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  • Models, Biological  (59)
  • American Association for the Advancement of Science (AAAS)  (59)
  • Periodicals Archive Online (PAO)
  • 2010-2014  (59)
  • 1955-1959
  • 1940-1944
  • 2011  (59)
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  • 2010-2014  (59)
  • 1955-1959
  • 1940-1944
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  • 1
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    Acceleration of emergence of bacterial antibiotic resistance in connected microenvironments (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-24
    Description: The emergence of bacterial antibiotic resistance is a growing problem, yet the variables that influence the rate of emergence of resistance are not well understood. In a microfluidic device designed to mimic naturally occurring bacterial niches, resistance of Escherichia coli to the antibiotic ciprofloxacin developed within 10 hours. Resistance emerged with as few as 100 bacteria in the initial inoculation. Whole-genome sequencing of the resistant organisms revealed that four functional single-nucleotide polymorphisms attained fixation. Knowledge about the rapid emergence of antibiotic resistance in the heterogeneous conditions within the mammalian body may be helpful in understanding the emergence of drug resistance during cancer chemotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qiucen -- Lambert, Guillaume -- Liao, David -- Kim, Hyunsung -- Robin, Kristelle -- Tung, Chih-kuan -- Pourmand, Nader -- Austin, Robert H -- U54CA143803/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 23;333(6050):1764-7. doi: 10.1126/science.1208747.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21940899" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-Bacterial Agents/analysis/*pharmacology ; Ciprofloxacin/analysis/*pharmacology ; DNA Gyrase/genetics/metabolism ; Drug Resistance, Bacterial/*genetics ; Escherichia coli K12/*drug effects/genetics/growth & development/physiology ; Escherichia coli Proteins/genetics/metabolism ; *Evolution, Molecular ; Genes, Bacterial ; Genome, Bacterial ; Membrane Transport Proteins/genetics/metabolism ; Microbial Sensitivity Tests ; Microfluidic Analytical Techniques ; Models, Biological ; Movement ; Mutation, Missense ; *Polymorphism, Single Nucleotide ; Repressor Proteins/genetics/metabolism
    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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  • 2
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    Generation of spatial patterns through cell polarity switching (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-10
    Description: The mechanisms that generate dynamic spatial patterns within proliferating tissues are poorly understood, largely because of difficulties in unravelling interactions between cell specification, polarity, asymmetric division, rearrangements, and growth. We address this problem for stomatal spacing in plants, which offer the simplifying advantage that cells do not rearrange. By tracking lineages and gene activities over extended periods, we show that limited stem cell behavior of stomatal precursors depends on maintenance of the SPEECHLESS (SPCH) transcription factor in single daughter cells. Modeling shows how this property can lead to observed stereotypical stomata lineages through a postmitotic polarity-switching mechanism. The model predicts the location of a polarity determinant BASL over multiple divisions, which we validate experimentally. Our results highlight the dynamic two-way interactions between stem cells and their neighborhood during developmental patterning.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383840/" 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/PMC3383840/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, Sarah -- Barbier de Reuille, Pierre -- Chan, Jordi -- Bergmann, Dominique -- Prusinkiewicz, Przemyslaw -- Coen, Enrico -- 1R01GM086632-02/GM/NIGMS NIH HHS/ -- BB/F005997/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- R01 GM086632/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 9;333(6048):1436-40. doi: 10.1126/science.1202185.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉John Innes Centre, Norwich Research Park, Colney, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21903812" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*cytology/genetics ; Arabidopsis Proteins/genetics/*metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Cell Cycle Proteins/genetics/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; *Cell Polarity ; Cell Size ; Meristem/*cytology ; Microscopy, Confocal ; Models, Biological ; Plant Epidermis/cytology ; Plant Leaves/cytology ; Plant Stomata/*cytology ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Interconversion between intestinal stem cell populations in distinct niches (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: Intestinal epithelial stem cell identity and location have been the subject of substantial research. Cells in the +4 niche are slow-cycling and label-retaining, whereas a different stem cell niche located at the crypt base is occupied by crypt base columnar (CBC) cells. CBCs are distinct from +4 cells, and the relationship between them is unknown, though both give rise to all intestinal epithelial lineages. We demonstrate that Hopx, an atypical homeobox protein, is a specific marker of +4 cells. Hopx-expressing cells give rise to CBCs and all mature intestinal epithelial lineages. Conversely, CBCs can give rise to +4 Hopx-positive cells. These findings demonstrate a bidirectional lineage relationship between active and quiescent stem cells in their niches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705713/" 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/PMC3705713/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Norifumi -- Jain, Rajan -- LeBoeuf, Matthew R -- Wang, Qiaohong -- Lu, Min Min -- Epstein, Jonathan A -- R01 HL071546/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1420-4. doi: 10.1126/science.1213214. Epub 2011 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22075725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epithelial Cells/*cytology ; Homeodomain Proteins/analysis/genetics ; Intestinal Mucosa/*cytology/drug effects ; Intestine, Small/*cytology/drug effects ; Mice ; Models, Biological ; Multipotent Stem Cells/*cytology/physiology ; Paneth Cells/cytology ; *Stem Cell Niche ; Tamoxifen/pharmacology
    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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  • 4
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    Chirality in planar cell shape contributes to left-right asymmetric epithelial morphogenesis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: Some organs in animals display left-right (LR) asymmetry. To better understand LR asymmetric morphogenesis in Drosophila, we studied LR directional rotation of the hindgut epithelial tube. Hindgut epithelial cells adopt a LR asymmetric (chiral) cell shape within their plane, and we refer to this cell behavior as planar cell-shape chirality (PCC). Drosophila E-cadherin (DE-Cad) is distributed to cell boundaries with LR asymmetry, which is responsible for the PCC formation. Myosin ID switches the LR polarity found in PCC and in DE-Cad distribution, which coincides with the direction of rotation. An in silico simulation showed that PCC is sufficient to induce the directional rotation of this tissue. Thus, the intrinsic chirality of epithelial cells in vivo is an underlying mechanism for LR asymmetric tissue morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taniguchi, Kiichiro -- Maeda, Reo -- Ando, Tadashi -- Okumura, Takashi -- Nakazawa, Naotaka -- Hatori, Ryo -- Nakamura, Mitsutoshi -- Hozumi, Shunya -- Fujiwara, Hiroo -- Matsuno, Kenji -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):339-41. doi: 10.1126/science.1200940.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science and Technology, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764746" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions ; Animals ; Body Patterning ; Cadherins/*metabolism ; Cell Polarity ; *Cell Shape ; Computer Simulation ; Drosophila/cytology/*embryology/genetics ; Drosophila Proteins/genetics/*metabolism ; Epithelial Cells/*cytology ; Intestines/cytology/embryology ; Models, Biological ; Morphogenesis ; Myosin Type I/genetics/*metabolism ; Rotation
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  • 5
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    De-AMPylation of the small GTPase Rab1 by the pathogen Legionella pneumophila (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-18
    Description: The bacterial pathogen Legionella pneumophila exploits host cell vesicle transport by transiently manipulating the activity of the small guanosine triphosphatase (GTPase) Rab1. The effector protein SidM recruits Rab1 to the Legionella-containing vacuole (LCV), where it activates Rab1 and then AMPylates it by covalently adding adenosine monophosphate (AMP). L. pneumophila GTPase-activating protein LepB inactivates Rab1 before its removal from LCVs. Because LepB cannot bind AMPylated Rab1, the molecular events leading to Rab1 inactivation are unknown. We found that the effector protein SidD from L. pneumophila catalyzed AMP release from Rab1, generating de-AMPylated Rab1 accessible for inactivation by LepB. L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying SidD as the missing link connecting the processes of early Rab1 accumulation and subsequent Rab1 removal during infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209958/" 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/PMC3209958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neunuebel, M Ramona -- Chen, Yang -- Gaspar, Andrew H -- Backlund, Peter S Jr -- Yergey, Alfred -- Machner, Matthias P -- ZIA HD008893-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 22;333(6041):453-6. doi: 10.1126/science.1207193. Epub 2011 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680813" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Monophosphate/*metabolism ; Animals ; Bacterial Proteins/genetics/*metabolism ; COS Cells ; Cercopithecus aethiops ; Golgi Apparatus/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Guanosine Monophosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Legionella pneumophila/*metabolism/pathogenicity ; Ligands ; Macrophages/metabolism/microbiology ; Mice ; Mice, Inbred A ; Models, Biological ; Mutant Proteins/metabolism ; U937 Cells ; Vacuoles/metabolism/*microbiology ; rab1 GTP-Binding Proteins/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Single-base pair unwinding and asynchronous RNA release by the hepatitis C virus NS3 helicase (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-24
    Description: Nonhexameric helicases use adenosine triphosphate (ATP) to unzip base pairs in double-stranded nucleic acids (dsNAs). Studies have suggested that these helicases unzip dsNAs in single-base pair increments, consuming one ATP molecule per base pair, but direct evidence for this mechanism is lacking. We used optical tweezers to follow the unwinding of double-stranded RNA by the hepatitis C virus NS3 helicase. Single-base pair steps by NS3 were observed, along with nascent nucleotide release that was asynchronous with base pair opening. Asynchronous release of nascent nucleotides rationalizes various observations of its dsNA unwinding and may be used to coordinate the translocation speed of NS3 along the RNA during viral replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172460/" 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/PMC4172460/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Wei -- Arunajadai, Srikesh G -- Moffitt, Jeffrey R -- Tinoco, Ignacio Jr -- Bustamante, Carlos -- 5R01GM010840/GM/NIGMS NIH HHS/ -- 5R01GM032543/GM/NIGMS NIH HHS/ -- R01 GM010840/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 23;333(6050):1746-9. doi: 10.1126/science.1206023.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA. chengwe@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21940894" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Algorithms ; Base Pairing ; Hepacivirus/*enzymology ; Kinetics ; Models, Biological ; Nucleic Acid Conformation ; Optical Tweezers ; RNA Helicases/*metabolism ; RNA, Double-Stranded/chemistry/*metabolism ; RNA, Viral/chemistry/*metabolism ; Viral Nonstructural Proteins/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Early warnings of regime shifts: a whole-ecosystem experiment (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-30
    Description: Catastrophic ecological regime shifts may be announced in advance by statistical early warning signals such as slowing return rates from perturbation and rising variance. The theoretical background for these indicators is rich, but real-world tests are rare, especially for whole ecosystems. We tested the hypothesis that these statistics would be early warning signals for an experimentally induced regime shift in an aquatic food web. We gradually added top predators to a lake over 3 years to destabilize its food web. An adjacent lake was monitored simultaneously as a reference ecosystem. Warning signals of a regime shift were evident in the manipulated lake during reorganization of the food web more than a year before the food web transition was complete, corroborating theory for leading indicators of ecological regime shifts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carpenter, S R -- Cole, J J -- Pace, M L -- Batt, R -- Brock, W A -- Cline, T -- Coloso, J -- Hodgson, J R -- Kitchell, J F -- Seekell, D A -- Smith, L -- Weidel, B -- New York, N.Y. -- Science. 2011 May 27;332(6033):1079-82. doi: 10.1126/science.1203672. Epub 2011 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Limnology, University of Wisconsin, Madison, WI 53706, USA. srcarpen@wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21527677" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bass ; Biomass ; Chlorophyll/analysis ; *Ecosystem ; *Fishes ; *Food Chain ; *Fresh Water/chemistry ; Models, Biological ; Nonlinear Dynamics ; *Phytoplankton ; Population Dynamics ; *Zooplankton
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  • 8
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    The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" 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/PMC3164325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Round, June L -- Lee, S Melanie -- Li, Jennifer -- Tran, Gloria -- Jabri, Bana -- Chatila, Talal A -- Mazmanian, Sarkis K -- AI 080002/AI/NIAID NIH HHS/ -- AI 088626/AI/NIAID NIH HHS/ -- DK 078938/DK/NIDDK NIH HHS/ -- DK 083633/DK/NIDDK NIH HHS/ -- R01 AI085090/AI/NIAID NIH HHS/ -- R01 AI085090-01/AI/NIAID NIH HHS/ -- R01 AI085090-01S1/AI/NIAID NIH HHS/ -- R01 AI085090-02/AI/NIAID NIH HHS/ -- R01 AI085090-03/AI/NIAID NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI080002/AI/NIAID NIH HHS/ -- R21 AI080002-01/AI/NIAID NIH HHS/ -- R21 AI080002-02/AI/NIAID NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):974-7. doi: 10.1126/science.1206095. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. jround@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides fragilis/*growth & development/*immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; Humans ; *Immune Tolerance ; Immunity, Mucosal ; Interleukin-10/metabolism ; Intestinal Mucosa/*immunology/*microbiology ; Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Polysaccharides, Bacterial/immunology/*metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms ; Symbiosis ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Toll-Like Receptor 2/immunology/*metabolism
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  • 9
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    Animal migration and infectious disease risk (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-22
    Description: Animal migrations are often spectacular, and migratory species harbor zoonotic pathogens of importance to humans. Animal migrations are expected to enhance the global spread of pathogens and facilitate cross-species transmission. This does happen, but new research has also shown that migration allows hosts to escape from infected habitats, reduces disease levels when infected animals do not migrate successfully, and may lead to the evolution of less-virulent pathogens. Migratory demands can also reduce immune function, with consequences for host susceptibility and mortality. Studies of pathogen dynamics in migratory species and how these will respond to global change are urgently needed to predict future disease risks for wildlife and humans alike.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altizer, Sonia -- Bartel, Rebecca -- Han, Barbara A -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):296-302. doi: 10.1126/science.1194694.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Odum School of Ecology, University of Georgia, Athens, GA 30602, USA. saltizer@uga.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21252339" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; Biological Evolution ; Climate Change ; *Communicable Diseases/epidemiology/immunology/transmission/veterinary ; Disease Susceptibility ; Ecosystem ; Human Activities ; Humans ; Immunity ; Models, Biological ; Risk
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  • 10
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    Sequential establishment of stripe patterns in an expanding cell population (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: Periodic stripe patterns are ubiquitous in living organisms, yet the underlying developmental processes are complex and difficult to disentangle. We describe a synthetic genetic circuit that couples cell density and motility. This system enabled programmed Escherichia coli cells to form periodic stripes of high and low cell densities sequentially and autonomously. Theoretical and experimental analyses reveal that the spatial structure arises from a recurrent aggregation process at the front of the continuously expanding cell population. The number of stripes formed could be tuned by modulating the basal expression of a single gene. The results establish motility control as a simple route to establishing recurrent structures without requiring an extrinsic pacemaker.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Chenli -- Fu, Xiongfei -- Liu, Lizhong -- Ren, Xiaojing -- Chau, Carlos K L -- Li, Sihong -- Xiang, Lu -- Zeng, Hualing -- Chen, Guanhua -- Tang, Lei-Han -- Lenz, Peter -- Cui, Xiaodong -- Huang, Wei -- Hwa, Terence -- Huang, Jian-Dong -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):238-41. doi: 10.1126/science.1209042.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, The University of Hong Kong, Pokfulam, Hong Kong, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998392" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl-Butyrolactones/metabolism ; Bacterial Load ; Cell Proliferation ; Culture Media ; Diffusion ; Escherichia coli K12/cytology/genetics/*growth & development/*physiology ; Gene Expression Regulation, Bacterial ; Gene Regulatory Networks ; Kinetics ; Models, Biological ; Movement ; Quorum Sensing ; Synthetic Biology
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