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  • Animals  (6)
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  • 1
    Publication Date: 2008-05-30
    Description: Malaria parasites and related Apicomplexans are the causative agents of the some of the most serious infectious diseases of humans, companion animals, livestock and wildlife. These parasites must undergo sexual reproduction to transmit from vertebrate hosts to vectors, and their sex ratios are consistently female-biased. Sex allocation theory, a cornerstone of evolutionary biology, is remarkably successful at explaining female-biased sex ratios in multicellular taxa, but has proved controversial when applied to malaria parasites. Here we show that, as predicted by theory, sex ratio is an important fitness-determining trait and Plasmodium chabaudi parasites adjust their sex allocation in response to the presence of unrelated conspecifics. This suggests that P. chabaudi parasites use kin discrimination to evaluate the genetic diversity of their infections, and they adjust their behaviour in response to environmental cues. Malaria parasites provide a novel way to test evolutionary theory, and support the generality and power of a darwinian approach.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3807728/" 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/PMC3807728/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reece, Sarah E -- Drew, Damien R -- Gardner, Andy -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 May 29;453(7195):609-14. doi: 10.1038/nature06954.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Evolutionary Biology, Ashworth Laboratories, School of Biological Science, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK. sarah.reece@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cues ; Female ; Fertility/genetics/physiology ; Genetic Variation ; Genotype ; Humans ; Malaria/*parasitology ; Male ; Models, Biological ; Plasmodium chabaudi/genetics/*physiology ; *Sex Ratio
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drew, Liam J -- MacDermott, Amy B -- England -- Nature. 2009 Dec 3;462(7273):580-1. doi: 10.1038/462580a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19956249" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Mice ; Neuronal Plasticity/physiology ; Neurosciences ; Pain/*physiopathology ; Sensory Receptor Cells/*physiology ; Touch/*physiology ; Vesicular Glutamate Transport Proteins/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-04-19
    Description: T-helper cells that produce interleukin-17 (T(H)17 cells) are a recently identified CD4(+) T-cell subset with characterized pathological roles in autoimmune diseases. The nuclear receptors retinoic-acid-receptor-related orphan receptors alpha and gammat (RORalpha and RORgammat, respectively) have indispensible roles in the development of this cell type. Here we present SR1001, a high-affinity synthetic ligand-the first in a new class of compound-that is specific to both RORalpha and RORgammat and which inhibits T(H)17 cell differentiation and function. SR1001 binds specifically to the ligand-binding domains of RORalpha and RORgammat, inducing a conformational change within the ligand-binding domain that encompasses the repositioning of helix 12 and leads to diminished affinity for co-activators and increased affinity for co-repressors, resulting in suppression of the receptors' transcriptional activity. SR1001 inhibited the development of murine T(H)17 cells, as demonstrated by inhibition of interleukin-17A gene expression and protein production. Furthermore, SR1001 inhibited the expression of cytokines when added to differentiated murine or human T(H)17 cells. Finally, SR1001 effectively suppressed the clinical severity of autoimmune disease in mice. Our data demonstrate the feasibility of targeting the orphan receptors RORalpha and RORgammat to inhibit specifically T(H)17 cell differentiation and function, and indicate that this novel class of compound has potential utility in the treatment of autoimmune diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148894/" 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/PMC3148894/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solt, Laura A -- Kumar, Naresh -- Nuhant, Philippe -- Wang, Yongjun -- Lauer, Janelle L -- Liu, Jin -- Istrate, Monica A -- Kamenecka, Theodore M -- Roush, William R -- Vidovic, Dusica -- Schurer, Stephan C -- Xu, Jihong -- Wagoner, Gail -- Drew, Paul D -- Griffin, Patrick R -- Burris, Thomas P -- DK080201/DK/NIDDK NIH HHS/ -- DK088499/DK/NIDDK NIH HHS/ -- DK089984/DK/NIDDK NIH HHS/ -- GM084041/GM/NIGMS NIH HHS/ -- MH084512/MH/NIMH NIH HHS/ -- R01 DK080201/DK/NIDDK NIH HHS/ -- R01 DK080201-06/DK/NIDDK NIH HHS/ -- R01 GM084041/GM/NIGMS NIH HHS/ -- R01 MH092769/MH/NIMH NIH HHS/ -- U54 MH084512/MH/NIMH NIH HHS/ -- U54 MH084512-02/MH/NIMH NIH HHS/ -- U54MH074404/MH/NIMH NIH HHS/ -- England -- Nature. 2011 Apr 28;472(7344):491-4. doi: 10.1038/nature10075. Epub 2011 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, Florida 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21499262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity/*drug effects/immunology ; Cell Differentiation/*drug effects ; Drug Inverse Agonism ; HEK293 Cells ; Humans ; Interleukin-17/biosynthesis/immunology ; Interleukins/biosynthesis/immunology ; Ligands ; Mice ; Mice, Inbred C57BL ; Models, Molecular ; Nuclear Receptor Subfamily 1, Group F, Member 1/antagonists & ; inhibitors/genetics/metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 3/antagonists & ; inhibitors/genetics/metabolism ; Sulfonamides/*pharmacology ; Th17 Cells/*cytology/drug effects/*immunology/secretion ; Thiazoles/*pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2011-12-24
    Description: Antidepressant drugs and psychotherapy combined are more effective in treating mood disorders than either treatment alone, but the neurobiological basis of this interaction is unknown. To investigate how antidepressants influence the response of mood-related systems to behavioral experience, we used a fear-conditioning and extinction paradigm in mice. Combining extinction training with chronic fluoxetine, but neither treatment alone, induced an enduring loss of conditioned fear memory in adult animals. Fluoxetine treatment increased synaptic plasticity, converted the fear memory circuitry to a more immature state, and acted through local brain-derived neurotrophic factor. Fluoxetine-induced plasticity may allow fear erasure by extinction-guided remodeling of the memory circuitry. Thus, the pharmacological effects of antidepressants need to be combined with psychological rehabilitation to reorganize networks rendered more plastic by the drug treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929964/" 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/PMC3929964/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karpova, Nina N -- Pickenhagen, Anouchka -- Lindholm, Jesse -- Tiraboschi, Ettore -- Kulesskaya, Natalia -- Agustsdottir, Arna -- Antila, Hanna -- Popova, Dina -- Akamine, Yumiko -- Bahi, Amine -- Sullivan, Regina -- Hen, Rene -- Drew, Liam J -- Castren, Eero -- DC 003906/DC/NIDCD NIH HHS/ -- DC 009910/DC/NIDCD NIH HHS/ -- R01 DC009910/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1731-4. doi: 10.1126/science.1214592.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sigrid Juselius Laboratory, Neuroscience Center, University of Helsinki, Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194582" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/drug effects/physiology ; Animals ; Antidepressive Agents, Second-Generation/pharmacology/*therapeutic use ; Anxiety Disorders/*therapy ; *Behavior Therapy ; Brain-Derived Neurotrophic Factor/genetics/metabolism ; Combined Modality Therapy ; Conditioning, Classical ; Excitatory Postsynaptic Potentials/drug effects ; *Extinction, Psychological ; *Fear ; Fluoxetine/pharmacology/*therapeutic use ; Interneurons/drug effects/physiology ; Male ; Memory ; Mice ; Mice, Inbred C57BL ; Nerve Net/drug effects/physiology ; Neuronal Plasticity/*drug effects ; Neurons/cytology/drug effects ; Synaptic Transmission/drug effects
    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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  • 5
    Publication Date: 1979-12-14
    Description: Brief inhalation exposure of rats to three or six puffs of cigarette smoke significantly decreases elastase inhibitory capacity per milligram of alpha 1-antitrypsin in lung lavage fluid. This effect is not observed in ozone-tolerant rats and can be reversed by treating the lung lavage fluid from smoke-exposed rats with reducing agents. Samples of human serum obtained immediately after smoking also show decreased elastase inhibitory capacity per milligram of alpha 1-antitrypsin. Again, elastase inhibitory capacity can be restored by treatment with a reducing agent. Cigarette smoking may cause emphysema by inactivating alpha 1-antitrypsin through oxidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janoff, A -- Carp, H -- Lee, D K -- Drew, R T -- New York, N.Y. -- Science. 1979 Dec 14;206(4424):1313-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/316187" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Tolerance ; Lung/drug effects/*enzymology ; Male ; Oxidation-Reduction ; Ozone ; Pancreatic Elastase/metabolism ; Plants, Toxic ; Rats ; Smoke ; Smoking/*physiopathology ; Tobacco ; alpha 1-Antitrypsin/*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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  • 6
    Publication Date: 2015-09-08
    Description: Macromolecular complexes are essential to conserved biological processes, but their prevalence across animals is unclear. By combining extensive biochemical fractionation with quantitative mass spectrometry, here we directly examined the composition of soluble multiprotein complexes among diverse metazoan models. Using an integrative approach, we generated a draft conservation map consisting of more than one million putative high-confidence co-complex interactions for species with fully sequenced genomes that encompasses functional modules present broadly across all extant animals. Clustering reveals a spectrum of conservation, ranging from ancient eukaryotic assemblies that have probably served cellular housekeeping roles for at least one billion years, ancestral complexes that have accrued contemporary components, and rarer metazoan innovations linked to multicellularity. We validated these projections by independent co-fractionation experiments in evolutionarily distant species, affinity purification and functional analyses. The comprehensiveness, centrality and modularity of these reconstructed interactomes reflect their fundamental mechanistic importance and adaptive value to animal cell systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, Cuihong -- Borgeson, Blake -- Phanse, Sadhna -- Tu, Fan -- Drew, Kevin -- Clark, Greg -- Xiong, Xuejian -- Kagan, Olga -- Kwan, Julian -- Bezginov, Alexandr -- Chessman, Kyle -- Pal, Swati -- Cromar, Graham -- Papoulas, Ophelia -- Ni, Zuyao -- Boutz, Daniel R -- Stoilova, Snejana -- Havugimana, Pierre C -- Guo, Xinghua -- Malty, Ramy H -- Sarov, Mihail -- Greenblatt, Jack -- Babu, Mohan -- Derry, W Brent -- Tillier, Elisabeth R -- Wallingford, John B -- Parkinson, John -- Marcotte, Edward M -- Emili, Andrew -- F32 GM112495/GM/NIGMS NIH HHS/ -- F32GM112495/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2015 Sep 17;525(7569):339-44. doi: 10.1038/nature14877. Epub 2015 Sep 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; Center for Systems and Synthetic Biology, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, Texas 78712, USA. ; Department of Medical Biophysics, Toronto, Ontario M5G 1L7, Canada. ; Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada. ; Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada. ; Department of Biochemistry, University of Regina, Regina, Saskatchewan S4S 0A2, Canada. ; Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany. ; Department of Molecular Biosciences, University of Texas at Austin, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26344197" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Datasets as Topic ; *Evolution, Molecular ; Humans ; Multiprotein Complexes/*chemistry/*metabolism ; Protein Interaction Mapping ; *Protein Interaction Maps ; Reproducibility of Results ; Systems Biology ; Tandem Mass Spectrometry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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