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  • 1
    Publication Date: 2011-06-28
    Description: Author(s): A. R. Lopes, S. d’A. Sanchez, and M. H. F. Bettega In this work, we present integral, differential, and momentum transfer cross sections for elastic scattering of low-energy electrons by nitromethane, for energies up to 10 eV. We calculated the cross sections using the Schwinger multichannel method with pseudopotentials, in the static-exchange and i... [Phys. Rev. A 83, 062713] Published Mon Jun 27, 2011
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 2
    Publication Date: 2012-08-21
    Description: Author(s): Eliane M. de Oliveira, Sergio d’A. Sanchez, Márcio H. F. Bettega, Alexandra P. P. Natalense, Marco A. P. Lima, and Márcio T. do N. Varella We report integral cross sections for elastic electron scattering by the lignin subunits phenol, guaiacol, and p -coumaryl alcohol. Our calculations employed the Schwinger multichannel method with pseudopotentials and indicate three to four π * shape resonances for each of these systems, suggesting th... [Phys. Rev. A 86, 020701] Published Mon Aug 20, 2012
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 3
    Publication Date: 2012-04-12
    Description: Author(s): A. R. Lopes, M. H. F. Bettega, and S. d’A. Sanchez In this work, we present integral cross sections for elastic scattering of low-energy electrons by the nitro compounds nitroethylene, nitroethane, and 1-nitropropane, for energies up to 8 eV. We calculated the scattering cross sections using the Schwinger multichannel method with pseudopotentials in... [Phys. Rev. A 85, 044701] Published Wed Apr 11, 2012
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 4
    Publication Date: 2012-08-16
    Description: Author(s): Márcio H. F. Bettega, Sergio d'A. Sanchez, Márcio T. do N. Varella, Marco A. P. Lima, Luca Chiari, Antonio Zecca, Emanuele Trainotti, and Michael J. Brunger We present experimental and theoretical cross sections for positron collisions with ethene molecules. The experimental total cross sections (TCSs) were obtained with a linear transmission technique, for energies from 0.1 eV up to 70 eV. The calculations employed the Schwinger multichannel method and... [Phys. Rev. A 86, 022709] Published Wed Aug 15, 2012
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 5
    Publication Date: 2011-12-28
    Description: Author(s): T. C. Freitas, S. d’A. Sanchez, M. T. do N. Varella, and M. H. F. Bettega [Phys. Rev. A 84, 062714] Published Tue Dec 27, 2011
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 6
    Publication Date: 2012-01-20
    Description: Author(s): A. Zecca, L. Chiari, E. Trainotti, A. Sarkar, S. d’A. Sanchez, M. H. F. Bettega, M. T. do N. Varella, M. A. P. Lima, and M. J. Brunger We report on measurements of total cross sections for positron scattering from the fundamental organic molecule methane (CH 4 ). The energy range of these measurements was 0.1–50 eV, whereas the energy resolution was ∼ 100 meV when our Ni moderator was used and ∼ 260 meV when the W moderator was employe... [Phys. Rev. A 85, 012707] Published Thu Jan 19, 2012
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 7
    Publication Date: 2010-06-29
    Description: The accumulation of species-specific enemies around adults is hypothesized to maintain plant diversity by limiting the recruitment of conspecific seedlings relative to heterospecific seedlings. Although previous studies in forested ecosystems have documented patterns consistent with the process of negative feedback, these studies are unable to address which classes of enemies (for example, pathogens, invertebrates, mammals) exhibit species-specific effects strong enough to generate negative feedback, and whether negative feedback at the level of the individual tree is sufficient to influence community-wide forest composition. Here we use fully reciprocal shade-house and field experiments to test whether the performance of conspecific tree seedlings (relative to heterospecific seedlings) is reduced when grown in the presence of enemies associated with adult trees. Both experiments provide strong evidence for negative plant-soil feedback mediated by soil biota. In contrast, above-ground enemies (mammals, foliar herbivores and foliar pathogens) contributed little to negative feedback observed in the field. In both experiments, we found that tree species that showed stronger negative feedback were less common as adults in the forest community, indicating that susceptibility to soil biota may determine species relative abundance in these tropical forests. Finally, our simulation models confirm that the strength of local negative feedback that we measured is sufficient to produce the observed community-wide patterns in tree-species relative abundance. Our findings indicate that plant-soil feedback is an important mechanism that can maintain species diversity and explain patterns of tree-species relative abundance in tropical forests.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mangan, Scott A -- Schnitzer, Stefan A -- Herre, Edward A -- Mack, Keenan M L -- Valencia, Mariana C -- Sanchez, Evelyn I -- Bever, James D -- R01 GM092660/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):752-5. doi: 10.1038/nature09273.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Wisconsin-Milwaukee, Wisconsin 53201, USA. smangan37@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20581819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Biomass ; Computer Simulation ; Feedback, Physiological ; Food Chain ; Insects/physiology ; Models, Biological ; Panama ; Population Density ; Seedlings/growth & development ; Soil/*analysis ; *Soil Microbiology ; Species Specificity ; Trees/*classification/*growth & development/microbiology/parasitology ; *Tropical Climate ; Vertebrates/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2010-10-22
    Description: Circadian rhythms allow organisms to time biological processes to the most appropriate phases of the day-night cycle. Post-transcriptional regulation is emerging as an important component of circadian networks, but the molecular mechanisms linking the circadian clock to the control of RNA processing are largely unknown. Here we show that PROTEIN ARGININE METHYL TRANSFERASE 5 (PRMT5), which transfers methyl groups to arginine residues present in histones and Sm spliceosomal proteins, links the circadian clock to the control of alternative splicing in plants. Mutations in PRMT5 impair several circadian rhythms in Arabidopsis thaliana and this phenotype is caused, at least in part, by a strong alteration in alternative splicing of the core-clock gene PSEUDO RESPONSE REGULATOR 9 (PRR9). Furthermore, genome-wide studies show that PRMT5 contributes to the regulation of many pre-messenger-RNA splicing events, probably by modulating 5'-splice-site recognition. PRMT5 expression shows daily and circadian oscillations, and this contributes to the mediation of the circadian regulation of expression and alternative splicing of a subset of genes. Circadian rhythms in locomotor activity are also disrupted in dart5-1, a mutant affected in the Drosophila melanogaster PRMT5 homologue, and this is associated with alterations in splicing of the core-clock gene period and several clock-associated genes. Our results demonstrate a key role for PRMT5 in the regulation of alternative splicing and indicate that the interplay between the circadian clock and the regulation of alternative splicing by PRMT5 constitutes a common mechanism that helps organisms to synchronize physiological processes with daily changes in environmental conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Sabrina E -- Petrillo, Ezequiel -- Beckwith, Esteban J -- Zhang, Xu -- Rugnone, Matias L -- Hernando, C Esteban -- Cuevas, Juan C -- Godoy Herz, Micaela A -- Depetris-Chauvin, Ana -- Simpson, Craig G -- Brown, John W S -- Cerdan, Pablo D -- Borevitz, Justin O -- Mas, Paloma -- Ceriani, M Fernanda -- Kornblihtt, Alberto R -- Yanovsky, Marcelo J -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 4;468(7320):112-6. doi: 10.1038/nature09470. Epub 2010 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IFEVA, Facultad de Agronomia, UBA-CONICET, C1417DSE Buenos Aires, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962777" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Arabidopsis/enzymology/genetics/*physiology/radiation effects ; Arabidopsis Proteins/genetics/*metabolism ; Base Sequence ; Circadian Clocks/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Darkness ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/enzymology/genetics/*physiology/radiation effects ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Light ; Methylation ; Mutation ; Period Circadian Proteins/genetics ; Phenotype ; Protein Methyltransferases/genetics/*metabolism ; Protein-Arginine N-Methyltransferases/genetics/*metabolism ; RNA Precursors/genetics/metabolism ; RNA Splice Sites/genetics ; RNA, Messenger/genetics/metabolism ; Spliceosomes/metabolism ; Transcription Factors/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2010-06-25
    Description: The early development of teleost paired fins is strikingly similar to that of tetrapod limb buds and is controlled by similar mechanisms. One early morphological divergence between pectoral fins and limbs is in the fate of the apical ectodermal ridge (AER), the distal epidermis that rims the bud. Whereas the AER of tetrapods regresses after specification of the skeletal progenitors, the AER of teleost fishes forms a fold that elongates. Formation of the fin fold is accompanied by the synthesis of two rows of rigid, unmineralized fibrils called actinotrichia, which keep the fold straight and guide the migration of mesenchymal cells within the fold. The actinotrichia are made of elastoidin, the components of which, apart from collagen, are unknown. Here we show that two zebrafish proteins, which we name actinodin 1 and 2 (And1 and And2), are essential structural components of elastoidin. The presence of actinodin sequences in several teleost fishes and in the elephant shark (Callorhinchus milii, which occupies a basal phylogenetic position), but not in tetrapods, suggests that these genes have been lost during tetrapod species evolution. Double gene knockdown of and1 and and2 in zebrafish embryos results in the absence of actinotrichia and impaired fin folds. Gene expression profiles in embryos lacking and1 and and2 function are consistent with pectoral fin truncation and may offer a potential explanation for the polydactyly observed in early tetrapod fossils. We propose that the loss of both actinodins and actinotrichia during evolution may have led to the loss of lepidotrichia and may have contributed to the fin-to-limb transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jing -- Wagh, Purva -- Guay, Danielle -- Sanchez-Pulido, Luis -- Padhi, Bhaja K -- Korzh, Vladimir -- Andrade-Navarro, Miguel A -- Akimenko, Marie-Andree -- MC_U137761446/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jul 8;466(7303):234-7. doi: 10.1038/nature09137. Epub 2010 Jun 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CAREG, Department of Biology, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20574421" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Structures/*anatomy & histology/embryology/*physiology ; Animals ; *Biological Evolution ; Collagen/chemistry/metabolism ; Ectoderm/embryology/metabolism ; Embryo, Nonmammalian/anatomy & histology/embryology/metabolism ; Evolution, Molecular ; Extremities/anatomy & histology/embryology/*physiology ; Fish Proteins/*deficiency/genetics/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Limb Buds/anatomy & histology/embryology/metabolism ; Models, Biological ; Phylogeny ; Zebrafish/*anatomy & histology/embryology/genetics/*metabolism ; Zebrafish Proteins/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2010-11-26
    Description: Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumour suppressor pathways. Personalized cancer therapy that is based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumour suppressors and activation of oncogenes is essential in advanced cancers. Mutations in the p53 tumour-suppressor pathway are common in human cancer and significant efforts towards pharmaceutical reactivation of defective p53 pathways are underway. Here we show that restoration of p53 in established murine lung tumours leads to significant but incomplete tumour cell loss specifically in malignant adenocarcinomas, but not in adenomas. We define amplification of MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumour-suppressor expression. The response to p53 restoration in this context is critically dependent on the expression of Arf. We propose that p53 not only limits malignant progression by suppressing the acquisition of alterations that lead to tumour progression, but also, in the context of p53 restoration, responds to increased oncogenic signalling to mediate tumour regression. Our observations also underscore that the p53 pathway is not engaged by low levels of oncogene activity that are sufficient for early stages of lung tumour development. These data suggest that restoration of pathways important in tumour progression, as opposed to initiation, may lead to incomplete tumour regression due to the stage-heterogeneity of tumour cell populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003305/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003305/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feldser, David M -- Kostova, Kamena K -- Winslow, Monte M -- Taylor, Sarah E -- Cashman, Chris -- Whittaker, Charles A -- Sanchez-Rivera, Francisco J -- Resnick, Rebecca -- Bronson, Roderick -- Hemann, Michael T -- Jacks, Tyler -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-37/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30 CA014051-39/CA/NCI NIH HHS/ -- P30 CA014051-40/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 25;468(7323):572-5. doi: 10.1038/nature09535.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, Department of Biology, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107428" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/metabolism/*physiopathology ; Adenoma/metabolism/*physiopathology ; Animals ; Cell Proliferation ; *Disease Progression ; Lung Neoplasms/*physiopathology ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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