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  • 1
    Publication Date: 2012-10-03
    Description: Author(s): J. C. Cressoni, G. M. Viswanathan, A. S. Ferreira, and M. A. A. da Silva A non-Markovian one-dimensional random walk model is studied with emphasis on the phase-diagram, showing all the diffusion regimes, along with the exactly determined critical lines. The model, known as the Alzheimer walk, is endowed with memory-controlled diffusion, responsible for the model's long-... [Phys. Rev. E 86, 042101] Published Tue Oct 02, 2012
    Keywords: Statistical physics
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 2
    Publication Date: 2012-09-25
    Description: Author(s): S. A. Sotelo-López, M. C. Santos, E. P. Raposo, G. M. Viswanathan, and M. G. E. da Luz Intuitively, lower target densities and lower detection capabilities should demand more sophisticated search strategies for a random search reasonable outcome. In contrast, when targets are easily found, a simple Brownian random walk strategy is enough. But where is the threshold between these two s... [Phys. Rev. E 86, 031133] Published Mon Sep 24, 2012
    Keywords: Statistical physics
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 3
    Publication Date: 2012-12-05
    Description: Author(s): P. J. Ribeiro-Neto, E. P. Raposo, H. A. Araújo, C. L. Faustino, M. G. E. da Luz, and G. M. Viswanathan We investigate the problem of survival at the very low target-density limit and report on a second-order phase transition for one-dimensional random searches in which the energy cost of locomotion is a function of the distance traveled by the searcher. Surprisingly, from analytical calculations (als... [Phys. Rev. E 86, 061102] Published Tue Dec 04, 2012
    Keywords: Statistical physics
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 4
    Publication Date: 2012-08-28
    Description: Author(s): J. C. Cressoni, G. M. Viswanathan, A. S. Ferreira, and M. A. A. da Silva A poorly understood phenomenon seen in complex systems is diffusion characterized by Hurst exponent H ≈1/2 but with non-Gaussian statistics. Motivated by such empirical findings, we report an exact analytical solution for a non-Markovian random walk model that gives rise to weakly anomalous diffusion... [Phys. Rev. E 86, 022103] Published Mon Aug 27, 2012
    Keywords: Statistical physics
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 5
    Publication Date: 2009-07-07
    Description: The rarity and inaccessibility of the earliest primordial germ cells (PGCs) in the mouse embryo thwart efforts to investigate molecular mechanisms of germ-cell specification. stella (also called Dppa3) marks the rare founder population of the germ lineage. Here we differentiate mouse embryonic stem cells carrying a stella transgenic reporter into putative PGCs in vitro. The Stella(+) cells possess a transcriptional profile similar to embryo-derived PGCs, and like their counterparts in vivo, lose imprints in a time-dependent manner. Using inhibitory RNAs to screen candidate genes for effects on the development of Stella(+) cells in vitro, we discovered that Lin28, a negative regulator of let-7 microRNA processing, is essential for proper PGC development. Furthermore, we show that Blimp1 (also called Prdm1), a let-7 target and a master regulator of PGC specification, can rescue the effect of Lin28 deficiency during PGC development, thereby establishing a mechanism of action for Lin28 during PGC specification. Overexpression of Lin28 promotes formation of Stella(+) cells in vitro and PGCs in chimaeric embryos, and is associated with human germ-cell tumours. The differentiation of putative PGCs from embryonic stem cells in vitro recapitulates the early stages of gamete development in vivo, and provides an accessible system for discovering novel genes involved in germ-cell development and malignancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729657/" 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/PMC2729657/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Jason A -- Viswanathan, Srinivas R -- Yabuuchi, Akiko -- Cunniff, Kerianne -- Takeuchi, Ayumu -- Park, In-Hyun -- Sero, Julia E -- Zhu, Hao -- Perez-Atayde, Antonio -- Frazier, A Lindsay -- Surani, M Azim -- Daley, George Q -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- G0300723/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Aug 13;460(7257):909-13. doi: 10.1038/nature08210. Epub 2009 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and the Dana-Farber Cancer Institute, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19578360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Line ; Embryonic Stem Cells/cytology/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Germ Cells/*cytology/*metabolism/pathology ; Humans ; Mice ; Mice, Inbred C57BL ; Neoplasms, Germ Cell and Embryonal/genetics/*metabolism/*pathology ; RNA-Binding Proteins/genetics/*metabolism ; Repressor Proteins/genetics/metabolism ; Transcription Factors/metabolism ; Transgenes
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2009-11-11
    Description: Rapid antigenic evolution in the influenza A virus hemagglutinin precludes effective vaccination with existing vaccines. To understand this phenomenon, we passaged virus in mice immunized with influenza vaccine. Neutralizing antibodies selected mutants with single-amino acid hemagglutinin substitutions that increased virus binding to cell surface glycan receptors. Passaging these high-avidity binding mutants in naive mice, but not immune mice, selected for additional hemagglutinin substitutions that decreased cellular receptor binding avidity. Analyzing a panel of monoclonal antibody hemagglutinin escape mutants revealed a positive correlation between receptor binding avidity and escape from polyclonal antibodies. We propose that in response to variation in neutralizing antibody pressure between individuals, influenza A virus evolves by adjusting receptor binding avidity via amino acid substitutions throughout the hemagglutinin globular domain, many of which simultaneously alter antigenicity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" 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/PMC2784927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensley, Scott E -- Das, Suman R -- Bailey, Adam L -- Schmidt, Loren M -- Hickman, Heather D -- Jayaraman, Akila -- Viswanathan, Karthik -- Raman, Rahul -- Sasisekharan, Ram -- Bennink, Jack R -- Yewdell, Jonathan W -- GM 57073/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- Z01 AI001014-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):734-6. doi: 10.1126/science.1178258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900932" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Antigenic Variation/genetics/*immunology ; Cell Line ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology/*metabolism ; Influenza A Virus, H1N1 Subtype/genetics/*immunology ; Influenza Vaccines/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Immunological ; Mutation ; Receptors, Virus/*metabolism ; Serial Passage
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2008-02-23
    Description: MicroRNAs (miRNAs) play critical roles in development, and dysregulation of miRNA expression has been observed in human malignancies. Recent evidence suggests that the processing of several primary miRNA transcripts (pri-miRNAs) is blocked posttranscriptionally in embryonic stem cells, embryonal carcinoma cells, and primary tumors. Here we show that Lin28, a developmentally regulated RNA binding protein, selectively blocks the processing of pri-let-7 miRNAs in embryonic cells. Using in vitro and in vivo studies, we found that Lin28 is necessary and sufficient for blocking Microprocessor-mediated cleavage of pri-let-7 miRNAs. Our results identify Lin28 as a negative regulator of miRNA biogenesis and suggest that Lin28 may play a central role in blocking miRNA-mediated differentiation in stem cells and in certain cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368499/" 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/PMC3368499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viswanathan, Srinivas R -- Daley, George Q -- Gregory, Richard I -- DK70055/DK/NIDDK NIH HHS/ -- DP1 OD000256/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 4;320(5872):97-100. doi: 10.1126/science.1154040. Epub 2008 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Harvard Stem Cell Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18292307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Embryonal ; Cell Differentiation ; Cell Line, Transformed ; Cell Line, Tumor ; Cellular Reprogramming ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Embryonic Stem Cells/cytology/*metabolism ; Humans ; Mice ; MicroRNAs/*metabolism ; Pluripotent Stem Cells/cytology/metabolism ; Protein Binding ; RNA Interference ; *RNA Processing, Post-Transcriptional ; RNA-Binding Proteins/genetics/*metabolism ; Ribonuclease III/metabolism ; Transfection ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2009-07-04
    Description: Recent reports of mild to severe influenza-like illness in humans caused by a novel swine-origin 2009 A(H1N1) influenza virus underscore the need to better understand the pathogenesis and transmission of these viruses in mammals. In this study, selected 2009 A(H1N1) influenza isolates were assessed for their ability to cause disease in mice and ferrets and compared with a contemporary seasonal H1N1 virus for their ability to transmit to naive ferrets through respiratory droplets. In contrast to seasonal influenza H1N1 virus, 2009 A(H1N1) influenza viruses caused increased morbidity, replicated to higher titers in lung tissue, and were recovered from the intestinal tract of intranasally inoculated ferrets. The 2009 A(H1N1) influenza viruses exhibited less efficient respiratory droplet transmission in ferrets in comparison with the highly transmissible phenotype of a seasonal H1N1 virus. Transmission of the 2009 A(H1N1) influenza viruses was further corroborated by characterizing the binding specificity of the viral hemagglutinin to the sialylated glycan receptors (in the human host) by use of dose-dependent direct receptor-binding and human lung tissue-binding assays.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2953552/" 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/PMC2953552/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maines, Taronna R -- Jayaraman, Akila -- Belser, Jessica A -- Wadford, Debra A -- Pappas, Claudia -- Zeng, Hui -- Gustin, Kortney M -- Pearce, Melissa B -- Viswanathan, Karthik -- Shriver, Zachary H -- Raman, Rahul -- Cox, Nancy J -- Sasisekharan, Ram -- Katz, Jacqueline M -- Tumpey, Terrence M -- GM 57073/GM/NIGMS NIH HHS/ -- R01 GM057073/GM/NIGMS NIH HHS/ -- R01 GM057073-09/GM/NIGMS NIH HHS/ -- R37 GM057073/GM/NIGMS NIH HHS/ -- U54 GM062116/GM/NIGMS NIH HHS/ -- U54 GM062116-09/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):484-7. doi: 10.1126/science.1177238. Epub 2009 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574347" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Disease Models, Animal ; Female ; Ferrets ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/metabolism ; Humans ; Influenza A Virus, H1N1 Subtype/*pathogenicity ; Influenza, Human/transmission/*virology ; Intestines/virology ; Male ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Orthomyxoviridae Infections/*transmission/*virology ; Protein Binding ; Receptors, Virus/metabolism ; Respiratory System/virology ; Swine ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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