three groups: scientists, governments and the general public. The communication process is complicated further by the difficulty that geoscientists can have in identifying the appropriate communication pathways to use if their endeavours are to be successful. Such pathways are not generally taught during formal scientific education and, as a consequence, it may require considerable experience for individuals to understand the processes involved. The World Wide Web now makes that process much easier. As an example of the types of understanding required, this paper outlines the geoscience communication pathways that exist at present in Australia, with an emphasis on government pathways, for the communication of geoscience, both nationally and internationally. It is hoped that this Australian example may stimulate geoscientists in other countries to record and publish (in simplified formats) the appropriate pathways required for effective environmental geoscience communication in their country.
Environmental geoscience; communication challenges
Authors: Liverman David G. E. 
Published: October 2008

Abstract
Geologists whose research deals with environmental problems such as landslides, floods, earthquakes and other natural hazards that affect people's health and safety must communicate their results effectively to the public, policy-makers and politicians. There are many examples of geological studies being ignored in policy and public action; this is in due in part to geoscientists being poor communicators. Scientists often use complicated and difficult to understand language, talk mostly to other scientists, and are not trained to work with the media. They generally are not encouraged by their employers and funding agencies to communicate to non-scientists. Environmental geoscientists must make their research publications more accessible to the public by including plain-language summaries. They should work with media and communications professionals, and seek training in how to communicate better. They need to understand the different approaches that will work with different audiences. Universities, employers and funding agencies should encourage environmental geoscientists to improve communication skills, and to reward attempts to explain their research to non-scientists.
Altered priorities ahead; or how to develop fruitful relationships with the media
Authors: Nield Ted 
Published: October 2008

Abstract
This paper examines the conflict between scientists' usual conception of the media and the reality of working successfully with them when transmitting research findings. It suggests that if scientists rid themselves of some common misconceptions, they can begin to engage more effectively with the news media. By always bearing in mind two crucial facts (that the news media are not going to change the way they work to please scientists, and that they should be approached as a branch of the entertainment industry) all subsequent decisions and behaviours on the part of scientists and their companies or institutions will be more likely to be blessed with success. It concludes by reporting some case histories, as worked examples of how scientific institutions can promote themselves through their research by harnessing the potent power of enlightened self-interest.
Guidelines for landslide hazard mapping in the Andes: speaking one language
Authors:   Multinational Andean Project: Geosciences for Andean Communities GEMMA—Landslide Hazard Standards Group
Published: October 2008

Abstract

To maximize the use of geoscience information across institutions and international borders, data must be collected and stored in a uniform manner so that they are readily accessible and understandable. There is seldom consistency in the representation of these data delivered to users between countries (and, sometimes, even within institutions in the same country). The Multinational Andean Project: Geosciences for Andean Communities (MAP:GAC (2002–2008)), identified the need to research, design and develop a common terminology, techniques, classification system, cartographic symbols and databases for landslide studies. MAP:GAC produced regional guides for landslide studies and mapping, through the first regional group for landslide studies (GEMMA). It is expected that these guides will facilitate the transfer and appropriation of information, and that the generation of products will be more easily understood and applied by land-use planners, emergency-management planners and other users. The standards have been adopted by the seven Andean countries (Argentina, Bolivia, Chile, Colombia, Ecuador, Peru and Venezuela) and were published in the book
Movimientos en Masa en la Región Andina: Una Guía para la Evaluación de Amenazas
(
Landslide Hazards in the Andes
) in 2007.
GeoSure; a bridge between geology and decision-makers
Authors: Walsby Jennifer C. 
Published: October 2008

Abstract
How many people understand a geological map and use it to assess the ground on which they live or plan to develop? How many town planners, house owners or insurers know that geologists can identify areas prone to flooding, radon gas emissions, landslides and subsidence? Do decision-makers understand the relevance of geology? Concerned about these questions, geological and geographic information system (GIS) professionals at the British Geological Survey (BGS) have created datasets that make information about geological hazards (‘geohazards’) easy to obtain, use and understand. The term ‘geohazard’ is emotive. Many people think of natural hazards as being large-scale disasters, such as tsunami and major earthquakes. Appropriate terminology is required to explain the relevance of factors such as the potential cost and health implications of the usually less dramatic British geohazards. Using the vast data holdings and geoscientific knowledge within BGS and building on past thematic mapping activities, a series of national geohazard datasets has been developed. GIS datasets with ‘plain English’ descriptions have been created for natural gas emissions, landslides, swell–shrink clays, compressible and collapsible deposits, soluble rocks, running sands and groundwater flooding. Geological information is thus brought before a wider audience and in a form that reveals to the British public and industry how geology can be used in conjunction with other information and why it is relevant to their lives.
A History of Cancer Chemotherapy
Authors: DeVita Vincent T. , Chu Edward 
Published: October 2008

AbstractThe use of chemotherapy to treat cancer began at the start of the 20th century with attempts to narrow the universe of chemicals that might affect the disease by developing methods to screen chemicals using transplantable tumors in rodents. It was, however, four World War II–related programs, and the effects of drugs that evolved from them, that provided the impetus to establish in 1955 the national drug development effort known as the Cancer Chemotherapy National Service Center. The ability of combination chemotherapy to cure acute childhood leukemia and advanced Hodgkin's disease in the 1960s and early 1970s overcame the prevailing pessimism about the ability of drugs to cure advanced cancers, facilitated the study of adjuvant chemotherapy, and helped foster the national cancer program. Today, chemotherapy has changed as important molecular abnormalities are being used to screen for potential new drugs as well as for targeted treatments. [Cancer Res 2008;68(21):8643–53]
Tumor Regression in Mice by Delivery of Bcl-2 Small Interfering RNA with Pegylated Cationic Liposomes
Authors: Sonoke Satoru , Ueda Toshihiro , Fujiwara Kae , Sato Yohei , Takagaki Kazuchika , Hirabayashi Kazuko , Ohgi Tadaaki , Yano Junichi 
Published: October 2008

AbstractThe pharmacokinetics and antitumor activity of pegylated small interfering RNA (siRNA)/cationic liposome complexes were studied after systemic administration to mice. We designed pegylated-lipid carriers for achieving increased plasma concentrations of RNA and hence improved accumulation of RNA in tumors by the enhanced permeability and retention effect. We compared the pharmacokinetics of siRNA complexed with liposomes incorporating pegylated lipids with longer (C-17 or C-18), shorter (C-12 to C-16), or unsaturated (C-18:1) acyl chains. When longer acyl chains were used, the plasma concentrations of siRNA obtained were dramatically higher than when shorter or unsaturated chains were used. This may be explained by the higher gel-to-liquid-crystalline phase-transition temperature (Tc) of lipids with longer acyl chains, which may form more rigid liposomes with reduced uptake by the liver. We tested a siRNA that is sequence specific for the antiapoptotic bcl-2 mRNA complexed with a pegylated liposome incorporating a C-18 lipid (PEG-LIC) by i.v. administration in a mouse model of human prostate cancer. Three-fold higher accumulation of RNA in the tumors was achieved when PEG-LIC rather than nonpegylated liposomes was used, and sequence-specific antitumor activity was observed. Our siRNA/PEG-LIC complex showed no side effects on repeated administration and the strength of its antitumor activity may be attributed to its high uptake by the tumors. Pegylation of liposomes improved the plasma retention, uptake by s.c. tumors, and antitumor activity of the encapsulated siRNA. PEG-LIC is a promising candidate for siRNA cancer therapy. [Cancer Res 2008;68(21):8843–51]
Bryostatin-5 Blocks Stromal Cell–Derived Factor-1 Induced Chemotaxis via Desensitization and Down-regulation of Cell Surface CXCR4 Receptors
Authors: He Xing , Fang Liyan , Wang Jue , Yi Yanghua , Zhang Shuyu , Xie Xin 
Published: October 2008

AbstractThe chemokine receptor CXCR4 and its ligand, stromal cell–derived factor-1 (SDF-1), play important roles in hematopoiesis regulation, lymphocyte activation, and trafficking, as well as in developmental processes, including organogenesis, vascularization, and embryogenesis. The receptor is also involved in HIV infection and tumor growth and metastasis. Antagonists of CXCR4 have been widely evaluated for drugs against HIV and tumors. In an effort to identify novel CXCR4 antagonists, we screened a small library of compounds derived from marine organisms and found bryostatin-5, which potently inhibits chemotaxis induced by SDF-1 in Jurkat cells. Bryostatin-5 is a member of the macrolactones, and its analogue bryostatin-1 is currently being evaluated in clinical trials for its chemotherapeutic potential. The involvement of bryostatins in the SDF-1/CXCR4 signaling process has never been reported. In this study, we found that bryostatin-5 potently inhibits SDF-1–induced chemotaxis but does not affect serum-induced chemotaxis. Further studies indicate that this inhibitory effect is not due to receptor antagonism but rather to bryostatin-5–induced receptor desensitization and down-regulation of cell surface CXCR4. We also show that these effects are mediated by the activation of conventional protein kinase C. [Cancer Res 2008;68(21):8678–86]
Endogenous Interleukin-4 Promotes Tumor Development by Increasing Tumor Cell Resistance to Apoptosis
Authors: Li Zhiguang , Jiang Jing , Wang Zibing , Zhang Jinhua , Xiao Mingjie , Wang Chunhui , Lu Yu , Qin Zhihai 
Published: October 2008

AbstractThe increase of interleukin-4 (IL-4) level in tumor environment and the up-regulation of IL-4 receptor (IL-4R) on tumor cells have been long observed. However, their significance for tumor development has not been investigated. Here, we found that endogenous IL-4 promotes tumor growth because neutralizing IL-4 by 11B11 monoclonal antibody (mAb) significantly delayed the growth of MCA205 fibrosarcoma. We also observed that tumor cells with higher IL-4R expression have more chances to survive in immunocompetent mice. To investigate how endogenous IL-4 influences tumor growth, we established a pair of tumor cells with or without IL-4R expression from the common parental cells. IL-4R–competent tumors exhibit increased growth compared with its IL-4R–deficient counterparts when inoculated into syngeneic mice. This growth advantage was still kept in IL-4R knockout mice but was abrogated in mice given i.p. with IL-4 neutralizing mAb. In vitro analyses indicate that IL-4 neither affects the proliferation of tumor cells nor changes the expression of several immune-related molecules, such as MHC-I, Fas, and B7-H3. Nonetheless, IL-4 up-regulates antiapoptotic gene expression in tumor cells and reduces apoptosis of tumor cells in vivo, as evidenced by real-time PCR, immunoblotting, and TUNEL staining. These findings were helpful to understand the long clinical observation and revealed that endogenous IL-4, the product of host immune response, can be used by tumor cells to facilitate their growth. [Cancer Res 2008;68(21):8687–94]
Identification of Pbx1, a Potential Oncogene, as a Notch3 Target Gene in Ovarian Cancer
Authors: Park Joon T. , Shih Ie-Ming , Wang Tian-Li 
Published: October 2008

Abstract
Notch3 gene amplification has recently been identified in ovarian cancer but the Notch3 effectors that are involved in the development of ovarian cancer remain elusive. In this study, we have identified Pbx1, a proto-oncogene in hematopoietic malignancy, as a Notch3 target gene. Pbx1 expression is transcriptionally regulated by Notch3 activation, and Notch3/CSL protein complex directly binds to the Pbx1 promoter segment harboring the CSL-binding sequence. The growth-inhibitory effect of γ-secretase inhibitor could be partially reversed by ectopic Pbx1 expression. Furthermore, functional studies by Pbx1 short hairpin RNA knockdown show that Pbx1 is essential for cell proliferation and tumorigenicity. Taken together, the above findings indicate that Pbx1 is a direct Notch3-regulated gene that mediates the survival signal of Notch3 in ovarian cancer. [Cancer Res 2008;68(21):8852–60]
EWS-FLI1 Induces Developmental Abnormalities and Accelerates Sarcoma Formation in a Transgenic Mouse Model
Authors: Lin Patrick P. , Pandey Manoj K. , Jin Fenghua , Xiong Shunbin , Deavers Michael , Parant John M. , Lozano Guillermina 
Published: October 2008

Abstract
Ewing's sarcoma is characterized by the t(11;22)(q24:q12) reciprocal translocation. To study the effects of the fusion gene EWS-FLI1 on development and tumor formation, a transgenic mouse model was created. A strategy of conditional expression was used to limit the potentially deleterious effects of EWS-FLI1 to certain tissues. In the absence of Cre recombinase, EWS-FLI1 was not expressed in the EWS-FLI1 transgenic mice, and they had a normal phenotype. When crossed to the Prx1-Cre transgenic mouse, which expresses Cre recombinase in the primitive mesenchymal cells of the embryonic limb bud, the EF mice were noted to have a number of developmental defects of the limbs. These included shortening of the limbs, muscle atrophy, cartilage dysplasia, and immature bone. By itself, EWS-FLI1 did not induce the formation of tumors in the EF transgenic mice. However, in the setting of p53 deletion, EWS-FLI1 accelerated the formation of sarcomas from a median time of 50 to 21 weeks. Furthermore, EWS-FLI1 altered the type of tumor that formed. Conditional deletion of p53 in mesenchymal cells (Prx1-Cre p53lox/lox) produced osteosarcomas as the predominant tumor. The presence of EWS-FLI1 shifted the tumor phenotype to a poorly differentiated sarcoma. The results taken together suggest that EWS-FLI1 inhibits normal limb development and accelerates the formation of poorly differentiated sarcomas. [Cancer Res 2008;68(21):8968–75]
Roles for MicroRNAs, miR-93 and miR-130b, and Tumor Protein 53–Induced Nuclear Protein 1 Tumor Suppressor in Cell Growth Dysregulation by Human T-Cell Lymphotrophic Virus 1
Authors: Yeung Man Lung , Yasunaga Jun-ichirou , Bennasser Yamina , Dusetti Nelson , Harris David , Ahmad Nafees , Matsuoka Masao , Jeang Kuan-Teh 
Published: October 2008

AbstractA role for microRNAs (miRNA) in human T-cell leukemia virus 1 (HTLV-1)–mediated cellular transformation has not been described. Here, we profiled miRNA expression in HTLV-1–transformed human T-cell lines and primary peripheral blood mononuclear cells from adult T-cell leukemia patients. Analyses of 11 different profiles revealed six miRNAs that were consistently up-regulated. Two of the up-regulated miRNAs (miR-93 and miR-130b) target the 3′ untranslated region (3′UTR) of the mRNA for a tumor suppressor protein, tumor protein 53–induced nuclear protein 1 (TP53INP1). A low expression level of TP53INP1 protein was found in HTLV-1–transformed cells. Additionally, when antagomirs were used to knock down miR-93 and miR-130b in these cells, the expression of TP53INP1 was increased, suggesting that the latter is regulated inside cells by the former. A role for TP53INP1 in regulating cell growth was established by experiments that showed that enhanced TP53INP1 expression increased apoptosis. Collectively, the findings implicate a miR-93/miR-130b-TP53INP1 axis that affects the proliferation and survival of HTLV-1–infected/transformed cells. [Cancer Res 2008;68(21):8976–85]
p37Ing1b Regulates B-Cell Proliferation and Cooperates with p53 to Suppress Diffuse Large B-Cell Lymphomagenesis
Authors: Coles Andrew H. , Marfella Concetta G.A. , Imbalzano Anthony N. , Steinman Heather A. , Garlick David S. , Gerstein Rachel M. , Jones Stephen N. 
Published: October 2008

Abstract
The Inhibitor of Growth (ING) gene family encodes structurally related proteins that alter chromatin to regulate gene expression and cell growth. The initial member, ING1, has also been proposed to function as a tumor suppressor in human cancer based on its ability to suppress cell growth and transformation in vitro. Mouse Ing1 produces two proteins (p31 and p37) from differentially spliced transcripts. We have recently generated p37Ing1b-null mice and observed spontaneous follicular B-cell lymphomagenesis in this model to show that ING proteins can function in vivo as tumor suppressors. In this present report, we examine the role of p37Ing1b in the regulation of B-cell growth and explore the relationship between p37Ing1b and p53-mediated tumor suppression. Our results indicate that p37Ing1b inhibits the proliferation of B cells and follicular B cells regardless of p53 status, and loss of p53 greatly accelerates the rate of B-cell lymphomagenesis in p37Ing1b-null mice. However, in contrast to the highly penetrant follicular B-cell lymphomas observed in p37Ing1b-null mice, mice lacking both p37Ing1b and p53 typically present with aggressive diffuse large B-cell lymphomas (DLBL). Analysis of marker gene expression in p37Ing1b/p53 null tumors indicates that the double-null mice develop both nongerminal center and germinal center B-cell–like DLBL, and also documents up-regulation of nuclear factor-κB activity in p37Ing1b/p53-null B cells and B-cell tumors. These results confirm that p53 mutation is an important mechanistic step in the formation of diffuse large B-cell lymphomas and reveals a p53-independent role for Ing1b in suppressing B-cell tumorigenesis. [Cancer Res 2008;68(21):8705–14]
Deleted in Liver Cancer 1 Controls Cell Migration through a Dia1-Dependent Signaling Pathway
Authors: Holeiter Gerlinde , Heering Johanna , Erlmann Patrik , Schmid Simone , Jähne Ruth , Olayioye Monilola A. 
Published: October 2008

Abstract
Deleted in liver cancer (DLC) 1 and 2 are Rho GTPase-activating proteins that are frequently down-regulated in various types of cancer. Ectopic expression in carcinoma cell lines lacking these proteins has been shown to inhibit cell migration and invasion. However, whether the loss of DLC1 or DLC2 is the cause of aberrant Rho signaling in transformed cells has not been investigated. Here, we have down-regulated DLC1 and DLC2 expression in breast cancer cells using a RNA interference approach. Silencing of DLC1 led to the stabilization of stress fibers and focal adhesions and enhanced cell motility in wound-healing as well as chemotactic Transwell assays. We provide evidence that enhanced migration of cells lacking DLC1 is dependent on the Rho effector protein Dia1 but does not require the activity of Rho kinase. By contrast, DLC2 knockdown failed to affect the migratory behavior of cells, suggesting that the two proteins have distinct functions. This is most likely due to their differential subcellular localizations, with DLC1 found in focal adhesions and DLC2 being mainly cytosolic. Collectively, our data show that DLC1 is critically involved in the control of Rho signaling and actin cytoskeleton remodeling and that its cellular loss is sufficient for the acquisition of a more migratory phenotype of breast cancer cells. [Cancer Res 2008;68(21):8743–51]