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  • 1
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    Human oocytes reprogram somatic cells to a pluripotent state (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-08
    Description: The exchange of the oocyte's genome with the genome of a somatic cell, followed by the derivation of pluripotent stem cells, could enable the generation of specific cells affected in degenerative human diseases. Such cells, carrying the patient's genome, might be useful for cell replacement. Here we report that the development of human oocytes after genome exchange arrests at late cleavage stages in association with transcriptional abnormalities. In contrast, if the oocyte genome is not removed and the somatic cell genome is merely added, the resultant triploid cells develop to the blastocyst stage. Stem cell lines derived from these blastocysts differentiate into cell types of all three germ layers, and a pluripotent gene expression program is established on the genome derived from the somatic cell. This result demonstrates the feasibility of reprogramming human cells using oocytes and identifies removal of the oocyte genome as the primary cause of developmental failure after genome exchange.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noggle, Scott -- Fung, Ho-Lim -- Gore, Athurva -- Martinez, Hector -- Satriani, Kathleen Crumm -- Prosser, Robert -- Oum, Kiboong -- Paull, Daniel -- Druckenmiller, Sarah -- Freeby, Matthew -- Greenberg, Ellen -- Zhang, Kun -- Goland, Robin -- Sauer, Mark V -- Leibel, Rudolph L -- Egli, Dieter -- England -- Nature. 2011 Oct 5;478(7367):70-5. doi: 10.1038/nature10397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The New York Stem Cell Foundation Laboratory, New York, New York, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979046" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Blastocyst/cytology/metabolism ; Cell Differentiation ; *Cellular Reprogramming ; DNA Methylation ; Epigenesis, Genetic ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genome, Human/genetics ; Germ Layers/cytology/embryology/metabolism ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Oocyte Donation ; Oocytes/*cytology/growth & development/*physiology ; Primary Cell Culture ; Transcription, Genetic ; Triploidy ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Science addict (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉zur Hausen, Harald -- England -- Nature. 2011 Oct 12;478(7368):S12. doi: 10.1038/478S12a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21993819" target="_blank"〉PubMed〈/a〉
    Keywords: Behavior/physiology ; Drug Industry ; Female ; Germany ; Human papillomavirus 16/pathogenicity ; Human papillomavirus 18/pathogenicity ; Humans ; Mentors ; *Nobel Prize ; Oncogenic Viruses/isolation & purification/pathogenicity ; Papillomavirus Vaccines ; Smoking Cessation/psychology ; Uterine Cervical Neoplasms/*virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Animal behaviour: the nexus of sex and violence (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saper, Clifford B -- England -- Nature. 2011 Feb 10;470(7333):179-81. doi: 10.1038/470179a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307926" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/drug effects/*physiology ; Animals ; Cats ; Electric Stimulation ; Female ; Gene Expression Regulation/genetics ; Genes, fos/genetics ; Humans ; Male ; Mice ; Neural Inhibition/drug effects/genetics/physiology ; Neural Pathways/drug effects/physiology ; Neurons/drug effects/physiology ; Rats ; Sex Characteristics ; Sexual Behavior, Animal/drug effects/physiology ; Time Factors ; Ventromedial Hypothalamic Nucleus/anatomy & histology/*cytology/drug ; effects/*physiology ; Violence
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    The circadian molecular clock creates epidermal stem cell heterogeneity (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-15
    Description: Murine epidermal stem cells undergo alternate cycles of dormancy and activation, fuelling tissue renewal. However, only a subset of stem cells becomes active during each round of morphogenesis, indicating that stem cells coexist in heterogeneous responsive states. Using a circadian-clock reporter-mouse model, here we show that the dormant hair-follicle stem cell niche contains coexisting populations of cells at opposite phases of the clock, which are differentially predisposed to respond to homeostatic cues. The core clock protein Bmal1 modulates the expression of stem cell regulatory genes in an oscillatory manner, to create populations that are either predisposed, or less prone, to activation. Disrupting this clock equilibrium, through deletion of Bmal1 (also known as Arntl) or Per1/2, resulted in a progressive accumulation or depletion of dormant stem cells, respectively. Stem cell arrhythmia also led to premature epidermal ageing, and a reduction in the development of squamous tumours. Our results indicate that the circadian clock fine-tunes the temporal behaviour of epidermal stem cells, and that its perturbation affects homeostasis and the predisposition to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janich, Peggy -- Pascual, Gloria -- Merlos-Suarez, Anna -- Batlle, Eduard -- Ripperger, Jurgen -- Albrecht, Urs -- Cheng, Hai-Ying M -- Obrietan, Karl -- Di Croce, Luciano -- Benitah, Salvador Aznar -- England -- Nature. 2011 Nov 9;480(7376):209-14. doi: 10.1038/nature10649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genomic Regulation and UPF, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22080954" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/deficiency/genetics/metabolism ; Animals ; Carcinoma, Squamous Cell/genetics/pathology ; Cell Adhesion/genetics ; Cell Aging ; Cell Cycle/genetics ; Cells, Cultured ; Circadian Clocks/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Cues ; Female ; Gene Expression Regulation/genetics ; Hair Follicle/*cytology ; Homeostasis/genetics/physiology ; Male ; Mice ; Mice, Knockout ; Skin Neoplasms/genetics/pathology ; Stem Cell Niche ; Stem Cells/*cytology/metabolism ; Transforming Growth Factor beta/genetics ; Wnt Signaling Pathway/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Reliability of flipper-banded penguins as indicators of climate change (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-14
    Description: In 2007, the Intergovernmental Panel on Climate Change highlighted an urgent need to assess the responses of marine ecosystems to climate change. Because they lie in a high-latitude region, the Southern Ocean ecosystems are expected to be strongly affected by global warming. Using top predators of this highly productive ocean (such as penguins) as integrative indicators may help us assess the impacts of climate change on marine ecosystems. Yet most available information on penguin population dynamics is based on the controversial use of flipper banding. Although some reports have found the effects of flipper bands to be deleterious, some short-term (one-year) studies have concluded otherwise, resulting in the continuation of extensive banding schemes and the use of data sets thus collected to predict climate impact on natural populations. Here we show that banding of free-ranging king penguins (Aptenodytes patagonicus) impairs both survival and reproduction, ultimately affecting population growth rate. Over the course of a 10-year longitudinal study, banded birds produced 41% [corrected] fewer chicks and had a survival rate 16 percentage points [corrected] lower than non-banded birds, demonstrating a massive long-term impact of banding and thus refuting the assumption that birds will ultimately adapt to being banded. Indeed, banded birds still arrived later for breeding at the study site and had longer foraging trips even after 10 years. One of our major findings is that responses of flipper-banded penguins to climate variability (that is, changes in sea surface temperature and in the Southern Oscillation index) differ from those of non-banded birds. We show that only long-term investigations may allow an evaluation of the impact of flipper bands and that every major life-history trait can be affected, calling into question the banding schemes still going on. In addition, our understanding of the effects of climate change on marine ecosystems based on flipper-band data should be reconsidered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saraux, Claire -- Le Bohec, Celine -- Durant, Joel M -- Viblanc, Vincent A -- Gauthier-Clerc, Michel -- Beaune, David -- Park, Young-Hyang -- Yoccoz, Nigel G -- Stenseth, Nils C -- Le Maho, Yvon -- England -- Nature. 2011 Jan 13;469(7329):203-6. doi: 10.1038/nature09630.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite de Strasbourg, Institut Pluridisciplinaire Hubert Curien, 23 rue Becquerel, 67087 Strasbourg, France. claire.saraux@c-strasbourg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21228875" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Identification Systems/ethics ; Animal Welfare/ethics/statistics & numerical data ; Animals ; Antarctic Regions ; *Artifacts ; Climate Change/*statistics & numerical data ; *Ecosystem ; Female ; Longitudinal Studies ; Male ; Oceans and Seas ; Population Dynamics ; Reproduction/physiology ; Seawater/chemistry ; Spheniscidae/growth & development/*physiology ; Survival Rate ; Temperature ; Time Factors
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  • 6
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    Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-08-26
    Description: Genetic manipulations of insect populations for pest control have been advocated for some time, but there are few cases where manipulated individuals have been released in the field and no cases where they have successfully invaded target populations. Population transformation using the intracellular bacterium Wolbachia is particularly attractive because this maternally-inherited agent provides a powerful mechanism to invade natural populations through cytoplasmic incompatibility. When Wolbachia are introduced into mosquitoes, they interfere with pathogen transmission and influence key life history traits such as lifespan. Here we describe how the wMel Wolbachia infection, introduced into the dengue vector Aedes aegypti from Drosophila melanogaster, successfully invaded two natural A. aegypti populations in Australia, reaching near-fixation in a few months following releases of wMel-infected A. aegypti adults. Models with plausible parameter values indicate that Wolbachia-infected mosquitoes suffered relatively small fitness costs, leading to an unstable equilibrium frequency 〈30% that must be exceeded for invasion. These findings demonstrate that Wolbachia-based strategies can be deployed as a practical approach to dengue suppression with potential for area-wide implementation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, A A -- Montgomery, B L -- Popovici, J -- Iturbe-Ormaetxe, I -- Johnson, P H -- Muzzi, F -- Greenfield, M -- Durkan, M -- Leong, Y S -- Dong, Y -- Cook, H -- Axford, J -- Callahan, A G -- Kenny, N -- Omodei, C -- McGraw, E A -- Ryan, P A -- Ritchie, S A -- Turelli, M -- O'Neill, S L -- England -- Nature. 2011 Aug 24;476(7361):454-7. doi: 10.1038/nature10356.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bio21 Institute, Department of Genetics, The University of Melbourne, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21866160" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*microbiology/physiology/*virology ; Animals ; Dengue/microbiology/*prevention & control/*transmission/virology ; Dengue Virus/isolation & purification/*physiology ; Drosophila melanogaster/microbiology ; Female ; Humans ; Insect Vectors/microbiology/physiology/virology ; Male ; Pest Control, Biological/*methods ; Queensland ; Time Factors ; Wolbachia/isolation & purification/*physiology
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  • 7
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    BRCA1 tumour suppression occurs via heterochromatin-mediated silencing (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-09
    Description: Mutations in the tumour suppressor gene BRCA1 lead to breast and/or ovarian cancer. Here we show that loss of Brca1 in mice results in transcriptional de-repression of the tandemly repeated satellite DNA. Brca1 deficiency is accompanied by a reduction of condensed DNA regions in the genome and loss of ubiquitylation of histone H2A at satellite repeats. BRCA1 binds to satellite DNA regions and ubiquitylates H2A in vivo. Ectopic expression of H2A fused to ubiquitin reverses the effects of BRCA1 loss, indicating that BRCA1 maintains heterochromatin structure via ubiquitylation of histone H2A. Satellite DNA de-repression was also observed in mouse and human BRCA1-deficient breast cancers. Ectopic expression of satellite DNA can phenocopy BRCA1 loss in centrosome amplification, cell-cycle checkpoint defects, DNA damage and genomic instability. We propose that the role of BRCA1 in maintaining global heterochromatin integrity accounts for many of its tumour suppressor functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240576/" 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/PMC3240576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Quan -- Pao, Gerald M -- Huynh, Alexis M -- Suh, Hoonkyo -- Tonnu, Nina -- Nederlof, Petra M -- Gage, Fred H -- Verma, Inder M -- NS50217/NS/NINDS NIH HHS/ -- NS52842/NS/NINDS NIH HHS/ -- R01 NS050217/NS/NINDS NIH HHS/ -- R01 NS050217-05/NS/NINDS NIH HHS/ -- R01 NS052842/NS/NINDS NIH HHS/ -- R01 NS052842-04/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Sep 7;477(7363):179-84. doi: 10.1038/nature10371.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21901007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/deficiency/genetics/*metabolism ; Breast/cytology ; Breast Neoplasms/*genetics/pathology ; Cell Line, Tumor ; Cells, Cultured ; DNA, Satellite/genetics ; Epithelial Cells/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Genes, BRCA1/*physiology ; Genomic Instability/genetics ; HeLa Cells ; Heterochromatin/*genetics/*metabolism ; Histones/metabolism ; Humans ; Mice ; Ovarian Neoplasms/genetics ; RNA, Messenger/genetics ; Transcription, Genetic/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitinated Proteins/metabolism ; Ubiquitination
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Visual place learning in Drosophila melanogaster (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-06-10
    Description: The ability of insects to learn and navigate to specific locations in the environment has fascinated naturalists for decades. The impressive navigational abilities of ants, bees, wasps and other insects demonstrate that insects are capable of visual place learning, but little is known about the underlying neural circuits that mediate these behaviours. Drosophila melanogaster (common fruit fly) is a powerful model organism for dissecting the neural circuitry underlying complex behaviours, from sensory perception to learning and memory. Drosophila can identify and remember visual features such as size, colour and contour orientation. However, the extent to which they use vision to recall specific locations remains unclear. Here we describe a visual place learning platform and demonstrate that Drosophila are capable of forming and retaining visual place memories to guide selective navigation. By targeted genetic silencing of small subsets of cells in the Drosophila brain, we show that neurons in the ellipsoid body, but not in the mushroom bodies, are necessary for visual place learning. Together, these studies reveal distinct neuroanatomical substrates for spatial versus non-spatial learning, and establish Drosophila as a powerful model for the study of spatial memories.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169673/" 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/PMC3169673/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ofstad, Tyler A -- Zuker, Charles S -- Reiser, Michael B -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jun 8;474(7350):204-7. doi: 10.1038/nature10131.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654803" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/physiology ; Conditioning (Psychology)/physiology ; Cues ; Drosophila melanogaster/anatomy & histology/cytology/*physiology ; Female ; Glass ; Learning/*physiology ; Locomotion/physiology ; Memory/physiology ; Models, Animal ; Models, Neurological ; Mushroom Bodies ; Odors ; Orientation/physiology ; Silicon Dioxide ; Temperature ; Time Factors ; Visual Perception/*physiology
    Print ISSN: 0028-0836
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    Physiology: On time metabolism (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-24
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3971995/" 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/PMC3971995/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bass, Joseph -- R01 DK090625/DK/NIDDK NIH HHS/ -- R01 HL097817/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Dec 21;480(7378):466-7. doi: 10.1038/480466a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22193099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Cryptochromes/*metabolism ; Female ; *Gene Expression Regulation ; Humans ; Receptors, Glucocorticoid/*metabolism
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  • 10
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    Control of Drosophila endocycles by E2F and CRL4(CDT2) (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-01
    Description: Endocycles are variant cell cycles comprised of DNA synthesis (S)- and gap (G)-phases but lacking mitosis. Such cycles facilitate post-mitotic growth in many invertebrate and plant cells, and are so ubiquitous that they may account for up to half the world's biomass. DNA replication in endocycling Drosophila cells is triggered by cyclin E/cyclin dependent kinase 2 (CYCE/CDK2), but this kinase must be inactivated during each G-phase to allow the assembly of pre-Replication Complexes (preRCs) for the next S-phase. How CYCE/CDK2 is periodically silenced to allow re-replication has not been established. Here, using genetic tests in parallel with computational modelling, we show that the endocycles of Drosophila are driven by a molecular oscillator in which the E2F1 transcription factor promotes CycE expression and S-phase initiation, S-phase then activates the CRL4(CDT2) ubiquitin ligase, and this in turn mediates the destruction of E2F1 (ref. 7). We propose that it is the transient loss of E2F1 during S phases that creates the window of low Cdk activity required for preRC formation. In support of this model overexpressed E2F1 accelerated endocycling, whereas a stabilized variant of E2F1 blocked endocycling by deregulating target genes, including CycE, as well as Cdk1 and mitotic cyclins. Moreover, we find that altering cell growth by changing nutrition or target of rapamycin (TOR) signalling impacts E2F1 translation, thereby making endocycle progression growth-dependent. Many of the regulatory interactions essential to this novel cell cycle oscillator are conserved in animals and plants, indicating that elements of this mechanism act in most growth-dependent cell cycles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3330263/" 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/PMC3330263/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zielke, Norman -- Kim, Kerry J -- Tran, Vuong -- Shibutani, Shusaku T -- Bravo, Maria-Jose -- Nagarajan, Sabarish -- van Straaten, Monique -- Woods, Brigitte -- von Dassow, George -- Rottig, Carmen -- Lehner, Christian F -- Grewal, Savraj S -- Duronio, Robert J -- Edgar, Bruce A -- 5 P50GM66050/GM/NIGMS NIH HHS/ -- GM51186/GM/NIGMS NIH HHS/ -- GM57859/GM/NIGMS NIH HHS/ -- MOP-86622/Canadian Institutes of Health Research/Canada -- R01 GM051186/GM/NIGMS NIH HHS/ -- R01 GM051186-14A1/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Oct 30;480(7375):123-7. doi: 10.1038/nature10579.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉German Cancer Research Center (DKFZ)-Zentrum fur Molekulare Biologie der Universitat Heidelberg Alliance, Im Neuenheimer Feld 282, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22037307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/*physiology ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/*cytology/*enzymology/growth & development/metabolism ; E2F Transcription Factors/*metabolism ; Female ; Male ; S Phase/physiology ; Salivary Glands/cytology ; Ubiquitin-Protein Ligases/*metabolism
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    Eutherian mammals use diverse strategies to initiate X-chromosome inactivation during development (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-08
    Description: X-chromosome inactivation (XCI) in female mammals allows dosage compensation for X-linked gene products between the sexes. The developmental regulation of this process has been extensively investigated in mice, where the X chromosome of paternal origin (Xp) is silenced during early embryogenesis owing to imprinted expression of the regulatory RNA, Xist (X-inactive specific transcript). Paternal XCI is reversed in the inner cell mass of the blastocyst and random XCI subsequently occurs in epiblast cells. Here we show that other eutherian mammals have very different strategies for initiating XCI. In rabbits and humans, the Xist homologue is not subject to imprinting and XCI begins later than in mice. Furthermore, Xist is upregulated on both X chromosomes in a high proportion of rabbit and human embryo cells, even in the inner cell mass. In rabbits, this triggers XCI on both X chromosomes in some cells. In humans, chromosome-wide XCI has not initiated even by the blastocyst stage, despite the upregulation of XIST. The choice of which X chromosome will finally become inactive thus occurs downstream of Xist upregulation in both rabbits and humans, unlike in mice. Our study demonstrates the remarkable diversity in XCI regulation and highlights differences between mammals in their requirement for dosage compensation during early embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamoto, Ikuhiro -- Patrat, Catherine -- Thepot, Dominique -- Peynot, Nathalie -- Fauque, Patricia -- Daniel, Nathalie -- Diabangouaya, Patricia -- Wolf, Jean-Philippe -- Renard, Jean-Paul -- Duranthon, Veronique -- Heard, Edith -- England -- Nature. 2011 Apr 21;472(7343):370-4. doi: 10.1038/nature09872. Epub 2011 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Developmental Epigenetics Group, Institut Curie, CNRS UMR 3215, INSERM U934, Paris 75248, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21471966" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Blastocyst/metabolism ; Chromosomes, Mammalian/*genetics ; Dosage Compensation, Genetic/genetics ; Embryo, Mammalian/embryology/metabolism ; Female ; Gene Expression Regulation, Developmental/*genetics ; Genes, X-Linked/genetics ; Genomic Imprinting/genetics ; Histones/metabolism ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Mammals/embryology/*genetics ; Mice ; Parthenogenesis ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Rabbits ; Species Specificity ; Up-Regulation/genetics ; X Chromosome/*genetics ; X Chromosome Inactivation/*genetics
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    Stem cells: Cloning advance calls for careful regulation (2011)
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    Publication Date: 2011-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hyun, Insoo -- Tesar, Paul -- England -- Nature. 2011 Oct 5;478(7367):36-7. doi: 10.1038/478036c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979034" target="_blank"〉PubMed〈/a〉
    Keywords: *Cellular Reprogramming ; Female ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Oocytes/*cytology/*physiology
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    Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders (2011)
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    Publication Date: 2011-11-04
    Description: Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues--such as adipose tissue, skeletal muscle and eye--in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468323/" 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/PMC3468323/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Darren J -- Wijshake, Tobias -- Tchkonia, Tamar -- LeBrasseur, Nathan K -- Childs, Bennett G -- van de Sluis, Bart -- Kirkland, James L -- van Deursen, Jan M -- AG13925/AG/NIA NIH HHS/ -- CA96985/CA/NCI NIH HHS/ -- P30 DK050456/DK/NIDDK NIH HHS/ -- R01 AG013925/AG/NIA NIH HHS/ -- R01 AG013925-14/AG/NIA NIH HHS/ -- R01 CA096985/CA/NCI NIH HHS/ -- R01 CA096985-10/CA/NCI NIH HHS/ -- England -- Nature. 2011 Nov 2;479(7372):232-6. doi: 10.1038/nature10600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22048312" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology/drug effects/pathology ; Aging/drug effects/*physiology ; Animals ; Bone Marrow Cells/cytology/drug effects ; Cell Aging/drug effects/*physiology ; Cell Count ; Cell Cycle Proteins ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/*metabolism ; Eye/cytology/drug effects/pathology ; Female ; Gene Expression ; Genotype ; Longevity/drug effects/physiology ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/drug effects/pathology ; Phenotype ; Progeria/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Tacrolimus/analogs & derivatives/pharmacology ; Time Factors ; Weaning
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    Increasing adult hippocampal neurogenesis is sufficient to improve pattern separation (2011)
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    Publication Date: 2011-04-05
    Description: Adult hippocampal neurogenesis is a unique form of neural circuit plasticity that results in the generation of new neurons in the dentate gyrus throughout life. Neurons that arise in adults (adult-born neurons) show heightened synaptic plasticity during their maturation and can account for up to ten per cent of the entire granule cell population. Moreover, levels of adult hippocampal neurogenesis are increased by interventions that are associated with beneficial effects on cognition and mood, such as learning, environmental enrichment, exercise and chronic treatment with antidepressants. Together, these properties of adult neurogenesis indicate that this process could be harnessed to improve hippocampal functions. However, despite a substantial number of studies demonstrating that adult-born neurons are necessary for mediating specific cognitive functions, as well as some of the behavioural effects of antidepressants, it is unknown whether an increase in adult hippocampal neurogenesis is sufficient to improve cognition and mood. Here we show that inducible genetic expansion of the population of adult-born neurons through enhancing their survival improves performance in a specific cognitive task in which two similar contexts need to be distinguished. Mice with increased adult hippocampal neurogenesis show normal object recognition, spatial learning, contextual fear conditioning and extinction learning but are more efficient in differentiating between overlapping contextual representations, which is indicative of enhanced pattern separation. Furthermore, stimulation of adult hippocampal neurogenesis, when combined with an intervention such as voluntary exercise, produces a robust increase in exploratory behaviour. However, increasing adult hippocampal neurogenesis alone does not produce a behavioural response like that induced by anxiolytic agents or antidepressants. Together, our findings suggest that strategies that are designed to increase adult hippocampal neurogenesis specifically, by targeting the cell death of adult-born neurons or by other mechanisms, may have therapeutic potential for reversing impairments in pattern separation and dentate gyrus dysfunction such as those seen during normal ageing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084370/" 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/PMC3084370/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sahay, Amar -- Scobie, Kimberly N -- Hill, Alexis S -- O'Carroll, Colin M -- Kheirbek, Mazen A -- Burghardt, Nesha S -- Fenton, Andre A -- Dranovsky, Alex -- Hen, Rene -- 1K99MH86615-01/MH/NIMH NIH HHS/ -- K08 MH079088/MH/NIMH NIH HHS/ -- K08 MH079088-01/MH/NIMH NIH HHS/ -- K08 MH079088-02/MH/NIMH NIH HHS/ -- K08 MH079088-03/MH/NIMH NIH HHS/ -- K08 MH079088-03S1/MH/NIMH NIH HHS/ -- K08 MH079088-04/MH/NIMH NIH HHS/ -- K08 MH079088-05/MH/NIMH NIH HHS/ -- K99 MH086615/MH/NIMH NIH HHS/ -- K99 MH086615-02/MH/NIMH NIH HHS/ -- R01 MH068542/MH/NIMH NIH HHS/ -- R01 MH091844/MH/NIMH NIH HHS/ -- R01 MH091844-01/MH/NIMH NIH HHS/ -- R01 MH091844-02/MH/NIMH NIH HHS/ -- R01 MH091844-03/MH/NIMH NIH HHS/ -- T32 HD007430/HD/NICHD NIH HHS/ -- England -- Nature. 2011 Apr 28;472(7344):466-70. doi: 10.1038/nature09817. Epub 2011 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Columbia University, New York, New York 10032, USA. as2619@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21460835" target="_blank"〉PubMed〈/a〉
    Keywords: Affect/*physiology ; Aging/drug effects/pathology/*physiology ; Animals ; Antidepressive Agents/pharmacology ; Anxiety/physiopathology/therapy ; Apoptosis/drug effects ; Cell Survival/drug effects ; Cognition/drug effects/*physiology ; Conditioning, Classical/drug effects/physiology ; Dentate Gyrus/cytology/pathology/physiology/physiopathology ; Exploratory Behavior/drug effects/physiology ; Extinction, Psychological/drug effects/physiology ; Fear/physiology/psychology ; Female ; Hippocampus/*cytology/pathology/*physiology/physiopathology ; Learning/drug effects/physiology ; Long-Term Potentiation/drug effects/physiology ; Male ; Memory/drug effects/physiology ; Mice ; Mice, Knockout ; Mice, Transgenic ; *Models, Neurological ; Neural Stem Cells/cytology/drug effects/metabolism ; Neurogenesis/drug effects/*physiology ; Neuronal Plasticity/drug effects/physiology ; Physical Conditioning, Animal/physiology ; Synapses/drug effects/metabolism ; bcl-2-Associated X Protein/deficiency/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Distinct stem cells contribute to mammary gland development and maintenance (2011)
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    Publication Date: 2011-10-11
    Description: The mammary epithelium is composed of several cell lineages including luminal, alveolar and myoepithelial cells. Transplantation studies have suggested that the mammary epithelium is maintained by the presence of multipotent mammary stem cells. To define the cellular hierarchy of the mammary gland during physiological conditions, we performed genetic lineage-tracing experiments and clonal analysis of the mouse mammary gland during development, adulthood and pregnancy. We found that in postnatal unperturbed mammary gland, both luminal and myoepithelial lineages contain long-lived unipotent stem cells that display extensive renewing capacities, as demonstrated by their ability to clonally expand during morphogenesis and adult life as well as undergo massive expansion during several cycles of pregnancy. The demonstration that the mammary gland contains different types of long-lived stem cells has profound implications for our understanding of mammary gland physiology and will be instrumental in unravelling the cells at the origin of breast cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Keymeulen, Alexandra -- Rocha, Ana Sofia -- Ousset, Marielle -- Beck, Benjamin -- Bouvencourt, Gaelle -- Rock, Jason -- Sharma, Neha -- Dekoninck, Sophie -- Blanpain, Cedric -- England -- Nature. 2011 Oct 9;479(7372):189-93. doi: 10.1038/nature10573.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21983963" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Differentiation ; *Cell Lineage ; Cell Transplantation ; Epithelium ; Female ; Homeostasis ; Lactation/physiology ; Mammary Glands, Animal/*cytology/*growth & development/physiology/transplantation ; Mice ; Multipotent Stem Cells/cytology ; Pregnancy ; Stem Cells/*cytology/metabolism
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    On the care and use of US lab animals (2011)
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    Publication Date: 2011-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garber, Janet C -- England -- Nature. 2011 Aug 10;476(7359):152. doi: 10.1038/476152a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833072" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Welfare/*standards ; Animals ; *Animals, Laboratory/physiology/psychology ; Female ; *Guidelines as Topic ; Male ; United States
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    Long-term evolution and transmission dynamics of swine influenza A virus (2011)
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    Publication Date: 2011-05-27
    Description: Swine influenza A viruses (SwIV) cause significant economic losses in animal husbandry as well as instances of human disease and occasionally give rise to human pandemics, including that caused by the H1N1/2009 virus. The lack of systematic and longitudinal influenza surveillance in pigs has hampered attempts to reconstruct the origins of this pandemic. Most existing swine data were derived from opportunistic samples collected from diseased pigs in disparate geographical regions, not from prospective studies in defined locations, hence the evolutionary and transmission dynamics of SwIV are poorly understood. Here we quantify the epidemiological, genetic and antigenic dynamics of SwIV in Hong Kong using a data set of more than 650 SwIV isolates and more than 800 swine sera from 12 years of systematic surveillance in this region, supplemented with data stretching back 34 years. Intercontinental virus movement has led to reassortment and lineage replacement, creating an antigenically and genetically diverse virus population whose dynamics are quantitatively different from those previously observed for human influenza viruses. Our findings indicate that increased antigenic drift is associated with reassortment events and offer insights into the emergence of influenza viruses with epidemic potential in swine and humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vijaykrishna, Dhanasekaran -- Smith, Gavin J D -- Pybus, Oliver G -- Zhu, Huachen -- Bhatt, Samir -- Poon, Leo L M -- Riley, Steven -- Bahl, Justin -- Ma, Siu K -- Cheung, Chung L -- Perera, Ranawaka A P M -- Chen, Honglin -- Shortridge, Kennedy F -- Webby, Richard J -- Webster, Robert G -- Guan, Yi -- Peiris, J S Malik -- HHSN26600700005C/PHS HHS/ -- MC_G0902096/Medical Research Council/United Kingdom -- England -- Nature. 2011 May 26;473(7348):519-22. doi: 10.1038/nature10004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Emerging Infectious Diseases & Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21614079" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/virology ; *Evolution, Molecular ; Female ; Hong Kong/epidemiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/genetics/isolation & ; purification/*physiology ; Influenza in Birds/transmission/virology ; Influenza, Human/epidemiology/transmission/virology ; Male ; Molecular Epidemiology ; Molecular Sequence Data ; Orthomyxoviridae Infections/epidemiology/transmission/*veterinary/virology ; Phylogeny ; Population Surveillance ; Reassortant Viruses/genetics/immunology/isolation & purification/physiology ; Swine/blood/*virology ; Swine Diseases/blood/epidemiology/*transmission/*virology ; Zoonoses/epidemiology/transmission/*virology
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    The ageing systemic milieu negatively regulates neurogenesis and cognitive function (2011)
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    Publication Date: 2011-09-03
    Description: In the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions. Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise. Here, using heterochronic parabiosis we show that blood-borne factors present in the systemic milieu can inhibit or promote adult neurogenesis in an age-dependent fashion in mice. Accordingly, exposing a young mouse to an old systemic environment or to plasma from old mice decreased synaptic plasticity, and impaired contextual fear conditioning and spatial learning and memory. We identify chemokines--including CCL11 (also known as eotaxin)--the plasma levels of which correlate with reduced neurogenesis in heterochronic parabionts and aged mice, and the levels of which are increased in the plasma and cerebrospinal fluid of healthy ageing humans. Lastly, increasing peripheral CCL11 chemokine levels in vivo in young mice decreased adult neurogenesis and impaired learning and memory. Together our data indicate that the decline in neurogenesis and cognitive impairments observed during ageing can be in part attributed to changes in blood-borne factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170097/" 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/PMC3170097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Villeda, Saul A -- Luo, Jian -- Mosher, Kira I -- Zou, Bende -- Britschgi, Markus -- Bieri, Gregor -- Stan, Trisha M -- Fainberg, Nina -- Ding, Zhaoqing -- Eggel, Alexander -- Lucin, Kurt M -- Czirr, Eva -- Park, Jeong-Soo -- Couillard-Despres, Sebastien -- Aigner, Ludwig -- Li, Ge -- Peskind, Elaine R -- Kaye, Jeffrey A -- Quinn, Joseph F -- Galasko, Douglas R -- Xie, Xinmin S -- Rando, Thomas A -- Wyss-Coray, Tony -- 1 F31 AG034045-01/AG/NIA NIH HHS/ -- 1 F31 NS066676-01A1/NS/NINDS NIH HHS/ -- DP1 OD000392/OD/NIH HHS/ -- DP1 OD000392-01/OD/NIH HHS/ -- DP1 OD000392-02/OD/NIH HHS/ -- DP1 OD000392-03/OD/NIH HHS/ -- DP1 OD000392-04/OD/NIH HHS/ -- DP1 OD000392-05/OD/NIH HHS/ -- F31 AG034045/AG/NIA NIH HHS/ -- F31 AG034045-01/AG/NIA NIH HHS/ -- F31 AG034045-02/AG/NIA NIH HHS/ -- F31 AG034045-03/AG/NIA NIH HHS/ -- P30AG08017/AG/NIA NIH HHS/ -- P50 AG005136/AG/NIA NIH HHS/ -- R01 AG027505/AG/NIA NIH HHS/ -- R01 AG027505-01A1/AG/NIA NIH HHS/ -- R01 AG027505-02/AG/NIA NIH HHS/ -- R01 AG027505-03/AG/NIA NIH HHS/ -- R01 AG027505-04/AG/NIA NIH HHS/ -- R01 AG027505-05/AG/NIA NIH HHS/ -- R01 AR056849/AR/NIAMS NIH HHS/ -- R01 MH078194/MH/NIMH NIH HHS/ -- R01AG027505/AG/NIA NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 31;477(7362):90-4. doi: 10.1038/nature10357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21886162" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Chemokine CCL11/blood/cerebrospinal fluid/metabolism/pharmacology ; Chemokines/*blood/cerebrospinal fluid/*metabolism ; Female ; Learning/drug effects/*physiology ; Learning Disorders/blood/cerebrospinal fluid/physiopathology ; Male ; Memory Disorders/blood/cerebrospinal fluid/physiopathology ; Mice ; Mice, Inbred C57BL ; Neurogenesis/drug effects/*physiology ; Parabiosis ; Plasma/chemistry ; Time Factors
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    Science education: Research on the reservation (2011)
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    Publication Date: 2011-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corbyn, Zoe -- England -- Nature. 2011 Mar 3;471(7336):25-6. doi: 10.1038/471025a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368800" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Indians, North American/*education/*statistics & numerical data ; Mercury/analysis ; Research/*manpower/statistics & numerical data ; Students/statistics & numerical data ; Trout ; Universities/manpower/organization & administration/statistics & numerical data
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    Epidemiology: Study of a lifetime (2011)
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    Publication Date: 2011-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearson, Helen -- MC_U123092720/Medical Research Council/United Kingdom -- England -- Nature. 2011 Mar 3;471(7336):20-4. doi: 10.1038/471020a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368799" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; *Aging/genetics/physiology ; Archives ; Child ; Child, Preschool ; *Cohort Studies ; Environment ; Epigenesis, Genetic ; Epigenomics ; Female ; Genetic Predisposition to Disease/genetics ; Great Britain/epidemiology ; *Health Surveys/economics/history/trends ; History, 20th Century ; History, 21st Century ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Obesity/etiology/genetics ; Phenotype ; Socioeconomic Factors ; Survival Rate ; Young Adult
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    Reproductive biology: bone returns the favour (2011)
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    Publication Date: 2011-04-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuh-Huerta, Sonya M -- Pera, Renee A Reijo -- England -- Nature. 2011 Apr 7;472(7341):46-7. doi: 10.1038/472046a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21475191" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Bone and Bones/*metabolism ; Energy Metabolism ; Estrogens/physiology ; Female ; Fertility/genetics/*physiology ; Humans ; Male ; Mice ; Osteoblasts/secretion ; Osteocalcin/deficiency/genetics/*metabolism/secretion ; Osteogenesis/physiology ; Receptors, G-Protein-Coupled/metabolism ; Sex Characteristics ; Testis/physiology/secretion ; Testosterone/*biosynthesis/blood
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    Animal behaviour: Why promiscuity pays (2011)
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    Publication Date: 2011-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bellamy, Lawrence -- Pomiankowski, Andrew -- England -- Nature. 2011 Nov 9;479(7372):184-6. doi: 10.1038/479184a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22071760" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Female ; Genetic Fitness/physiology ; Male ; Mating Preference, Animal/physiology ; Pair Bond ; Reproduction/*physiology ; Sexual Behavior, Animal/*physiology ; Songbirds/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Flagging flora: help from bacteriocins? (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotter, Paul D -- Ross, R Paul -- Hill, Colin -- England -- Nature. 2011 Sep 7;477(7363):162. doi: 10.1038/477162c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21900999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*adverse effects ; Bacteria/*drug effects/*isolation & purification ; Female ; Humans ; Metagenome/*drug effects/*physiology ; Microbial Viability/*drug effects ; Pregnancy
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Ageing: Old cells under attack (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peeper, Daniel S -- England -- Nature. 2011 Nov 9;479(7372):186-7. doi: 10.1038/479186a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22071762" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Cell Aging/*physiology ; Cyclin-Dependent Kinase Inhibitor p16/*metabolism ; Female ; Male
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-04-09
    Description: Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine--choline, trimethylamine N-oxide (TMAO) and betaine--were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086762/" 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/PMC3086762/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Zeneng -- Klipfell, Elizabeth -- Bennett, Brian J -- Koeth, Robert -- Levison, Bruce S -- Dugar, Brandon -- Feldstein, Ariel E -- Britt, Earl B -- Fu, Xiaoming -- Chung, Yoon-Mi -- Wu, Yuping -- Schauer, Phil -- Smith, Jonathan D -- Allayee, Hooman -- Tang, W H Wilson -- DiDonato, Joseph A -- Lusis, Aldons J -- Hazen, Stanley L -- K99 HL102223/HL/NHLBI NIH HHS/ -- K99 HL102223-01A1/HL/NHLBI NIH HHS/ -- P01 HL028481/HL/NHLBI NIH HHS/ -- P01 HL028481-26A1/HL/NHLBI NIH HHS/ -- P01 HL030568/HL/NHLBI NIH HHS/ -- P01 HL030568-27/HL/NHLBI NIH HHS/ -- P01 HL076491/HL/NHLBI NIH HHS/ -- P01 HL076491-05/HL/NHLBI NIH HHS/ -- P01 HL087018/HL/NHLBI NIH HHS/ -- P01 HL087018-02/HL/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- P01 HL098055-02/HL/NHLBI NIH HHS/ -- P01 HL28481/HL/NHLBI NIH HHS/ -- P01 HL30568/HL/NHLBI NIH HHS/ -- P01HL087018-020001/HL/NHLBI NIH HHS/ -- P20 AA017837/AA/NIAAA NIH HHS/ -- R01 DK080732/DK/NIDDK NIH HHS/ -- R01 DK080732-02/DK/NIDDK NIH HHS/ -- R01 HL098193/HL/NHLBI NIH HHS/ -- R01 HL103866/HL/NHLBI NIH HHS/ -- R01 HL103866-02/HL/NHLBI NIH HHS/ -- R01 HL103931/HL/NHLBI NIH HHS/ -- R01 HL103931-02/HL/NHLBI NIH HHS/ -- T32 DK007789/DK/NIDDK NIH HHS/ -- T32 DK007789-10/DK/NIDDK NIH HHS/ -- T32-DK07789/DK/NIDDK NIH HHS/ -- UL1 RR024989/RR/NCRR NIH HHS/ -- UL1 RR024989-05/RR/NCRR NIH HHS/ -- England -- Nature. 2011 Apr 7;472(7341):57-63. doi: 10.1038/nature09922.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cleveland Clinic, Cleveland, Ohio 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21475195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atherosclerosis/chemically induced/genetics/metabolism/microbiology ; Betaine/blood/metabolism ; Biomarkers/blood/metabolism ; Cardiovascular Diseases/blood/diagnosis/*metabolism/*microbiology ; Cholesterol, HDL/blood ; Choline/administration & dosage/blood/metabolism/pharmacology ; Diet/adverse effects ; Dietary Fats/blood/metabolism/pharmacology ; Female ; Gastrointestinal Tract/*metabolism/*microbiology ; Gene Expression Regulation ; Germ-Free Life ; Humans ; Liver/enzymology ; Macrophages/metabolism ; Metabolomics ; Methylamines/blood/metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Oxygenases/genetics/metabolism ; Phenotype ; Phosphatidylcholines/administration & dosage/blood/*metabolism/pharmacology ; Receptors, Scavenger/metabolism ; Risk Assessment
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Experimental therapies for Parkinson's disease: Why fake it? (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsnelson, Alla -- England -- Nature. 2011 Aug 10;476(7359):142-4. doi: 10.1038/476142a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833065" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/transplantation ; Adult ; Controlled Clinical Trials as Topic/*ethics/*methods ; Female ; Humans ; Male ; Multicenter Studies as Topic ; Parkinson Disease/*drug therapy/*surgery ; Placebo Effect ; *Placebos/adverse effects
    Print ISSN: 0028-0836
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    Scientists and the media must give a balanced view (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shelton, James -- England -- Nature. 2011 Nov 2;479(7371):7. doi: 10.1038/479007a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bureau for Global Health, US Agency for International Development, Washington DC, USA. jshelton@usaid.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22051636" target="_blank"〉PubMed〈/a〉
    Keywords: Bias (Epidemiology) ; Condoms/utilization ; Contraceptive Agents, Female/administration & dosage/*adverse effects ; Contraceptives, Oral, Hormonal/adverse effects ; Female ; HIV Infections/*epidemiology/*etiology/transmission ; Humans ; Injections ; Male ; Newspapers as Topic/standards ; Periodicals as Topic/*standards ; Reproducibility of Results ; Research Personnel/*standards ; Risk Assessment ; Uncertainty ; Virus Shedding
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    Pharmacogenomics: playing the odds (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maxmen, Amy -- England -- Nature. 2011 Jun 8;474(7350):S9-10. doi: 10.1038/474S9a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21666735" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; *Genetic Testing ; Hepatitis C/*drug therapy/*genetics ; Humans ; Interferon-alpha/pharmacology/therapeutic use ; Interleukins/*genetics ; *Pharmacogenetics ; Polymorphism, Single Nucleotide/genetics ; *Precision Medicine ; Ribavirin/pharmacology/therapeutic use
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    A critical role for TCF-1 in T-lineage specification and differentiation (2011)
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    Publication Date: 2011-08-05
    Description: The vertebrate thymus provides an inductive environment for T-cell development. Within the mouse thymus, Notch signals are indispensable for imposing the T-cell fate on multipotential haematopoietic progenitors, but the downstream effectors that impart T-lineage specification and commitment are not well understood. Here we show that a transcription factor, T-cell factor 1 (TCF-1; also known as transcription factor 7, T-cell specific, TCF7), is a critical regulator in T-cell specification. TCF-1 is highly expressed in the earliest thymic progenitors, and its expression is upregulated by Notch signals. Most importantly, when TCF-1 is forcibly expressed in bone marrow (BM) progenitors, it drives the development of T-lineage cells in the absence of T-inductive Notch1 signals. Further characterization of these TCF-1-induced cells revealed expression of many T-lineage genes, including T-cell-specific transcription factors Gata3 and Bcl11b, and components of the T-cell receptor. Our data suggest a model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upregulating expression of T-cell essential genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156435/" 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/PMC3156435/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, Brittany Nicole -- Chi, Anthony Wei-Shine -- Chavez, Alejandro -- Yashiro-Ohtani, Yumi -- Yang, Qi -- Shestova, Olga -- Bhandoola, Avinash -- AI059621/AI/NIAID NIH HHS/ -- R01 AI059621/AI/NIAID NIH HHS/ -- R01 AI059621-09/AI/NIAID NIH HHS/ -- RC1 HL099758/HL/NHLBI NIH HHS/ -- RC1 HL099758-01/HL/NHLBI NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- T32AI055428/AI/NIAID NIH HHS/ -- T32CA09140/CA/NCI NIH HHS/ -- England -- Nature. 2011 Aug 3;476(7358):63-8. doi: 10.1038/nature10279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; *Cell Lineage ; Female ; Genes, Essential ; HEK293 Cells ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Receptor, Notch1/metabolism ; Signal Transduction ; T Cell Transcription Factor 1/deficiency/genetics/*metabolism ; T-Lymphocytes/*cytology/*metabolism ; Up-Regulation
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    Intravenous delivery of a multi-mechanistic cancer-targeted oncolytic poxvirus in humans (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-03
    Description: The efficacy and safety of biological molecules in cancer therapy, such as peptides and small interfering RNAs (siRNAs), could be markedly increased if high concentrations could be achieved and amplified selectively in tumour tissues versus normal tissues after intravenous administration. This has not been achievable so far in humans. We hypothesized that a poxvirus, which evolved for blood-borne systemic spread in mammals, could be engineered for cancer-selective replication and used as a vehicle for the intravenous delivery and expression of transgenes in tumours. JX-594 is an oncolytic poxvirus engineered for replication, transgene expression and amplification in cancer cells harbouring activation of the epidermal growth factor receptor (EGFR)/Ras pathway, followed by cell lysis and anticancer immunity. Here we show in a clinical trial that JX-594 selectively infects, replicates and expresses transgene products in cancer tissue after intravenous infusion, in a dose-related fashion. Normal tissues were not affected clinically. This platform technology opens up the possibility of multifunctional products that selectively express high concentrations of several complementary therapeutic and imaging molecules in metastatic solid tumours in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breitbach, Caroline J -- Burke, James -- Jonker, Derek -- Stephenson, Joe -- Haas, Andrew R -- Chow, Laura Q M -- Nieva, Jorge -- Hwang, Tae-Ho -- Moon, Anne -- Patt, Richard -- Pelusio, Adina -- Le Boeuf, Fabrice -- Burns, Joe -- Evgin, Laura -- De Silva, Naomi -- Cvancic, Sara -- Robertson, Terri -- Je, Ji-Eun -- Lee, Yeon-Sook -- Parato, Kelley -- Diallo, Jean-Simon -- Fenster, Aaron -- Daneshmand, Manijeh -- Bell, John C -- Kirn, David H -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Aug 31;477(7362):99-102. doi: 10.1038/nature10358.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jennerex Inc., 450 Sansome Street, 16th floor, San Francisco, California 94111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21886163" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; DNA, Viral/blood ; Female ; Gene Expression Regulation, Enzymologic ; Humans ; Infusions, Intravenous ; Male ; Middle Aged ; Neoplasms/pathology/surgery/*therapy/virology ; *Oncolytic Virotherapy ; Oncolytic Viruses/*physiology ; Organisms, Genetically Modified/physiology ; Poxviridae/*physiology ; Transgenes/genetics ; beta-Galactosidase/genetics/metabolism
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    Bring on the biomarkers (2011)
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    Publication Date: 2011-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poste, George -- England -- Nature. 2011 Jan 13;469(7329):156-7. doi: 10.1038/469156a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Complex Adaptive Systems Initiative, Arizona State University, Scottsdale, Arizona 85257, USA. george.poste@asu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21228852" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Specimen Banks/supply & distribution ; Biomarkers/*analysis ; Biomedical Research/economics/standards/trends ; Cell Line ; Female ; Gene Expression Profiling ; Genetics, Medical/economics/*methods/standards/*trends ; Health Care Costs/trends ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Pharmacogenetics/economics/standards/trends ; Precision Medicine/economics/standards/*trends ; Proteomics ; Reproducibility of Results ; Sample Size ; Specimen Handling/methods/standards
    Print ISSN: 0028-0836
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    Evolution: Big brains explained (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potts, Richard -- England -- Nature. 2011 Nov 30;480(7375):43-4. doi: 10.1038/480043a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22129720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Brain/*anatomy & histology ; Energy Metabolism/*physiology ; Female ; Humans
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    Vaccine trial's ethics criticized (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shetty, Priya -- England -- Nature. 2011 Jun 22;474(7352):427-8. doi: 10.1038/474427a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21697918" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Child ; Clinical Trials as Topic/*ethics ; Ethics, Research ; Female ; Guidelines as Topic ; Humans ; India ; International Cooperation ; Papillomavirus Infections/prevention & control ; *Papillomavirus Vaccines/adverse effects ; Registries
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    Neuroethics: Give memory-altering drugs a chance (2011)
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    Publication Date: 2011-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolber, Adam -- England -- Nature. 2011 Aug 17;476(7360):275-6. doi: 10.1038/476275a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brooklyn Law School, New York 11201, USA. adam.kolber@brooklaw.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21850084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethical Issues/legislation & jurisprudence ; Female ; Humans ; Male ; Memory/*drug effects/*physiology ; Stress Disorders, Post-Traumatic/*drug therapy/*psychology/therapy ; Stress, Psychological/drug therapy/physiopathology/psychology
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    Stem cells: Triple genomes go far (2011)
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    Publication Date: 2011-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, George Q -- Solbakk, Jan Helge -- England -- Nature. 2011 Oct 5;478(7367):40-1. doi: 10.1038/478040a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979039" target="_blank"〉PubMed〈/a〉
    Keywords: *Cellular Reprogramming ; Female ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Oocytes/*cytology/*physiology
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    Chemoprevention: First line of defence (2011)
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    Publication Date: 2011-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gravitz, Lauren -- England -- Nature. 2011 Mar 24;471(7339):S5-7. doi: 10.1038/471S5a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430719" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/adverse effects/pharmacology ; Celecoxib ; Clinical Trials, Phase II as Topic ; Colonic Neoplasms/drug therapy/genetics/pathology ; Cyclooxygenase Inhibitors/adverse effects/pharmacology ; Disease Models, Animal ; Disease Progression ; Female ; Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Genistein/pharmacology ; Humans ; Inflammation/drug therapy/prevention & control ; Male ; Matrix Metalloproteinase 2/biosynthesis/metabolism ; Mice ; Neoplasm Metastasis/drug therapy/prevention & control ; Neoplasms/blood supply/drug therapy/*pathology/*prevention & control ; Neovascularization, Pathologic/drug therapy/prevention & control ; Polyamines/metabolism ; Precancerous Conditions/drug therapy/metabolism/pathology/prevention & control ; Prostatic Neoplasms/drug therapy/pathology ; Pyrazoles/adverse effects/pharmacology ; Risk Assessment ; Sulfonamides/adverse effects/pharmacology
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    Pharmaceuticals: Reduce drug waste in the environment (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Depledge, Michael -- England -- Nature. 2011 Oct 5;478(7367):36. doi: 10.1038/478036a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Drug Industry ; Female ; Fishes/*abnormalities ; Industrial Waste/*adverse effects ; Male ; *Waste Disposal, Fluid
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    Hedgehog/Wnt feedback supports regenerative proliferation of epithelial stem cells in bladder (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-11
    Description: Epithelial integrity in metazoan organs is maintained through the regulated proliferation and differentiation of organ-specific stem and progenitor cells. Although the epithelia of organs such as the intestine regenerate constantly and thus remain continuously proliferative, other organs, such as the mammalian urinary bladder, shift from near-quiescence to a highly proliferative state in response to epithelial injury. The cellular and molecular mechanisms underlying this injury-induced mode of regenerative response are poorly defined. Here we show in mice that the proliferative response to bacterial infection or chemical injury within the bladder is regulated by signal feedback between basal cells of the urothelium and the stromal cells that underlie them. We demonstrate that these basal cells include stem cells capable of regenerating all cell types within the urothelium, and are marked by expression of the secreted protein signal Sonic hedgehog (Shh). On injury, Shh expression in these basal cells increases and elicits increased stromal expression of Wnt protein signals, which in turn stimulate the proliferation of both urothelial and stromal cells. The heightened activity of this signal feedback circuit and the associated increase in cell proliferation appear to be required for restoration of urothelial function and, in the case of bacterial injury, may help clear and prevent further spread of infection. Our findings provide a conceptual framework for injury-induced epithelial regeneration in endodermal organs, and may provide a basis for understanding the roles of signalling pathways in cancer growth and metastasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676169/" 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/PMC3676169/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Kunyoo -- Lee, John -- Guo, Nini -- Kim, James -- Lim, Agnes -- Qu, Lishu -- Mysorekar, Indira U -- Beachy, Philip A -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 7;472(7341):110-4. doi: 10.1038/nature09851. Epub 2011 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Institute for Stem Cell Biology and Regenerative Medicine, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. kunyoos@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21389986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Proliferation ; Epithelial Cells/*cytology/metabolism ; Feedback, Physiological ; Female ; Fibroblast Growth Factors/metabolism ; Hedgehog Proteins/*metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Mice ; Organoids/cytology ; Regeneration/*physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; Stromal Cells/cytology/metabolism ; Urinary Bladder/*cytology/drug effects/injuries/metabolism ; Urinary Bladder Diseases/chemically induced/metabolism/microbiology/pathology ; Uropathogenic Escherichia coli/physiology ; Urothelium/cytology ; Wnt Proteins/*metabolism
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    Behavioural neuroscience: Fruity aphrodisiacs (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prud'homme, Benjamin -- Gompel, Nicolas -- England -- Nature. 2011 Oct 12;478(7368):190-1. doi: 10.1038/478190a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21993752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Courtship ; Drosophila melanogaster/*physiology ; Female ; *Food ; Male ; Odors/*analysis ; Olfactory Receptor Neurons/*metabolism ; Sexual Behavior, Animal/*physiology
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    Developmental biology: Remarkable role for the placenta (2011)
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    Publication Date: 2011-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKay, Ron -- England -- Nature. 2011 Apr 21;472(7343):298-9. doi: 10.1038/472298a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512563" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*embryology/*metabolism ; Female ; Fetus/cytology/embryology/*metabolism ; Humans ; Maternal-Fetal Exchange/*physiology ; Mice ; Placenta/cytology/*metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; Serotonin/*biosynthesis/metabolism
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    Primary motor cortex underlies multi-joint integration for fast feedback control (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-04
    Description: A basic difficulty for the nervous system is integrating locally ambiguous sensory information to form accurate perceptions about the outside world. This local-to-global problem is also fundamental to motor control of the arm, because complex mechanical interactions between shoulder and elbow allow a particular amount of motion at one joint to arise from an infinite combination of shoulder and elbow torques. Here we show, in humans and rhesus monkeys, that a transcortical pathway through primary motor cortex (M1) resolves this ambiguity during fast feedback control. We demonstrate that single M1 neurons of behaving monkeys can integrate shoulder and elbow motion information into motor commands that appropriately counter the underlying torque within about 50 milliseconds of a mechanical perturbation. Moreover, we reveal a causal link between M1 processing and multi-joint integration in humans by showing that shoulder muscle responses occurring approximately 50 milliseconds after pure elbow displacement can be potentiated by transcranial magnetic stimulation. Taken together, our results show that transcortical processing through M1 permits feedback responses to express a level of sophistication that rivals voluntary control; this provides neurophysiological support for influential theories positing that voluntary movement is generated by the intelligent manipulation of sensory feedback.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pruszynski, J Andrew -- Kurtzer, Isaac -- Nashed, Joseph Y -- Omrani, Mohsen -- Brouwer, Brenda -- Scott, Stephen H -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Sep 28;478(7369):387-90. doi: 10.1038/nature10436.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21964335" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Biomechanical Phenomena/physiology ; Elbow/*physiology ; Evoked Potentials, Motor/physiology ; Feedback, Sensory/*physiology ; Female ; Humans ; Macaca mulatta ; Male ; Motor Cortex/*cytology/*physiology ; Motor Neurons/physiology ; Muscle, Skeletal/physiology ; Shoulder/*physiology ; Time Factors
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    A transient placental source of serotonin for the fetal forebrain (2011)
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    Publication Date: 2011-04-23
    Description: Serotonin (5-hydroxytryptamine or 5-HT) is thought to regulate neurodevelopmental processes through maternal-fetal interactions that have long-term mental health implications. It is thought that beyond fetal 5-HT neurons there are significant maternal contributions to fetal 5-HT during pregnancy but this has not been tested empirically. To examine putative central and peripheral sources of embryonic brain 5-HT, we used Pet1(-/-) (also called Fev) mice in which most dorsal raphe neurons lack 5-HT. We detected previously unknown differences in accumulation of 5-HT between the forebrain and hindbrain during early and late fetal stages, through an exogenous source of 5-HT which is not of maternal origin. Using additional genetic strategies, a new technology for studying placental biology ex vivo and direct manipulation of placental neosynthesis, we investigated the nature of this exogenous source. We uncovered a placental 5-HT synthetic pathway from a maternal tryptophan precursor in both mice and humans. This study reveals a new, direct role for placental metabolic pathways in modulating fetal brain development and indicates that maternal-placental-fetal interactions could underlie the pronounced impact of 5-HT on long-lasting mental health outcomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084180/" 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/PMC3084180/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonnin, Alexandre -- Goeden, Nick -- Chen, Kevin -- Wilson, Melissa L -- King, Jennifer -- Shih, Jean C -- Blakely, Randy D -- Deneris, Evan S -- Levitt, Pat -- 1P50MH078280A1/MH/NIMH NIH HHS/ -- 5R21HD065287/HD/NICHD NIH HHS/ -- P50 MH078028/MH/NIMH NIH HHS/ -- P50 MH078028-01A1/MH/NIMH NIH HHS/ -- P50 MH078028-02/MH/NIMH NIH HHS/ -- P50 MH078028-03/MH/NIMH NIH HHS/ -- P50 MH078028-04/MH/NIMH NIH HHS/ -- P50 MH078028-05/MH/NIMH NIH HHS/ -- R01MH39085/MH/NIMH NIH HHS/ -- R21 HD065287/HD/NICHD NIH HHS/ -- R21 HD065287-01/HD/NICHD NIH HHS/ -- R21 HD065287-02/HD/NICHD NIH HHS/ -- England -- Nature. 2011 Apr 21;472(7343):347-50. doi: 10.1038/nature09972.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zilkha Neurogenetic Institute, Keck School of Medicine of USC, Los Angeles, California 90089, USA. bonnin@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo, Mammalian/metabolism ; Female ; Fetus/embryology/*metabolism ; Humans ; In Vitro Techniques ; Maternal-Fetal Exchange/*physiology ; Mice ; Placenta/*metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; Prosencephalon/*embryology/*metabolism ; Raphe Nuclei/cytology ; Rhombencephalon/embryology/metabolism ; Serotonin/analysis/*biosynthesis/metabolism ; Time Factors ; Transcription Factors/deficiency/genetics
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    Dopamine neurons derived from human ES cells efficiently engraft in animal models of Parkinson's disease (2011)
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    Publication Date: 2011-11-08
    Description: Human pluripotent stem cells (PSCs) are a promising source of cells for applications in regenerative medicine. Directed differentiation of PSCs into specialized cells such as spinal motoneurons or midbrain dopamine (DA) neurons has been achieved. However, the effective use of PSCs for cell therapy has lagged behind. Whereas mouse PSC-derived DA neurons have shown efficacy in models of Parkinson's disease, DA neurons from human PSCs generally show poor in vivo performance. There are also considerable safety concerns for PSCs related to their potential for teratoma formation or neural overgrowth. Here we present a novel floor-plate-based strategy for the derivation of human DA neurons that efficiently engraft in vivo, suggesting that past failures were due to incomplete specification rather than a specific vulnerability of the cells. Midbrain floor-plate precursors are derived from PSCs 11 days after exposure to small molecule activators of sonic hedgehog (SHH) and canonical WNT signalling. Engraftable midbrain DA neurons are obtained by day 25 and can be maintained in vitro for several months. Extensive molecular profiling, biochemical and electrophysiological data define developmental progression and confirm identity of PSC-derived midbrain DA neurons. In vivo survival and function is demonstrated in Parkinson's disease models using three host species. Long-term engraftment in 6-hydroxy-dopamine-lesioned mice and rats demonstrates robust survival of midbrain DA neurons derived from human embryonic stem (ES) cells, complete restoration of amphetamine-induced rotation behaviour and improvements in tests of forelimb use and akinesia. Finally, scalability is demonstrated by transplantation into parkinsonian monkeys. Excellent DA neuron survival, function and lack of neural overgrowth in the three animal models indicate promise for the development of cell-based therapies in Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245796/" 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/PMC3245796/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kriks, Sonja -- Shim, Jae-Won -- Piao, Jinghua -- Ganat, Yosif M -- Wakeman, Dustin R -- Xie, Zhong -- Carrillo-Reid, Luis -- Auyeung, Gordon -- Antonacci, Chris -- Buch, Amanda -- Yang, Lichuan -- Beal, M Flint -- Surmeier, D James -- Kordower, Jeffrey H -- Tabar, Viviane -- Studer, Lorenz -- NS052671/NS/NINDS NIH HHS/ -- P50 NS047085/NS/NINDS NIH HHS/ -- P50 NS071669/NS/NINDS NIH HHS/ -- P50 NS071669-03/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Nov 6;480(7378):547-51. doi: 10.1038/nature10648.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Stem Cell Biology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22056989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Tissue Transplantation ; Cell Differentiation ; Cell Line ; Cell Survival ; Dopaminergic Neurons/*cytology/*transplantation ; Embryonic Stem Cells/*cytology ; Female ; Humans ; Macaca mulatta ; Mesencephalon/cytology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Parkinson Disease/*therapy ; Rats ; Rats, Sprague-Dawley
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    Animal behaviour: Born leaders (2011)
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    Publication Date: 2011-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissing, Franz J -- England -- Nature. 2011 Jun 15;474(7351):288-9. doi: 10.1038/474288a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21677739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/physiology ; Biological Evolution ; Family Characteristics ; Female ; Game Theory ; Group Processes ; Humans ; *Leadership ; Male ; *Models, Biological ; Selection, Genetic ; Smegmamorpha/physiology ; *Social Behavior ; Social Dominance
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    Flagging flora: heart disease link (2011)
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    Publication Date: 2011-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davidson, Sean -- England -- Nature. 2011 Sep 7;477(7363):162. doi: 10.1038/477162d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21900997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*adverse effects ; Bacteria/*drug effects/*isolation & purification ; Cardiovascular Diseases/*metabolism/*microbiology ; Female ; Gastrointestinal Tract/*metabolism/*microbiology ; Humans ; Metagenome/*drug effects/*physiology ; Microbial Viability/*drug effects ; Phosphatidylcholines/*metabolism ; Pregnancy
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    A synthetic homing endonuclease-based gene drive system in the human malaria mosquito (2011)
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    Publication Date: 2011-04-22
    Description: Genetic methods of manipulating or eradicating disease vector populations have long been discussed as an attractive alternative to existing control measures because of their potential advantages in terms of effectiveness and species specificity. The development of genetically engineered malaria-resistant mosquitoes has shown, as a proof of principle, the possibility of targeting the mosquito's ability to serve as a disease vector. The translation of these achievements into control measures requires an effective technology to spread a genetic modification from laboratory mosquitoes to field populations. We have suggested previously that homing endonuclease genes (HEGs), a class of simple selfish genetic elements, could be exploited for this purpose. Here we demonstrate that a synthetic genetic element, consisting of mosquito regulatory regions and the homing endonuclease gene I-SceI, can substantially increase its transmission to the progeny in transgenic mosquitoes of the human malaria vector Anopheles gambiae. We show that the I-SceI element is able to invade receptive mosquito cage populations rapidly, validating mathematical models for the transmission dynamics of HEGs. Molecular analyses confirm that expression of I-SceI in the male germline induces high rates of site-specific chromosomal cleavage and gene conversion, which results in the gain of the I-SceI gene, and underlies the observed genetic drive. These findings demonstrate a new mechanism by which genetic control measures can be implemented. Our results also show in principle how sequence-specific genetic drive elements like HEGs could be used to take the step from the genetic engineering of individuals to the genetic engineering of populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093433/" 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/PMC3093433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Windbichler, Nikolai -- Menichelli, Miriam -- Papathanos, Philippos Aris -- Thyme, Summer B -- Li, Hui -- Ulge, Umut Y -- Hovde, Blake T -- Baker, David -- Monnat, Raymond J Jr -- Burt, Austin -- Crisanti, Andrea -- CA133831/CA/NCI NIH HHS/ -- RL1 CA133831/CA/NCI NIH HHS/ -- RL1 CA133831-01/CA/NCI NIH HHS/ -- RL1 CA133831-02/CA/NCI NIH HHS/ -- RL1 CA133831-03/CA/NCI NIH HHS/ -- RL1 CA133831-04/CA/NCI NIH HHS/ -- RL1 CA133831-05/CA/NCI NIH HHS/ -- RL1 GM084433/GM/NIGMS NIH HHS/ -- RL1 GM084433-01/GM/NIGMS NIH HHS/ -- RL1 GM084433-02/GM/NIGMS NIH HHS/ -- RL1 GM084433-03/GM/NIGMS NIH HHS/ -- RL1 GM084433-04/GM/NIGMS NIH HHS/ -- RL1 GM084433-05/GM/NIGMS NIH HHS/ -- T32 CA080416/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 May 12;473(7346):212-5. doi: 10.1038/nature09937. Epub 2011 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial College London, Department of Life Sciences, South Kensington Campus, London, SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21508956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Anopheles gambiae/*genetics ; Deoxyribonucleases, Type II Site-Specific/genetics ; Female ; Genes, Reporter/genetics ; *Genetic Engineering ; Genotype ; Insect Vectors/*genetics ; Male ; Molecular Sequence Data ; Mosquito Control/*methods ; Saccharomyces cerevisiae Proteins/genetics
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    Integrated genomic analyses of ovarian carcinoma (2011)
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    Publication Date: 2011-07-02
    Description: A catalogue of molecular aberrations that cause ovarian cancer is critical for developing and deploying therapies that will improve patients' lives. The Cancer Genome Atlas project has analysed messenger RNA expression, microRNA expression, promoter methylation and DNA copy number in 489 high-grade serous ovarian adenocarcinomas and the DNA sequences of exons from coding genes in 316 of these tumours. Here we report that high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumours (96%); low prevalence but statistically recurrent somatic mutations in nine further genes including NF1, BRCA1, BRCA2, RB1 and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes. Analyses delineated four ovarian cancer transcriptional subtypes, three microRNA subtypes, four promoter methylation subtypes and a transcriptional signature associated with survival duration, and shed new light on the impact that tumours with BRCA1/2 (BRCA1 or BRCA2) and CCNE1 aberrations have on survival. Pathway analyses suggested that homologous recombination is defective in about half of the tumours analysed, and that NOTCH and FOXM1 signalling are involved in serous ovarian cancer pathophysiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163504/" 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/PMC3163504/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cancer Genome Atlas Research Network -- R01 CA140323/CA/NCI NIH HHS/ -- R01 HG005690/HG/NHGRI NIH HHS/ -- R21 CA135877/CA/NCI NIH HHS/ -- R21 CA135877-01/CA/NCI NIH HHS/ -- R21 CA135877-02/CA/NCI NIH HHS/ -- U24 CA126551/CA/NCI NIH HHS/ -- U24 CA126561/CA/NCI NIH HHS/ -- U24CA126543/CA/NCI NIH HHS/ -- U24CA126544/CA/NCI NIH HHS/ -- U24CA126546/CA/NCI NIH HHS/ -- U24CA126551/CA/NCI NIH HHS/ -- U24CA126554/CA/NCI NIH HHS/ -- U24CA126561/CA/NCI NIH HHS/ -- U24CA126563/CA/NCI NIH HHS/ -- U24CA143731/CA/NCI NIH HHS/ -- U24CA143835/CA/NCI NIH HHS/ -- U24CA143840/CA/NCI NIH HHS/ -- U24CA143843/CA/NCI NIH HHS/ -- U24CA143845/CA/NCI NIH HHS/ -- U24CA143848/CA/NCI NIH HHS/ -- U24CA143858/CA/NCI NIH HHS/ -- U24CA143866/CA/NCI NIH HHS/ -- U24CA143867/CA/NCI NIH HHS/ -- U24CA143882/CA/NCI NIH HHS/ -- U24CA144025/CA/NCI NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- U54HG003079/HG/NHGRI NIH HHS/ -- U54HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2011 Jun 29;474(7353):609-15. doi: 10.1038/nature10166.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21720365" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Carcinoma/*genetics/physiopathology ; DNA Methylation ; Female ; Gene Dosage ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; *Genomics ; Humans ; MicroRNAs/metabolism ; Middle Aged ; Mutation/genetics ; Ovarian Neoplasms/*genetics/physiopathology ; RNA, Messenger/metabolism
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    Secrets of the human genome disclosed (2011)
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    Publication Date: 2011-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2011 Oct 4;478(7367):17. doi: 10.1038/478017a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979022" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Genetic Counseling/*ethics ; Genetic Testing/*ethics ; Genome, Human/*genetics ; Genomics/*ethics ; Humans ; Infant ; Male ; Pregnancy ; Truth Disclosure/ethics
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    Post-traumatic stress disorder is associated with PACAP and the PAC1 receptor (2011)
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    Details
    Publication Date: 2011-02-26
    Description: Pituitary adenylate cyclase-activating polypeptide (PACAP) is known to broadly regulate the cellular stress response. In contrast, it is unclear if the PACAP-PAC1 receptor pathway has a role in human psychological stress responses, such as post-traumatic stress disorder (PTSD). Here we find, in heavily traumatized subjects, a sex-specific association of PACAP blood levels with fear physiology, PTSD diagnosis and symptoms in females. We examined 44 single nucleotide polymorphisms (SNPs) spanning the PACAP (encoded by ADCYAP1) and PAC1 (encoded by ADCYAP1R1) genes, demonstrating a sex-specific association with PTSD. A single SNP in a putative oestrogen response element within ADCYAP1R1, rs2267735, predicts PTSD diagnosis and symptoms in females only. This SNP also associates with fear discrimination and with ADCYAP1R1 messenger RNA expression in human brain. Methylation of ADCYAP1R1 in peripheral blood is also associated with PTSD. Complementing these human data, ADCYAP1R1 mRNA is induced with fear conditioning or oestrogen replacement in rodent models. These data suggest that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress responses underlying PTSD. These sex-specific effects may occur via oestrogen regulation of ADCYAP1R1. PACAP levels and ADCYAP1R1 SNPs may serve as useful biomarkers to further our mechanistic understanding of PTSD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046811/" 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/PMC3046811/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ressler, Kerry J -- Mercer, Kristina B -- Bradley, Bekh -- Jovanovic, Tanja -- Mahan, Amy -- Kerley, Kimberly -- Norrholm, Seth D -- Kilaru, Varun -- Smith, Alicia K -- Myers, Amanda J -- Ramirez, Manuel -- Engel, Anzhelika -- Hammack, Sayamwong E -- Toufexis, Donna -- Braas, Karen M -- Binder, Elisabeth B -- May, Victor -- AG034504/AG/NIA NIH HHS/ -- DA019624/DA/NIDA NIH HHS/ -- HD27468/HD/NICHD NIH HHS/ -- M01RR00039/RR/NCRR NIH HHS/ -- MH071537/MH/NIMH NIH HHS/ -- P20RR16435/RR/NCRR NIH HHS/ -- R01 AG034504/AG/NIA NIH HHS/ -- R01 HD027468/HD/NICHD NIH HHS/ -- R01 HD027468-13/HD/NICHD NIH HHS/ -- UL1 TR000454/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 24;470(7335):492-7. doi: 10.1038/nature09856.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA. kressle@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350482" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Conditioning, Classical/physiology ; CpG Islands/genetics ; DNA Methylation ; Estrogens/metabolism/pharmacology ; Fear/physiology ; Female ; Gene Expression Regulation/drug effects ; Genetic Association Studies ; Genetic Predisposition to Disease/*genetics ; Humans ; Male ; Mice ; Pituitary Adenylate Cyclase-Activating Polypeptide/*blood/chemistry ; Polymorphism, Single Nucleotide/genetics ; RNA, Messenger/analysis/biosynthesis/genetics ; Rats ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I/*genetics ; Response Elements/genetics ; Septal Nuclei/drug effects/metabolism ; Sex Characteristics ; Stress Disorders, Post-Traumatic/*blood/*genetics/physiopathology/psychology
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    HIV drug-prevention strategy carries risks (2011)
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    Publication Date: 2011-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2011 Aug 16;476(7360):260-1. doi: 10.1038/476260a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21850077" target="_blank"〉PubMed〈/a〉
    Keywords: Chemoprevention/*adverse effects/*psychology ; Clinical Trials as Topic ; Deoxycytidine/analogs & derivatives/pharmacology/supply & ; distribution/therapeutic use ; Drug Combinations ; Emtricitabine, Tenofovir Disoproxil Fumarate Drug Combination ; Female ; HIV Infections/economics/*prevention & control/*psychology ; Health ; Humans ; Male ; Organophosphorus Compounds/pharmacology/supply & distribution/therapeutic use ; United States ; United States Food and Drug Administration ; Unsafe Sex/*drug effects/*psychology/statistics & numerical data
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    An olfactory receptor for food-derived odours promotes male courtship in Drosophila (2011)
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    Publication Date: 2011-10-04
    Description: Many animals attract mating partners through the release of volatile sex pheromones, which can convey information on the species, gender and receptivity of the sender to induce innate courtship and mating behaviours by the receiver. Male Drosophila melanogaster fruitflies display stereotyped reproductive behaviours towards females, and these behaviours are controlled by the neural circuitry expressing male-specific isoforms of the transcription factor Fruitless (FRU(M)). However, the volatile pheromone ligands, receptors and olfactory sensory neurons (OSNs) that promote male courtship have not been identified in this important model organism. Here we describe a novel courtship function of Ionotropic receptor 84a (IR84a), which is a member of the chemosensory ionotropic glutamate receptor family, in a previously uncharacterized population of FRU(M)-positive OSNs. IR84a-expressing neurons are activated not by fly-derived chemicals but by the aromatic odours phenylacetic acid and phenylacetaldehyde, which are widely found in fruit and other plant tissues that serve as food sources and oviposition sites for drosophilid flies. Mutation of Ir84a abolishes both odour-evoked and spontaneous electrophysiological activity in these neurons and markedly reduces male courtship behaviour. Conversely, male courtship is increased--in an IR84a-dependent manner--in the presence of phenylacetic acid but not in the presence of another fruit odour that does not activate IR84a. Interneurons downstream of IR84a-expressing OSNs innervate a pheromone-processing centre in the brain. Whereas IR84a orthologues and phenylacetic-acid-responsive neurons are present in diverse drosophilid species, IR84a is absent from insects that rely on long-range sex pheromones. Our results suggest a model in which IR84a couples food presence to the activation of the fru(M) courtship circuitry in fruitflies. These findings reveal an unusual but effective evolutionary solution to coordinate feeding and oviposition site selection with reproductive behaviours through a specific sensory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grosjean, Yael -- Rytz, Raphael -- Farine, Jean-Pierre -- Abuin, Liliane -- Cortot, Jerome -- Jefferis, Gregory S X E -- Benton, Richard -- MC_U105188491/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Sep 28;478(7368):236-40. doi: 10.1038/nature10428.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, CH-1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21964331" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/analogs & derivatives/metabolism/pharmacology ; Animals ; *Courtship ; Drosophila melanogaster/anatomy & histology/drug effects/genetics/*physiology ; Female ; *Food ; Fruit/chemistry ; Genotype ; Male ; Odors/*analysis ; Olfactory Receptor Neurons/drug effects/*metabolism ; Oviposition/physiology ; Phenylacetates/metabolism/pharmacology ; Receptors, Ionotropic Glutamate/genetics/metabolism ; Sex Attractants/metabolism/pharmacology ; Sexual Behavior, Animal/drug effects/*physiology
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    Perspective: The big C - for Chemoprevention (2011)
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    Publication Date: 2011-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sporn, Michael B -- England -- Nature. 2011 Mar 24;471(7339):S10-1. doi: 10.1038/471S10a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dartmouth Medical School, Hanover, New Hampshire, USA. michael.b.sporn@dartmouth.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430710" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Combined Chemotherapy Protocols/economics/pharmacology/therapeutic ; use ; Clinical Trials as Topic/legislation & jurisprudence/standards ; Cooperative Behavior ; Disease Progression ; Female ; Humans ; Male ; Neoplasms/drug therapy/epidemiology/pathology/*prevention & control ; Precision Medicine/trends ; Risk ; Time Factors ; Tumor Microenvironment/drug effects ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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    Earliest evidence of mammalian social behaviour in the basal Tertiary of Bolivia (2011)
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    Publication Date: 2011-05-10
    Description: The vast majority of Mesozoic and early Cenozoic metatherian mammals (extinct relatives of modern marsupials) are known only from partial jaws or isolated teeth, which give insight into their probable diets and phylogenetic relationships but little else. The few skulls known are generally crushed, incomplete or both, and associated postcranial material is extremely rare. Here we report the discovery of an exceptionally large number of almost undistorted, nearly complete skulls and skeletons of a stem-metatherian, Pucadelphys andinus, in the early Palaeocene epoch of Tiupampa in Bolivia. These give an unprecedented glimpse into early metatherian morphology, evolutionary relationships and, especially, ecology. The remains of 35 individuals have been collected, with 22 of these represented by nearly complete skulls and associated postcrania. These individuals were probably buried in a single catastrophic event, and so almost certainly belong to the same population. The preservation of multiple adult, sub-adult and juvenile individuals in close proximity (〈1 m(2)) is indicative of gregarious social behaviour or at least a high degree of social tolerance and frequent interaction. Such behaviour is unknown in living didelphids, which are highly solitary and have been regarded, perhaps wrongly, as the most generalized living marsupials. The Tiupampan P. andinus population also exhibits strong sexual dimorphism, which, in combination with gregariousness, suggests strong male-male competition and polygyny. Our study shows that social interactions occurred in metatherians as early as the basal Palaeocene and that solitary behaviour may not be plesiomorphic for Metatheria as a whole.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ladeveze, Sandrine -- de Muizon, Christian -- Beck, Robin M D -- Germain, Damien -- Cespedes-Paz, Ricardo -- England -- Nature. 2011 Jun 2;474(7349):83-6. doi: 10.1038/nature09987. Epub 2011 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Paleontology, Royal Belgian Institute of Natural Sciences, 29 rue Vautier, B-1000 Brussels, Belgium. sandrine.ladeveze@naturalsciences.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21552278" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bolivia ; Female ; *Fossils ; Male ; Marsupialia/anatomy & histology/*classification ; Sex Characteristics ; *Social Behavior
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    Over the limit (2011)
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    Publication Date: 2011-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2011 Mar 10;471(7337):136. doi: 10.1038/471136a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21390085" target="_blank"〉PubMed〈/a〉
    Keywords: Bias (Epidemiology) ; Cost-Benefit Analysis ; Female ; Global Warming ; Human Rights ; Humans ; Insurance, Accident/economics/*statistics & numerical data ; Insurance, Life/economics/*statistics & numerical data ; Male ; *Policy Making ; *Risk Assessment/methods/standards ; *Sex Characteristics
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    Asymmetric cell divisions promote Notch-dependent epidermal differentiation (2011)
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    Publication Date: 2011-02-19
    Description: Stem and progenitor cells use asymmetric cell divisions to balance proliferation and differentiation. Evidence from invertebrates shows that this process is regulated by proteins asymmetrically distributed at the cell cortex during mitosis: Par3-Par6-aPKC, which confer polarity, and Galpha(i)-LGN/AGS3-NuMA-dynein/dynactin, which govern spindle positioning. Here we focus on developing mouse skin, where progenitor cells execute a switch from symmetric to predominantly asymmetric divisions concomitant with stratification. Using in vivo skin-specific lentiviral RNA interference, we investigate spindle orientation regulation and provide direct evidence that LGN (also called Gpsm2), NuMA and dynactin (Dctn1) are involved. In compromising asymmetric cell divisions, we uncover profound defects in stratification, differentiation and barrier formation, and implicate Notch signalling as an important effector. Our study demonstrates the efficacy of applying RNA interference in vivo to mammalian systems, and the ease of uncovering complex genetic interactions, here to gain insights into how changes in spindle orientation are coupled to establishing proper tissue architecture during skin development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077085/" 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/PMC3077085/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Scott E -- Beronja, Slobodan -- Pasolli, H Amalia -- Fuchs, Elaine -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01 AR050452-07/AR/NIAMS NIH HHS/ -- R01AR27883/AR/NIAMS NIH HHS/ -- R37 AR027883/AR/NIAMS NIH HHS/ -- R37 AR027883-30/AR/NIAMS NIH HHS/ -- R37 AR027883-30S1/AR/NIAMS NIH HHS/ -- R37 AR027883-31/AR/NIAMS NIH HHS/ -- R37 AR027883-32/AR/NIAMS NIH HHS/ -- R37 AR027883-33/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 17;470(7334):353-8. doi: 10.1038/nature09793.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331036" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; *Cell Differentiation ; *Cell Division ; Cells, Cultured ; Epidermis/*cytology ; Female ; Gene Knockdown Techniques ; Keratinocytes/cytology ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/genetics/metabolism ; Nuclear Proteins/deficiency/genetics/metabolism ; Receptors, Notch/genetics/*metabolism ; Signal Transduction ; Skin/cytology/embryology ; Spindle Apparatus/metabolism
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    Psychiatry: A molecular shield from trauma (2011)
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    Publication Date: 2011-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stein, Murray B -- England -- Nature. 2011 Feb 24;470(7335):468-9. doi: 10.1038/470468a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350472" target="_blank"〉PubMed〈/a〉
    Keywords: Estrogens/metabolism/pharmacology ; Fear/physiology ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease/*genetics ; Humans ; Male ; Pituitary Adenylate Cyclase-Activating Polypeptide/*blood ; Polymorphism, Single Nucleotide/genetics ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I/*genetics ; Response Elements/genetics ; *Sex Characteristics ; Stress Disorders, Post-Traumatic/*blood/*genetics/physiopathology/psychology
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    Cryptochromes mediate rhythmic repression of the glucocorticoid receptor (2011)
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    Publication Date: 2011-12-16
    Description: Mammalian metabolism is highly circadian and major hormonal circuits involving nuclear hormone receptors display interlinked diurnal cycling. However, mechanisms that logically explain the coordination of nuclear hormone receptors and the clock are poorly understood. Here we show that two circadian co-regulators, cryptochromes 1 and 2, interact with the glucocorticoid receptor in a ligand-dependent fashion and globally alter the transcriptional response to glucocorticoids in mouse embryonic fibroblasts: cryptochrome deficiency vastly decreases gene repression and approximately doubles the number of dexamethasone-induced genes, suggesting that cryptochromes broadly oppose glucocorticoid receptor activation and promote repression. In mice, genetic loss of cryptochrome 1 and/or 2 results in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced suppression of the hypothalamic-pituitary-adrenal axis coupled with increased glucocorticoid transactivation in the liver. Genomically, cryptochromes 1 and 2 associate with a glucocorticoid response element in the phosphoenolpyruvate carboxykinase 1 promoter in a hormone-dependent manner, and dexamethasone-induced transcription of the phosphoenolpyruvate carboxykinase 1 gene was strikingly increased in cryptochrome-deficient livers. These results reveal a specific mechanism through which cryptochromes couple the activity of clock and receptor target genes to complex genomic circuits underpinning normal metabolic homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245818/" 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/PMC3245818/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Papp, Stephanie J -- Yu, Ruth T -- Barish, Grant D -- Uhlenhaut, N Henriette -- Jonker, Johan W -- Downes, Michael -- Evans, Ronald M -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188-01/DK/NIDDK NIH HHS/ -- K01 DK090188-02/DK/NIDDK NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-22/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Dec 14;480(7378):552-6. doi: 10.1038/nature10700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. klamia@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22170608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Corticosterone/blood ; Cryptochromes/genetics/*metabolism ; Dexamethasone/pharmacology ; Female ; *Gene Expression Regulation/drug effects ; Glucocorticoids/pharmacology ; Glucose Intolerance/genetics ; HEK293 Cells ; Humans ; Liver/enzymology/metabolism ; Mice ; Phosphoenolpyruvate Carboxykinase (GTP)/blood/metabolism ; Receptors, Glucocorticoid/*metabolism
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    Fancd2 counteracts the toxic effects of naturally produced aldehydes in mice (2011)
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    Publication Date: 2011-07-08
    Description: Reactive aldehydes are common carcinogens. They are also by-products of several metabolic pathways and, without enzymatic catabolism, may accumulate and cause DNA damage. Ethanol, which is metabolised to acetaldehyde, is both carcinogenic and teratogenic in humans. Here we find that the Fanconi anaemia DNA repair pathway counteracts acetaldehyde-induced genotoxicity in mice. Our results show that the acetaldehyde-catabolising enzyme Aldh2 is essential for the development of Fancd2(-/-) embryos. Nevertheless, acetaldehyde-catabolism-competent mothers (Aldh2(+/-)) can support the development of double-mutant (Aldh2(-/-)Fancd2(-/-)) mice. However, these embryos are unusually sensitive to ethanol exposure in utero, and ethanol consumption by postnatal double-deficient mice rapidly precipitates bone marrow failure. Lastly, Aldh2(-/-)Fancd2(-/-) mice spontaneously develop acute leukaemia. Acetaldehyde-mediated DNA damage may critically contribute to the genesis of fetal alcohol syndrome in fetuses, as well as to abnormal development, haematopoietic failure and cancer predisposition in Fanconi anaemia patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langevin, Frederic -- Crossan, Gerry P -- Rosado, Ivan V -- Arends, Mark J -- Patel, Ketan J -- MC_U105178811/Medical Research Council/United Kingdom -- England -- Nature. 2011 Jul 6;475(7354):53-8. doi: 10.1038/nature10192.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734703" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/metabolism/toxicity ; Aldehyde Dehydrogenase/deficiency/genetics/metabolism ; Aldehydes/*antagonists & inhibitors/metabolism/*toxicity ; Alleles ; Animals ; B-Lymphocytes/drug effects/metabolism ; Bone Marrow/drug effects/pathology/physiopathology ; Cell Line ; Cell Survival/drug effects ; Chickens ; Clone Cells/drug effects ; DNA Damage/genetics ; DNA Repair/genetics ; Embryo Loss/chemically induced/etiology ; Embryo, Mammalian/abnormalities/drug effects/embryology ; Ethanol/metabolism/toxicity ; Fanconi Anemia/genetics/pathology ; Fanconi Anemia Complementation Group D2 Protein/deficiency/genetics/*metabolism ; Female ; Fetal Alcohol Spectrum Disorders/etiology ; Gene Deletion ; Genes, Essential ; Hematopoiesis/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/chemically induced/etiology ; Pregnancy ; Teratogens/metabolism/toxicity ; Weaning
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Inclusive fitness theory and eusociality (2011)
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    Details
    Publication Date: 2011-03-25
    Description: Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Nowak et al. argue that inclusive fitness theory has been of little value in explaining the natural world, and that it has led to negligible progress in explaining the evolution of eusociality. However, we believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature. We will focus our comments on three general issues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836173/" 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/PMC3836173/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbot, Patrick -- Abe, Jun -- Alcock, John -- Alizon, Samuel -- Alpedrinha, Joao A C -- Andersson, Malte -- Andre, Jean-Baptiste -- van Baalen, Minus -- Balloux, Francois -- Balshine, Sigal -- Barton, Nick -- Beukeboom, Leo W -- Biernaskie, Jay M -- Bilde, Trine -- Borgia, Gerald -- Breed, Michael -- Brown, Sam -- Bshary, Redouan -- Buckling, Angus -- Burley, Nancy T -- Burton-Chellew, Max N -- Cant, Michael A -- Chapuisat, Michel -- Charnov, Eric L -- Clutton-Brock, Tim -- Cockburn, Andrew -- Cole, Blaine J -- Colegrave, Nick -- Cosmides, Leda -- Couzin, Iain D -- Coyne, Jerry A -- Creel, Scott -- Crespi, Bernard -- Curry, Robert L -- Dall, Sasha R X -- Day, Troy -- Dickinson, Janis L -- Dugatkin, Lee Alan -- El Mouden, Claire -- Emlen, Stephen T -- Evans, Jay -- Ferriere, Regis -- Field, Jeremy -- Foitzik, Susanne -- Foster, Kevin -- Foster, William A -- Fox, Charles W -- Gadau, Juergen -- Gandon, Sylvain -- Gardner, Andy -- Gardner, Michael G -- Getty, Thomas -- Goodisman, Michael A D -- Grafen, Alan -- Grosberg, Rick -- Grozinger, Christina M -- Gouyon, Pierre-Henri -- Gwynne, Darryl -- Harvey, Paul H -- Hatchwell, Ben J -- Heinze, Jurgen -- Helantera, Heikki -- Helms, Ken R -- Hill, Kim -- Jiricny, Natalie -- Johnstone, Rufus A -- Kacelnik, Alex -- Kiers, E Toby -- Kokko, Hanna -- Komdeur, Jan -- Korb, Judith -- Kronauer, Daniel -- Kummerli, Rolf -- Lehmann, Laurent -- Linksvayer, Timothy A -- Lion, Sebastien -- Lyon, Bruce -- Marshall, James A R -- McElreath, Richard -- Michalakis, Yannis -- Michod, Richard E -- Mock, Douglas -- Monnin, Thibaud -- Montgomerie, Robert -- Moore, Allen J -- Mueller, Ulrich G -- Noe, Ronald -- Okasha, Samir -- Pamilo, Pekka -- Parker, Geoff A -- Pedersen, Jes S -- Pen, Ido -- Pfennig, David -- Queller, David C -- Rankin, Daniel J -- Reece, Sarah E -- Reeve, Hudson K -- Reuter, Max -- Roberts, Gilbert -- Robson, Simon K A -- Roze, Denis -- Rousset, Francois -- Rueppell, Olav -- Sachs, Joel L -- Santorelli, Lorenzo -- Schmid-Hempel, Paul -- Schwarz, Michael P -- Scott-Phillips, Tom -- Shellmann-Sherman, Janet -- Sherman, Paul W -- Shuker, David M -- Smith, Jeff -- Spagna, Joseph C -- Strassmann, Beverly -- Suarez, Andrew V -- Sundstrom, Liselotte -- Taborsky, Michael -- Taylor, Peter -- Thompson, Graham -- Tooby, John -- Tsutsui, Neil D -- Tsuji, Kazuki -- Turillazzi, Stefano -- Ubeda, Francisco -- Vargo, Edward L -- Voelkl, Bernard -- Wenseleers, Tom -- West, Stuart A -- West-Eberhard, Mary Jane -- Westneat, David F -- Wiernasz, Diane C -- Wild, Geoff -- Wrangham, Richard -- Young, Andrew J -- Zeh, David W -- Zeh, Jeanne A -- Zink, Andrew -- BB/H022716/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2011 Mar 24;471(7339):E1-4; author reply E9-10. doi: 10.1038/nature09831.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430721" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Game Theory ; *Genetic Fitness ; Genetics, Population ; Heredity ; Humans ; Male ; *Models, Biological ; Phenotype ; Reproducibility of Results ; *Selection, Genetic ; Sex Ratio
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    Entomology: Royal aspirations (2011)
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    Publication Date: 2011-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, Gene E -- England -- Nature. 2011 May 26;473(7348):454-5. doi: 10.1038/473454a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21614066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bees/*drug effects/genetics/*growth & development/physiology ; Body Size/drug effects ; Drosophila melanogaster/drug effects/enzymology/growth & development/physiology ; Fat Body/drug effects/metabolism ; Fatty Acids/chemistry/*pharmacology ; Female ; Fertility/drug effects ; Glycoproteins/isolation & purification/pharmacology ; Insect Proteins/isolation & purification/pharmacology ; Juvenile Hormones/metabolism ; Larva/drug effects/growth & development ; Longevity/drug effects ; Ovary/drug effects/growth & development ; Phenotype ; Protein Stability ; Receptor, Epidermal Growth Factor/metabolism ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Signal Transduction/drug effects ; *Social Dominance
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    Licence rules hinder work on rare disease (2011)
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    Publication Date: 2011-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2011 Feb 17;470(7334):318-9. doi: 10.1038/470318a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/economics/*legislation & jurisprudence ; *Disease Models, Animal ; Female ; Humans ; Internationality ; Licensure/*legislation & jurisprudence ; Methyl-CpG-Binding Protein 2/genetics/immunology ; Mice ; Models, Immunological ; National Institutes of Health (U.S.) ; *Rare Diseases ; *Rett Syndrome/genetics/immunology/therapy ; Time Factors ; United States
    Print ISSN: 0028-0836
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    Reversing pathological neural activity using targeted plasticity (2011)
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    Publication Date: 2011-01-14
    Description: Brain changes in response to nerve damage or cochlear trauma can generate pathological neural activity that is believed to be responsible for many types of chronic pain and tinnitus. Several studies have reported that the severity of chronic pain and tinnitus is correlated with the degree of map reorganization in somatosensory and auditory cortex, respectively. Direct electrical or transcranial magnetic stimulation of sensory cortex can temporarily disrupt these phantom sensations. However, there is as yet no direct evidence for a causal role of plasticity in the generation of pain or tinnitus. Here we report evidence that reversing the brain changes responsible can eliminate the perceptual impairment in an animal model of noise-induced tinnitus. Exposure to intense noise degrades the frequency tuning of auditory cortex neurons and increases cortical synchronization. Repeatedly pairing tones with brief pulses of vagus nerve stimulation completely eliminated the physiological and behavioural correlates of tinnitus in noise-exposed rats. These improvements persisted for weeks after the end of therapy. This method for restoring neural activity to normal may be applicable to a variety of neurological disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295231/" 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/PMC3295231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engineer, Navzer D -- Riley, Jonathan R -- Seale, Jonathan D -- Vrana, Will A -- Shetake, Jai A -- Sudanagunta, Sindhu P -- Borland, Michael S -- Kilgard, Michael P -- R43 DC010084-01/DC/NIDCD NIH HHS/ -- R44 DC010084-03/DC/NIDCD NIH HHS/ -- England -- Nature. 2011 Feb 3;470(7332):101-4. doi: 10.1038/nature09656. Epub 2011 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cortical Plasticity Laboratory, Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, Texas 75080, USA. navzer@utdallas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21228773" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Auditory Perception/physiology ; Behavior, Animal/physiology ; Disease Models, Animal ; Electric Stimulation ; Female ; Models, Neurological ; Neuronal Plasticity/*physiology ; Noise/adverse effects ; Rats ; Rats, Sprague-Dawley ; Tinnitus/etiology/pathology/*physiopathology/*therapy ; Vagus Nerve/physiology
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    NIH: FDA key for speed and safety (2011)
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    Publication Date: 2011-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reichmann, James P -- England -- Nature. 2011 Jun 8;474(7350):161. doi: 10.1038/474161c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654788" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; *Drug Approval ; Female ; Humans ; *National Institutes of Health (U.S.) ; Orphan Drug Production/legislation & jurisprudence ; Pregnancy ; Premature Birth/prevention & control ; Time Factors ; United States ; *United States Food and Drug Administration/legislation & jurisprudence
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    Translational research: 4 ways to fix the clinical trial (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2011 Sep 28;477(7366):526-8. doi: 10.1038/477526a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21956311" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clinical Trials as Topic/economics/*methods/*trends ; Database Management Systems ; Disease Models, Animal ; Drug Evaluation, Preclinical/methods ; Female ; Humans ; Male ; Mice ; Multicenter Studies as Topic/methods ; Precision Medicine/economics/methods/trends ; Translational Medical Research/economics/methods/trends ; United States ; United States Food and Drug Administration/legislation & jurisprudence
    Print ISSN: 0028-0836
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    Control of TH17 cells occurs in the small intestine (2011)
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    Publication Date: 2011-07-19
    Description: Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148838/" 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/PMC3148838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esplugues, Enric -- Huber, Samuel -- Gagliani, Nicola -- Hauser, Anja E -- Town, Terrence -- Wan, Yisong Y -- O'Connor, William Jr -- Rongvaux, Anthony -- Van Rooijen, Nico -- Haberman, Ann M -- Iwakura, Yoichiro -- Kuchroo, Vijay K -- Kolls, Jay K -- Bluestone, Jeffrey A -- Herold, Kevan C -- Flavell, Richard A -- DK45735/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-20/DK/NIDDK NIH HHS/ -- R01 HL061271/HL/NHLBI NIH HHS/ -- R01 HL062052/HL/NHLBI NIH HHS/ -- R21 HL104601/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jul 17;475(7357):514-8. doi: 10.1038/nature10228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21765430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology/pharmacology ; Antigens, CD3/immunology ; CD4-Positive T-Lymphocytes/immunology/transplantation ; Cell Movement/drug effects ; Chemokine CCL20/immunology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Gene Expression Profiling ; Gene Expression Regulation/immunology ; Influenza A virus/immunology ; Interleukin-17/immunology ; Intestine, Small/cytology/*immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Orthomyxoviridae Infections/immunology ; Receptors, CCR6/immunology ; Sepsis/immunology ; Staphylococcal Infections/immunology ; Th17 Cells/*immunology
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    NLRP6 negatively regulates innate immunity and host defence against bacterial pathogens (2012)
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    Publication Date: 2012-07-06
    Description: Members of the intracellular nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family contribute to immune responses through activation of nuclear factor-kappaB (NF-kappaB), type I interferon and inflammasome signalling. Mice lacking the NLR family member NLRP6 were recently shown to be susceptible to colitis and colorectal tumorigenesis, but the role of NLRP6 in microbial infections and the nature of the inflammatory signalling pathways regulated by NLRP6 remain unclear. Here we show that Nlrp6-deficient mice are highly resistant to infection with the bacterial pathogens Listeria monocytogenes, Salmonella typhimurium and Escherichia coli. Infected Nlrp6-deficient mice had increased numbers of monocytes and neutrophils in circulation, and NLRP6 signalling in both haematopoietic and radioresistant cells contributed to increased susceptibility. Nlrp6 deficiency enhanced activation of mitogen-activated protein kinase (MAPK) and the canonical NF-kappaB pathway after Toll-like receptor ligation, but not cytosolic NOD1/2 ligation, in vitro. Consequently, infected Nlrp6-deficient cells produced increased levels of NF-kappaB- and MAPK-dependent cytokines and chemokines. Thus, our results reveal NLRP6 as a negative regulator of inflammatory signalling, and demonstrate a role for this NLR in impeding clearance of both Gram-positive and -negative bacterial pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422416/" 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/PMC3422416/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anand, Paras K -- Malireddi, R K Subbarao -- Lukens, John R -- Vogel, Peter -- Bertin, John -- Lamkanfi, Mohamed -- Kanneganti, Thirumala-Devi -- AI101935/AI/NIAID NIH HHS/ -- AR056296/AR/NIAMS NIH HHS/ -- R01 AI101935/AI/NIAID NIH HHS/ -- R01 AR056296/AR/NIAMS NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):389-93. doi: 10.1038/nature11250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Susceptibility/immunology ; Escherichia coli/*immunology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Immunity, Innate/*immunology ; Listeria monocytogenes/*immunology ; MAP Kinase Signaling System ; Mice ; Monocytes/cytology/enzymology/immunology/metabolism ; NF-kappa B/metabolism ; Neutrophils/cytology/enzymology/immunology/metabolism ; Receptors, Cell Surface/deficiency/genetics/immunology/*metabolism ; Salmonella typhimurium/*immunology
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    Toxicology: The learning curve (2012)
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    Publication Date: 2012-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagin, Dan -- England -- Nature. 2012 Oct 25;490(7421):462-5. doi: 10.1038/490462a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23099381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzhydryl Compounds ; Diethylhexyl Phthalate/administration & dosage/toxicity ; Diethylstilbestrol/administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Endocrine Disruptors/*administration & dosage/*toxicity ; Estradiol/administration & dosage/toxicity ; Female ; Humans ; Male ; Mice ; National Institute of Environmental Health Sciences (U.S.) ; Phenols/administration & dosage/toxicity ; Risk Assessment/*methods ; Tamoxifen/administration & dosage/adverse effects/pharmacology ; Toxicology/*methods ; United States
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    Microbiology: Learning about who we are (2012)
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    Publication Date: 2012-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Relman, David A -- England -- Nature. 2012 Jun 13;486(7402):194-5. doi: 10.1038/486194a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699602" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*classification/*genetics ; *Biodiversity ; Female ; *Health ; Humans ; Male ; *Metagenome ; Metagenomics/*methods
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    The split brain: a tale of two halves (2012)
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    Publication Date: 2012-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolman, David -- England -- Nature. 2012 Mar 14;483(7389):260-3. doi: 10.1038/483260a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422242" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Age Factors ; Animals ; Brain/*physiology/*physiopathology/surgery ; Cohort Studies ; Corpus Callosum/physiology/physiopathology/*surgery ; Epilepsy/history/surgery ; Female ; Functional Laterality/*physiology ; History, 20th Century ; History, 21st Century ; Humans ; Magnetic Resonance Imaging ; Male ; Morals ; Neurosciences/*history ; Seizures/history/surgery
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    Ageing: Mixed results for dieting monkeys (2012)
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    Publication Date: 2012-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Austad, Steven N -- England -- Nature. 2012 Sep 13;489(7415):210-11. doi: 10.1038/nature11484.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932269" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Female ; *Health ; Humans ; Longevity/*physiology ; Male ; *National Institute on Aging (U.S.)
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    Non-invasive prenatal measurement of the fetal genome (2012)
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    Details
    Publication Date: 2012-07-06
    Description: The vast majority of prenatal genetic testing requires invasive sampling. However, this poses a risk to the fetus, so one must make a decision that weighs the desire for genetic information against the risk of an adverse outcome due to hazards of the testing process. These issues are not required to be coupled, and it would be desirable to discover genetic information about the fetus without incurring a health risk. Here we demonstrate that it is possible to non-invasively sequence the entire prenatal genome. Our results show that molecular counting of parental haplotypes in maternal plasma by shotgun sequencing of maternal plasma DNA allows the inherited fetal genome to be deciphered non-invasively. We also applied the counting principle directly to each allele in the fetal exome by performing exome capture on maternal plasma DNA before shotgun sequencing. This approach enables non-invasive exome screening of clinically relevant and deleterious alleles that were paternally inherited or had arisen as de novo germline mutations, and complements the haplotype counting approach to provide a comprehensive view of the fetal genome. Non-invasive determination of the fetal genome may ultimately facilitate the diagnosis of all inherited and de novo genetic disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561905/" 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/PMC3561905/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, H Christina -- Gu, Wei -- Wang, Jianbin -- Blumenfeld, Yair J -- El-Sayed, Yasser Y -- Quake, Stephen R -- DP1 OD000251/OD/NIH HHS/ -- U54 CA151459/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jul 19;487(7407):320-4. doi: 10.1038/nature11251.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Clark Center Rm E300, 318 Campus Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763444" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human/genetics ; DNA/*analysis/blood ; Exome/genetics ; Female ; Fetus ; *Genome, Human ; Haplotypes ; Humans ; Male ; Pregnancy ; Prenatal Diagnosis/*methods ; Sensitivity and Specificity
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    Fetal tests spur legal battle (2012)
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    Publication Date: 2012-06-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2012 Jun 27;486(7404):454. doi: 10.1038/486454a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22739292" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Female ; Fetus/blood supply/*metabolism ; Genetic Testing/economics/*legislation & jurisprudence/utilization ; Humans ; Patents as Topic/legislation & jurisprudence ; Pregnancy/*blood ; *Prenatal Diagnosis/economics/utilization
    Print ISSN: 0028-0836
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    Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: Autism spectrum disorder (ASD) is a group of conditions characterized by impaired social interaction and communication, and restricted and repetitive behaviours. ASD is a highly heritable disorder involving various genetic determinants. Shank2 (also known as ProSAP1) is a multi-domain scaffolding protein and signalling adaptor enriched at excitatory neuronal synapses, and mutations in the human SHANK2 gene have recently been associated with ASD and intellectual disability. Although ASD-associated genes are being increasingly identified and studied using various approaches, including mouse genetics, further efforts are required to delineate important causal mechanisms with the potential for therapeutic application. Here we show that Shank2-mutant (Shank2(-/-)) mice carrying a mutation identical to the ASD-associated microdeletion in the human SHANK2 gene exhibit ASD-like behaviours including reduced social interaction, reduced social communication by ultrasonic vocalizations, and repetitive jumping. These mice show a marked decrease in NMDA (N-methyl-D-aspartate) glutamate receptor (NMDAR) function. Direct stimulation of NMDARs with D-cycloserine, a partial agonist of NMDARs, normalizes NMDAR function and improves social interaction in Shank2(-/-) mice. Furthermore, treatment of Shank2(-/-) mice with a positive allosteric modulator of metabotropic glutamate receptor 5 (mGluR5), which enhances NMDAR function via mGluR5 activation, also normalizes NMDAR function and markedly enhances social interaction. These results suggest that reduced NMDAR function may contribute to the development of ASD-like phenotypes in Shank2(-/-) mice, and mGluR modulation of NMDARs offers a potential strategy to treat ASD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Won, Hyejung -- Lee, Hye-Ryeon -- Gee, Heon Yung -- Mah, Won -- Kim, Jae-Ick -- Lee, Jiseok -- Ha, Seungmin -- Chung, Changuk -- Jung, Eun Suk -- Cho, Yi Sul -- Park, Sae-Geun -- Lee, Jung-Soo -- Lee, Kyungmin -- Kim, Daesoo -- Bae, Yong Chul -- Kaang, Bong-Kiun -- Lee, Min Goo -- Kim, Eunjoon -- England -- Nature. 2012 Jun 13;486(7402):261-5. doi: 10.1038/nature11208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, KAIST, Daejeon 305-701, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699620" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*genetics ; Animals ; Antimetabolites/pharmacology ; *Autistic Disorder/genetics/metabolism ; Behavior, Animal/*drug effects/physiology ; Benzamides/*pharmacology ; Cycloserine/*pharmacology ; Disease Models, Animal ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/*genetics ; Pyrazoles/*pharmacology ; Receptors, N-Methyl-D-Aspartate/*agonists/*metabolism
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    Metastasis: The rude awakening (2012)
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    Publication Date: 2012-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, Jocelyn -- England -- Nature. 2012 May 30;485(7400):S55-7. doi: 10.1038/485S55a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22648500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*pathology/therapy ; Female ; Humans ; Mice ; Neoplasm Metastasis/*pathology/therapy ; Neoplastic Cells, Circulating/pathology ; Recurrence
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    Sensory science: partners in flavour (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakalar, Nicholas -- England -- Nature. 2012 Jun 20;486(7403):S4-5. doi: 10.1038/486S4a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22717401" target="_blank"〉PubMed〈/a〉
    Keywords: Amniotic Fluid/chemistry ; Electroencephalography ; Female ; Fetus/drug effects/physiology ; Flavoring Agents/*pharmacology ; *Food ; Food Habits/physiology ; Hearing/physiology ; Humans ; Odors ; Pregnancy ; Smell/physiology ; Taste/drug effects/*physiology ; Temperature ; Vision, Ocular/physiology
    Print ISSN: 0028-0836
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    Neuroscience: Sibling neurons bond to share sensations (2012)
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    Publication Date: 2012-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mrsic-Flogel, Thomas D -- Bonhoeffer, Tobias -- 095074/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Jun 6;486(7401):41-2. doi: 10.1038/486041a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; *Cell Lineage ; *Electric Conductivity ; Electrical Synapses/*physiology ; Female ; Gap Junctions/*metabolism ; Male ; Neocortex/*cytology ; Neurons/*cytology/*physiology ; Visual Cortex/*cytology
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    Stem cells: a sporadic super state (2012)
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    Publication Date: 2012-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surani, Azim -- Tischler, Julia -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- England -- Nature. 2012 Jul 4;487(7405):43-5. doi: 10.1038/487043a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK. a.surani@gurdon.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Dedifferentiation/*genetics ; Embryonic Stem Cells/*cytology/*metabolism ; Endogenous Retroviruses/*genetics ; Female ; Pluripotent Stem Cells/*cytology ; Totipotent Stem Cells/*cytology/*metabolism
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    Sequence analysis of mutations and translocations across breast cancer subtypes (2012)
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    Publication Date: 2012-06-23
    Description: Breast carcinoma is the leading cause of cancer-related mortality in women worldwide, with an estimated 1.38 million new cases and 458,000 deaths in 2008 alone. This malignancy represents a heterogeneous group of tumours with characteristic molecular features, prognosis and responses to available therapy. Recurrent somatic alterations in breast cancer have been described, including mutations and copy number alterations, notably ERBB2 amplifications, the first successful therapy target defined by a genomic aberration. Previous DNA sequencing studies of breast cancer genomes have revealed additional candidate mutations and gene rearrangements. Here we report the whole-exome sequences of DNA from 103 human breast cancers of diverse subtypes from patients in Mexico and Vietnam compared to matched-normal DNA, together with whole-genome sequences of 22 breast cancer/normal pairs. Beyond confirming recurrent somatic mutations in PIK3CA, TP53, AKT1, GATA3 and MAP3K1, we discovered recurrent mutations in the CBFB transcription factor gene and deletions of its partner RUNX1. Furthermore, we have identified a recurrent MAGI3-AKT3 fusion enriched in triple-negative breast cancer lacking oestrogen and progesterone receptors and ERBB2 expression. The MAGI3-AKT3 fusion leads to constitutive activation of AKT kinase, which is abolished by treatment with an ATP-competitive AKT small-molecule inhibitor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148686/" 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/PMC4148686/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerji, Shantanu -- Cibulskis, Kristian -- Rangel-Escareno, Claudia -- Brown, Kristin K -- Carter, Scott L -- Frederick, Abbie M -- Lawrence, Michael S -- Sivachenko, Andrey Y -- Sougnez, Carrie -- Zou, Lihua -- Cortes, Maria L -- Fernandez-Lopez, Juan C -- Peng, Shouyong -- Ardlie, Kristin G -- Auclair, Daniel -- Bautista-Pina, Veronica -- Duke, Fujiko -- Francis, Joshua -- Jung, Joonil -- Maffuz-Aziz, Antonio -- Onofrio, Robert C -- Parkin, Melissa -- Pho, Nam H -- Quintanar-Jurado, Valeria -- Ramos, Alex H -- Rebollar-Vega, Rosa -- Rodriguez-Cuevas, Sergio -- Romero-Cordoba, Sandra L -- Schumacher, Steven E -- Stransky, Nicolas -- Thompson, Kristin M -- Uribe-Figueroa, Laura -- Baselga, Jose -- Beroukhim, Rameen -- Polyak, Kornelia -- Sgroi, Dennis C -- Richardson, Andrea L -- Jimenez-Sanchez, Gerardo -- Lander, Eric S -- Gabriel, Stacey B -- Garraway, Levi A -- Golub, Todd R -- Melendez-Zajgla, Jorge -- Toker, Alex -- Getz, Gad -- Hidalgo-Miranda, Alfredo -- Meyerson, Matthew -- CA089393/CA/NCI NIH HHS/ -- CA122099/CA/NCI NIH HHS/ -- R01 CA122099/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 20;486(7403):405-9. doi: 10.1038/nature11154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722202" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Breast Neoplasms/*classification/*genetics/pathology ; Core Binding Factor Alpha 2 Subunit/genetics ; Core Binding Factor beta Subunit/genetics ; DNA Mutational Analysis ; Exome/genetics ; Female ; Gene Fusion/genetics ; Humans ; Membrane Proteins/genetics ; Mexico ; Mutation/*genetics ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/genetics/metabolism ; Translocation, Genetic/*genetics ; Vietnam
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    A restricted cell population propagates glioblastoma growth after chemotherapy (2012)
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    Publication Date: 2012-08-03
    Description: Glioblastoma multiforme is the most common primary malignant brain tumour, with a median survival of about one year. This poor prognosis is due to therapeutic resistance and tumour recurrence after surgical removal. Precisely how recurrence occurs is unknown. Using a genetically engineered mouse model of glioma, here we identify a subset of endogenous tumour cells that are the source of new tumour cells after the drug temozolomide (TMZ) is administered to transiently arrest tumour growth. A nestin-DeltaTK-IRES-GFP (Nes-DeltaTK-GFP) transgene that labels quiescent subventricular zone adult neural stem cells also labels a subset of endogenous glioma tumour cells. On arrest of tumour cell proliferation with TMZ, pulse-chase experiments demonstrate a tumour re-growth cell hierarchy originating with the Nes-DeltaTK-GFP transgene subpopulation. Ablation of the GFP+ cells with chronic ganciclovir administration significantly arrested tumour growth, and combined TMZ and ganciclovir treatment impeded tumour development. Thus, a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed for cancer stem cells, is responsible for sustaining long-term tumour growth through the production of transient populations of highly proliferative cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427400/" 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/PMC3427400/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Jian -- Li, Yanjiao -- Yu, Tzong-Shiue -- McKay, Renee M -- Burns, Dennis K -- Kernie, Steven G -- Parada, Luis F -- R01 CA131313/CA/NCI NIH HHS/ -- R01 NS048192-01/NS/NINDS NIH HHS/ -- England -- Nature. 2012 Aug 23;488(7412):522-6. doi: 10.1038/nature11287.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9133, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22854781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents, Alkylating/pharmacology/therapeutic use ; Brain Neoplasms/*drug therapy/*pathology ; Cell Proliferation/drug effects ; Cell Tracking ; Dacarbazine/*analogs & derivatives/pharmacology/therapeutic use ; Disease Models, Animal ; Disease Progression ; Female ; Ganciclovir/pharmacology ; Glioblastoma/*drug therapy/*pathology ; Green Fluorescent Proteins/genetics/metabolism ; Male ; Mice ; Mice, Transgenic ; Neoplastic Stem Cells/*drug effects/*pathology ; Neural Stem Cells/drug effects/pathology ; Transgenes/genetics
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    Cancer metabolism: Tumour friend or foe (2012)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svensson, Robert U -- Shaw, Reuben J -- England -- Nature. 2012 May 31;485(7400):590-1. doi: 10.1038/485590a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660317" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Animals ; *Energy Metabolism ; Female ; *Homeostasis ; Male ; NADP/*metabolism ; Neoplasms/*metabolism/*pathology ; *Oxidative Stress
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    Tet1 controls meiosis by regulating meiotic gene expression (2012)
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    Publication Date: 2012-11-16
    Description: Meiosis is a germ-cell-specific cell division process through which haploid gametes are produced for sexual reproduction. Before the initiation of meiosis, mouse primordial germ cells undergo a series of epigenetic reprogramming steps, including the global erasure of DNA methylation at the 5-position of cytosine (5mC) in CpG-rich DNA. Although several epigenetic regulators, such as Dnmt3l and the histone methyltransferases G9a and Prdm9, have been reported to be crucial for meiosis, little is known about how the expression of meiotic genes is regulated and how their expression contributes to normal meiosis. Using a loss-of-function approach in mice, here we show that the 5mC-specific dioxygenase Tet1 has an important role in regulating meiosis in mouse oocytes. Tet1 deficiency significantly reduces female germ-cell numbers and fertility. Univalent chromosomes and unresolved DNA double-strand breaks are also observed in Tet1-deficient oocytes. Tet1 deficiency does not greatly affect the genome-wide demethylation that takes place in primordial germ cells, but leads to defective DNA demethylation and decreased expression of a subset of meiotic genes. Our study thus establishes a function for Tet1 in meiosis and meiotic gene activation in female germ cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3528851/" 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/PMC3528851/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Shinpei -- Hong, Kwonho -- Liu, Rui -- Shen, Li -- Inoue, Azusa -- Diep, Dinh -- Zhang, Kun -- Zhang, Yi -- R01GM097253/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- U01DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 20;492(7429):443-7. doi: 10.1038/nature11709. Epub 2012 Nov 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, WAB-149G, 200 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23151479" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Count ; DNA Breaks, Double-Stranded ; DNA Methylation/genetics ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Embryo, Mammalian/cytology/pathology ; Female ; Gene Expression Regulation/*genetics ; Infertility, Female/pathology ; Male ; Meiosis/*genetics ; Mice ; Mice, Knockout ; Oocytes/cytology/*metabolism/pathology ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Transcriptome
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    An RNA interference screen uncovers a new molecule in stem cell self-renewal and long-term regeneration (2012)
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    Publication Date: 2012-04-13
    Description: Adult stem cells sustain tissue maintenance and regeneration throughout the lifetime of an animal. These cells often reside in specific signalling niches that orchestrate the stem cell's balancing act between quiescence and cell-cycle re-entry based on the demand for tissue regeneration. How stem cells maintain their capacity to replenish themselves after tissue regeneration is poorly understood. Here we use RNA-interference-based loss-of-function screening as a powerful approach to uncover transcriptional regulators that govern the self-renewal capacity and regenerative potential of stem cells. Hair follicle stem cells provide an ideal model. These cells have been purified and characterized from their native niche in vivo and, in contrast to their rapidly dividing progeny, they can be maintained and passaged long-term in vitro. Focusing on the nuclear proteins and/or transcription factors that are enriched in stem cells compared with their progeny, we screened approximately 2,000 short hairpin RNAs for their effect on long-term, but not short-term, stem cell self-renewal in vitro. To address the physiological relevance of our findings, we selected one candidate that was uncovered in the screen: TBX1. This transcription factor is expressed in many tissues but has not been studied in the context of stem cell biology. By conditionally ablating Tbx1 in vivo, we showed that during homeostasis, tissue regeneration occurs normally but is markedly delayed. We then devised an in vivo assay for stem cell replenishment and found that when challenged with repetitive rounds of regeneration, the Tbx1-deficient stem cell niche becomes progressively depleted. Addressing the mechanism of TBX1 action, we discovered that TBX1 acts as an intrinsic rheostat of BMP signalling: it is a gatekeeper that governs the transition between stem cell quiescence and proliferation in hair follicles. Our results validate the RNA interference screen and underscore its power in unearthing new molecules that govern stem cell self-renewal and tissue-regenerative potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3600643/" 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/PMC3600643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Ting -- Heller, Evan -- Beronja, Slobodan -- Oshimori, Naoki -- Stokes, Nicole -- Fuchs, Elaine -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Apr 4;485(7396):104-8. doi: 10.1038/nature10940.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495305" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/metabolism ; Cell Proliferation ; Epidermis/cytology ; Female ; Hair Follicle/cytology ; Male ; Mice ; *RNA Interference ; Regeneration/genetics/*physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; T-Box Domain Proteins/deficiency/genetics/*metabolism
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    FTO genotype is associated with phenotypic variability of body mass index (2012)
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    Details
    Publication Date: 2012-09-18
    Description: There is evidence across several species for genetic control of phenotypic variation of complex traits, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using approximately 170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype), is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of approximately 0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI, possibly mediated by DNA methylation. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564953/" 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/PMC3564953/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Jian -- Loos, Ruth J F -- Powell, Joseph E -- Medland, Sarah E -- Speliotes, Elizabeth K -- Chasman, Daniel I -- Rose, Lynda M -- Thorleifsson, Gudmar -- Steinthorsdottir, Valgerdur -- Magi, Reedik -- Waite, Lindsay -- Smith, Albert Vernon -- Yerges-Armstrong, Laura M -- Monda, Keri L -- Hadley, David -- Mahajan, Anubha -- Li, Guo -- Kapur, Karen -- Vitart, Veronique -- Huffman, Jennifer E -- Wang, Sophie R -- Palmer, Cameron -- Esko, Tonu -- Fischer, Krista -- Zhao, Jing Hua -- Demirkan, Ayse -- Isaacs, Aaron -- Feitosa, Mary F -- Luan, Jian'an -- Heard-Costa, Nancy L -- White, Charles -- Jackson, Anne U -- Preuss, Michael -- Ziegler, Andreas -- Eriksson, Joel -- Kutalik, Zoltan -- Frau, Francesca -- Nolte, Ilja M -- Van Vliet-Ostaptchouk, Jana V -- Hottenga, Jouke-Jan -- Jacobs, Kevin B -- Verweij, Niek -- Goel, Anuj -- Medina-Gomez, Carolina -- Estrada, Karol -- Bragg-Gresham, Jennifer Lynn -- Sanna, Serena -- Sidore, Carlo -- Tyrer, Jonathan -- Teumer, Alexander -- Prokopenko, Inga -- Mangino, Massimo -- Lindgren, Cecilia M -- Assimes, Themistocles L -- Shuldiner, Alan R -- Hui, Jennie -- Beilby, John P -- McArdle, Wendy L -- Hall, Per -- Haritunians, Talin -- Zgaga, Lina -- Kolcic, Ivana -- Polasek, Ozren -- Zemunik, Tatijana -- Oostra, Ben A -- Junttila, M Juhani -- Gronberg, Henrik -- Schreiber, Stefan -- Peters, Annette -- Hicks, Andrew A -- Stephens, Jonathan -- Foad, Nicola S -- Laitinen, Jaana -- Pouta, Anneli -- Kaakinen, Marika -- Willemsen, Gonneke -- Vink, Jacqueline M -- Wild, Sarah H -- Navis, Gerjan -- Asselbergs, Folkert W -- Homuth, Georg -- John, Ulrich -- Iribarren, Carlos -- Harris, Tamara -- Launer, Lenore -- Gudnason, Vilmundur -- O'Connell, Jeffrey R -- Boerwinkle, Eric -- Cadby, Gemma -- Palmer, Lyle J -- James, Alan L -- Musk, Arthur W -- Ingelsson, Erik -- Psaty, Bruce M -- Beckmann, Jacques S -- Waeber, Gerard -- Vollenweider, Peter -- Hayward, Caroline -- Wright, Alan F -- Rudan, Igor -- Groop, Leif C -- Metspalu, Andres -- Khaw, Kay Tee -- van Duijn, Cornelia M -- Borecki, Ingrid B -- Province, Michael A -- Wareham, Nicholas J -- Tardif, Jean-Claude -- Huikuri, Heikki V -- Cupples, L Adrienne -- Atwood, Larry D -- Fox, Caroline S -- Boehnke, Michael -- Collins, Francis S -- Mohlke, Karen L -- Erdmann, Jeanette -- Schunkert, Heribert -- Hengstenberg, Christian -- Stark, Klaus -- Lorentzon, Mattias -- Ohlsson, Claes -- Cusi, Daniele -- Staessen, Jan A -- Van der Klauw, Melanie M -- Pramstaller, Peter P -- Kathiresan, Sekar -- Jolley, Jennifer D -- Ripatti, Samuli -- Jarvelin, Marjo-Riitta -- de Geus, Eco J C -- Boomsma, Dorret I -- Penninx, Brenda -- Wilson, James F -- Campbell, Harry -- Chanock, Stephen J -- van der Harst, Pim -- Hamsten, Anders -- Watkins, Hugh -- Hofman, Albert -- Witteman, Jacqueline C -- Zillikens, M Carola -- Uitterlinden, Andre G -- Rivadeneira, Fernando -- Kiemeney, Lambertus A -- Vermeulen, Sita H -- Abecasis, Goncalo R -- Schlessinger, David -- Schipf, Sabine -- Stumvoll, Michael -- Tonjes, Anke -- Spector, Tim D -- North, Kari E -- Lettre, Guillaume -- McCarthy, Mark I -- Berndt, Sonja I -- Heath, Andrew C -- Madden, Pamela A F -- Nyholt, Dale R -- Montgomery, Grant W -- Martin, Nicholas G -- McKnight, Barbara -- Strachan, David P -- Hill, William G -- Snieder, Harold -- Ridker, Paul M -- Thorsteinsdottir, Unnur -- Stefansson, Kari -- Frayling, Timothy M -- Hirschhorn, Joel N -- Goddard, Michael E -- Visscher, Peter M -- 090532/Wellcome Trust/United Kingdom -- 14136/Cancer Research UK/United Kingdom -- AA014041/AA/NIAAA NIH HHS/ -- AA07535/AA/NIAAA NIH HHS/ -- AA10248/AA/NIAAA NIH HHS/ -- AA13320/AA/NIAAA NIH HHS/ -- AA13321/AA/NIAAA NIH HHS/ -- AA13326/AA/NIAAA NIH HHS/ -- CZB/4/710/Chief Scientist Office/United Kingdom -- DA12854/DA/NIDA NIH HHS/ -- F32 AR059469/AR/NIAMS NIH HHS/ -- F32 DK079466/DK/NIDDK NIH HHS/ -- G0601261/Medical Research Council/United Kingdom -- G1000143/Medical Research Council/United Kingdom -- GM057091/GM/NIGMS NIH HHS/ -- HHSN268201100005C/HL/NHLBI NIH HHS/ -- HHSN268201100006C/HL/NHLBI NIH HHS/ -- HHSN268201100007C/HL/NHLBI NIH HHS/ -- HHSN268201100008C/HL/NHLBI NIH HHS/ -- HHSN268201100009C/HL/NHLBI NIH HHS/ -- HHSN268201100010C/HL/NHLBI NIH HHS/ -- HHSN268201100011C/HL/NHLBI NIH HHS/ -- HHSN268201100012C/HL/NHLBI NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- K23 DK080145/DK/NIDDK NIH HHS/ -- MC_PC_U127561128/Medical Research Council/United Kingdom -- MC_U106179471/Medical Research Council/United Kingdom -- MC_U127561128/Medical Research Council/United Kingdom -- N01 AG012100/AG/NIA NIH HHS/ -- N01 HC015103/HC/NHLBI NIH HHS/ -- N01 HC025195/HC/NHLBI NIH HHS/ -- N01 HC035129/HC/NHLBI NIH HHS/ -- N01 HC045133/HC/NHLBI NIH HHS/ -- N01 HC055222/HC/NHLBI NIH HHS/ -- N01 HC075150/HC/NHLBI NIH HHS/ -- N01 HC085079/HC/NHLBI NIH HHS/ -- N01 HG065403/HG/NHGRI NIH HHS/ -- N01HC85086/HL/NHLBI NIH HHS/ -- N02 HL64278/HL/NHLBI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK072488/DK/NIDDK NIH HHS/ -- R01 AA007535/AA/NIAAA NIH HHS/ -- R01 AA013320/AA/NIAAA NIH HHS/ -- R01 AA013321/AA/NIAAA NIH HHS/ -- R01 AA013326/AA/NIAAA NIH HHS/ -- R01 AA014041/AA/NIAAA NIH HHS/ -- R01 AG015928/AG/NIA NIH HHS/ -- R01 AG020098/AG/NIA NIH HHS/ -- R01 AG023629/AG/NIA NIH HHS/ -- R01 AG027058/AG/NIA NIH HHS/ -- R01 DA012854/DA/NIDA NIH HHS/ -- R01 DK062370/DK/NIDDK NIH HHS/ -- R01 DK072193/DK/NIDDK NIH HHS/ -- R01 DK073490/DK/NIDDK NIH HHS/ -- R01 DK075681/DK/NIDDK NIH HHS/ -- R01 DK075787/DK/NIDDK NIH HHS/ -- R01 HG002651/HG/NHGRI NIH HHS/ -- R01 HL043851/HL/NHLBI NIH HHS/ -- R01 HL059367/HL/NHLBI NIH HHS/ -- R01 HL075366/HL/NHLBI NIH HHS/ -- R01 HL080295/HL/NHLBI NIH HHS/ -- R01 HL086694/HL/NHLBI NIH HHS/ -- R01 HL087641/HL/NHLBI NIH HHS/ -- R01 HL087647/HL/NHLBI NIH HHS/ -- R01 HL087652/HL/NHLBI NIH HHS/ -- R01 HL087676/HL/NHLBI NIH HHS/ -- R01 HL087679/HL/NHLBI NIH HHS/ -- R01 HL105756/HL/NHLBI NIH HHS/ -- R01 LM010098/LM/NLM NIH HHS/ -- R01 MH063706/MH/NIMH NIH HHS/ -- RL1 MH083268/MH/NIMH NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 HG004402/HG/NHGRI NIH HHS/ -- U01 HL054527/HL/NHLBI NIH HHS/ -- U01 HL069757/HL/NHLBI NIH HHS/ -- U01 HL072515/HL/NHLBI NIH HHS/ -- U01 HL084729/HL/NHLBI NIH HHS/ -- U01 HL084756/HL/NHLBI NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- Z01 HG000024-14/Intramural NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):267-72. doi: 10.1038/nature11401. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Queensland Diamantina Institute, The University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982992" target="_blank"〉PubMed〈/a〉
    Keywords: Body Height/genetics ; *Body Mass Index ; Co-Repressor Proteins ; Female ; *Genetic Variation ; Genome-Wide Association Study ; Humans ; Male ; Nerve Tissue Proteins/genetics ; *Phenotype ; Polymorphism, Single Nucleotide ; Proteins/*genetics ; Repressor Proteins/genetics
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    Microbiology: Antibiotics and adiposity (2012)
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    Publication Date: 2012-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, Harry J -- England -- Nature. 2012 Aug 30;488(7413):601-2. doi: 10.1038/488601a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932383" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/*drug effects ; Animals ; Anti-Bacterial Agents/*administration & dosage/*pharmacology ; Colon/*drug effects/*microbiology ; Female ; Male ; Metagenome/*drug effects
    Print ISSN: 0028-0836
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    Circadian rhythms: No lazing on sunny afternoons (2012)
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    Publication Date: 2012-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rouyer, Francois -- England -- Nature. 2012 Apr 18;484(7394):325-6. doi: 10.1038/484325a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm/*physiology ; Drosophila melanogaster/*physiology ; *Environment ; Female ; Male
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    Alzheimer's: Put patients and researchers in touch (2012)
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    Publication Date: 2012-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murray, Matt -- England -- Nature. 2012 Aug 9;488(7410):157. doi: 10.1038/488157c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22874953" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Female ; Humans ; Male ; *Motivation ; Patients/*psychology ; Research Personnel/*psychology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Human gut microbiome viewed across age and geography (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: Gut microbial communities represent one source of human genetic and metabolic diversity. To examine how gut microbiomes differ among human populations, here we characterize bacterial species in fecal samples from 531 individuals, plus the gene content of 110 of them. The cohort encompassed healthy children and adults from the Amazonas of Venezuela, rural Malawi and US metropolitan areas and included mono- and dizygotic twins. Shared features of the functional maturation of the gut microbiome were identified during the first three years of life in all three populations, including age-associated changes in the genes involved in vitamin biosynthesis and metabolism. Pronounced differences in bacterial assemblages and functional gene repertoires were noted between US residents and those in the other two countries. These distinctive features are evident in early infancy as well as adulthood. Our findings underscore the need to consider the microbiome when evaluating human development, nutritional needs, physiological variations and the impact of westernization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376388/" 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/PMC3376388/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yatsunenko, Tanya -- Rey, Federico E -- Manary, Mark J -- Trehan, Indi -- Dominguez-Bello, Maria Gloria -- Contreras, Monica -- Magris, Magda -- Hidalgo, Glida -- Baldassano, Robert N -- Anokhin, Andrey P -- Heath, Andrew C -- Warner, Barbara -- Reeder, Jens -- Kuczynski, Justin -- Caporaso, J Gregory -- Lozupone, Catherine A -- Lauber, Christian -- Clemente, Jose Carlos -- Knights, Dan -- Knight, Rob -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- K01 DK090285/DK/NIDDK NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P01 DK078669-05/DK/NIDDK NIH HHS/ -- T32 HD049338-06/HD/NICHD NIH HHS/ -- T32-HD049338/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 May 9;486(7402):222-7. doi: 10.1038/nature11053.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699611" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Age Factors ; Aged ; Bacteria/*classification/*genetics ; *Biodiversity ; Child ; Child, Preschool ; Feces/microbiology ; Female ; Geography ; Humans ; Infant ; Intestines/*microbiology ; Malawi ; Male ; *Metagenome ; Middle Aged ; Phylogeny ; RNA, Ribosomal, 16S/genetics ; Twins, Dizygotic ; Twins, Monozygotic ; United States ; Venezuela ; Young Adult
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    Resurrection of endogenous retroviruses in antibody-deficient mice (2012)
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    Publication Date: 2012-10-30
    Description: The mammalian host has developed a long-standing symbiotic relationship with a considerable number of microbial species. These include the microbiota on environmental surfaces, such as the respiratory and gastrointestinal tracts, and also endogenous retroviruses (ERVs), comprising a substantial fraction of the mammalian genome. The long-term consequences for the host of interactions with these microbial species can range from mutualism to parasitism and are not always completely understood. The potential effect of one microbial symbiont on another is even less clear. Here we study the control of ERVs in the commonly used C57BL/6 (B6) mouse strain, which lacks endogenous murine leukaemia viruses (MLVs) able to replicate in murine cells. We demonstrate the spontaneous emergence of fully infectious ecotropic MLV in B6 mice with a range of distinct immune deficiencies affecting antibody production. These recombinant retroviruses establish infection of immunodeficient mouse colonies, and ultimately result in retrovirus-induced lymphomas. Notably, ERV activation in immunodeficient mice is prevented in husbandry conditions associated with reduced or absent intestinal microbiota. Our results shed light onto a previously unappreciated role for immunity in the control of ERVs and provide a potential mechanistic link between immune activation by microbial triggers and a range of pathologies associated with ERVs, including cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511586/" 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/PMC3511586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, George R -- Eksmond, Urszula -- Salcedo, Rosalba -- Alexopoulou, Lena -- Stoye, Jonathan P -- Kassiotis, George -- MC_U117512710/Medical Research Council/United Kingdom -- MC_U117581330/Medical Research Council/United Kingdom -- U.1175.02.005.00005(60891)/Medical Research Council/United Kingdom -- U.1175.02.006.00007(81330)/Medical Research Council/United Kingdom -- U117512710/Medical Research Council/United Kingdom -- U117581330/Medical Research Council/United Kingdom -- England -- Nature. 2012 Nov 29;491(7426):774-8. doi: 10.1038/nature11599. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunoregulation, MRC National Institute for Medical Research, The Ridgeway, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103862" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Antibodies, Viral/*biosynthesis/immunology ; Cell Transformation, Viral ; Endogenous Retroviruses/genetics/growth & development/immunology/*physiology ; Female ; Immunocompromised Host/*immunology ; Leukemia/virology ; Leukemia Virus, Murine/genetics/growth & development/immunology/physiology ; Lymphoma/virology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/deficiency/genetics ; Recombination, Genetic ; Viremia/immunology/virology ; *Virus Activation
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    Translational research: A UK tissue bank for breast tumours (2012)
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    Publication Date: 2012-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Alastair M -- England -- Nature. 2012 May 9;485(7397):174. doi: 10.1038/485174d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22575950" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/classification/*pathology ; Female ; Great Britain ; Humans ; Ireland ; *Tissue Banks ; *Translational Medical Research/trends
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    Fracking boom spurs environmental audit (2012)
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    Publication Date: 2012-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Helen -- England -- Nature. 2012 May 29;485(7400):556-7. doi: 10.1038/485556a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Confidentiality ; *Environment ; Environmental Exposure/*adverse effects/legislation & jurisprudence ; Environmental Monitoring ; Extraction and Processing Industry/economics/*legislation & jurisprudence ; Female ; Humans ; Livestock ; Ohio ; *Oil and Gas Fields ; Pregnancy ; *Public Health/legislation & jurisprudence ; Sentinel Surveillance ; United States ; United States Environmental Protection Agency
    Print ISSN: 0028-0836
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    Comprehensive molecular portraits of human breast tumours (2012)
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    Publication Date: 2012-09-25
    Description: We analysed primary breast cancers by genomic DNA copy number arrays, DNA methylation, exome sequencing, messenger RNA arrays, microRNA sequencing and reverse-phase protein arrays. Our ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity. Somatic mutations in only three genes (TP53, PIK3CA and GATA3) occurred at 〉10% incidence across all breast cancers; however, there were numerous subtype-associated and novel gene mutations including the enrichment of specific mutations in GATA3, PIK3CA and MAP3K1 with the luminal A subtype. We identified two novel protein-expression-defined subgroups, possibly produced by stromal/microenvironmental elements, and integrated analyses identified specific signalling pathways dominant in each molecular subtype including a HER2/phosphorylated HER2/EGFR/phosphorylated EGFR signature within the HER2-enriched expression subtype. Comparison of basal-like breast tumours with high-grade serous ovarian tumours showed many molecular commonalities, indicating a related aetiology and similar therapeutic opportunities. The biological finding of the four main breast cancer subtypes caused by different subsets of genetic and epigenetic abnormalities raises the hypothesis that much of the clinically observable plasticity and heterogeneity occurs within, and not across, these major biological subtypes of breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465532/" 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/PMC3465532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cancer Genome Atlas Network -- K08 CA148912/CA/NCI NIH HHS/ -- P30 CA016058/CA/NCI NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- P50 CA058223/CA/NCI NIH HHS/ -- P50 CA116201/CA/NCI NIH HHS/ -- P50CA116201/CA/NCI NIH HHS/ -- P50CA58223/CA/NCI NIH HHS/ -- R01 LM009722/LM/NLM NIH HHS/ -- U01 CA084955/CA/NCI NIH HHS/ -- U24 CA143799/CA/NCI NIH HHS/ -- U24 CA143848/CA/NCI NIH HHS/ -- U24 CA143866/CA/NCI NIH HHS/ -- U24 CA143882/CA/NCI NIH HHS/ -- U24CA143799/CA/NCI NIH HHS/ -- U24CA143835/CA/NCI NIH HHS/ -- U24CA143840/CA/NCI NIH HHS/ -- U24CA143845/CA/NCI NIH HHS/ -- U24CA143848/CA/NCI NIH HHS/ -- U24CA143858/CA/NCI NIH HHS/ -- U24CA143866/CA/NCI NIH HHS/ -- U24CA143867/CA/NCI NIH HHS/ -- U24CA143882/CA/NCI NIH HHS/ -- U24CA143883/CA/NCI NIH HHS/ -- U24CA144025/CA/NCI NIH HHS/ -- U54 HG004028/HG/NHGRI NIH HHS/ -- U54HG003079/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Oct 4;490(7418):61-70. doi: 10.1038/nature11412. Epub 2012 Sep 23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23000897" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/classification/*genetics/metabolism/*pathology ; DNA Copy Number Variations/genetics ; DNA Methylation ; DNA Mutational Analysis ; Exome/genetics ; Female ; GATA3 Transcription Factor/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Genes, Neoplasm/*genetics ; Genes, erbB-2/genetics ; Genes, p53/genetics ; *Genetic Heterogeneity ; Genome, Human/genetics ; Genomics ; Humans ; MAP Kinase Kinase Kinase 1/genetics ; MicroRNAs/genetics ; Mutation/*genetics ; Oligonucleotide Array Sequence Analysis ; Ovarian Neoplasms/genetics/pathology ; Phosphatidylinositol 3-Kinases/genetics ; Protein Array Analysis ; Proteomics ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics ; Receptors, Estrogen/metabolism ; Retinoblastoma Protein/genetics/metabolism
    Print ISSN: 0028-0836
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    Reach and grasp by people with tetraplegia using a neurally controlled robotic arm (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-05-19
    Description: Paralysis following spinal cord injury, brainstem stroke, amyotrophic lateral sclerosis and other disorders can disconnect the brain from the body, eliminating the ability to perform volitional movements. A neural interface system could restore mobility and independence for people with paralysis by translating neuronal activity directly into control signals for assistive devices. We have previously shown that people with long-standing tetraplegia can use a neural interface system to move and click a computer cursor and to control physical devices. Able-bodied monkeys have used a neural interface system to control a robotic arm, but it is unknown whether people with profound upper extremity paralysis or limb loss could use cortical neuronal ensemble signals to direct useful arm actions. Here we demonstrate the ability of two people with long-standing tetraplegia to use neural interface system-based control of a robotic arm to perform three-dimensional reach and grasp movements. Participants controlled the arm and hand over a broad space without explicit training, using signals decoded from a small, local population of motor cortex (MI) neurons recorded from a 96-channel microelectrode array. One of the study participants, implanted with the sensor 5 years earlier, also used a robotic arm to drink coffee from a bottle. Although robotic reach and grasp actions were not as fast or accurate as those of an able-bodied person, our results demonstrate the feasibility for people with tetraplegia, years after injury to the central nervous system, to recreate useful multidimensional control of complex devices directly from a small sample of neural signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640850/" 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/PMC3640850/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hochberg, Leigh R -- Bacher, Daniel -- Jarosiewicz, Beata -- Masse, Nicolas Y -- Simeral, John D -- Vogel, Joern -- Haddadin, Sami -- Liu, Jie -- Cash, Sydney S -- van der Smagt, Patrick -- Donoghue, John P -- HHSN275201100018C/HD/NICHD NIH HHS/ -- N01 HD053403/HD/NICHD NIH HHS/ -- N01HD10018/HD/NICHD NIH HHS/ -- N01HD53403/HD/NICHD NIH HHS/ -- NS25074/NS/NINDS NIH HHS/ -- R01 DC009899/DC/NIDCD NIH HHS/ -- R01 DC009899-02/DC/NIDCD NIH HHS/ -- R01 EB007401/EB/NIBIB NIH HHS/ -- R01 EB007401-05/EB/NIBIB NIH HHS/ -- R01DC009899/DC/NIDCD NIH HHS/ -- R01EB007401/EB/NIBIB NIH HHS/ -- R56 NS025074/NS/NINDS NIH HHS/ -- R56 NS025074-23/NS/NINDS NIH HHS/ -- RC1 HD063931/HD/NICHD NIH HHS/ -- RC1 HD063931-02/HD/NICHD NIH HHS/ -- RC1HD063931/HD/NICHD NIH HHS/ -- England -- Nature. 2012 May 16;485(7398):372-5. doi: 10.1038/nature11076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rehabilitation Research & Development Service, Department of Veterans Affairs, Providence, Rhode Island 02908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22596161" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Arm/*physiology ; Calibration ; Drinking/physiology ; Female ; Hand/physiology ; Hand Strength/*physiology ; Humans ; Male ; *Man-Machine Systems ; Microelectrodes ; Middle Aged ; Motor Cortex/cytology/physiology ; Movement/*physiology ; Psychomotor Performance ; Quadriplegia/*physiopathology ; Robotics/*instrumentation/*methods ; Time Factors
    Print ISSN: 0028-0836
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    Control of a Salmonella virulence locus by an ATP-sensing leader messenger RNA (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-16
    Description: The facultative intracellular pathogen Salmonella enterica resides within a membrane-bound compartment inside macrophages. This compartment must be acidified for Salmonella to survive within macrophages, possibly because acidic pH promotes expression of Salmonella virulence proteins. We reasoned that Salmonella might sense its surroundings have turned acidic not only upon protonation of the extracytoplasmic domain of a protein sensor but also by an increase in cytosolic ATP levels, because conditions that enhance the proton gradient across the bacterial inner membrane stimulate ATP synthesis. Here we report that an increase in cytosolic ATP promotes transcription of the coding region for the virulence gene mgtC, which is the most highly induced horizontally acquired gene when Salmonella is inside macrophages. This transcript is induced both upon media acidification and by physiological conditions that increase ATP levels independently of acidification. ATP is sensed by the coupling/uncoupling of transcription of the unusually long mgtC leader messenger RNA and translation of a short open reading frame located in this region. A mutation in the mgtC leader messenger RNA that eliminates the response to ATP hinders mgtC expression inside macrophages and attenuates Salmonella virulence in mice. Our results define a singular example of an ATP-sensing leader messenger RNA. Moreover, they indicate that pathogens can interpret extracellular cues by the impact they have on cellular metabolites.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711680/" 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/PMC3711680/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Eun-Jin -- Groisman, Eduardo A -- AI49561/AI/NIAID NIH HHS/ -- R01 AI049561/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jun 13;486(7402):271-5. doi: 10.1038/nature11090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale School of Medicine, Section of Microbial Pathogenesis, New Haven, Connecticut 06536-0812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699622" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/genetics/*physiology ; Adenosine Triphosphate/*metabolism ; Animals ; *Bacterial Proteins/genetics/metabolism ; Base Sequence ; *Cation Transport Proteins/genetics/metabolism ; Female ; Gene Expression Regulation, Bacterial ; Hydrogen-Ion Concentration ; Macrophages/microbiology ; Mice ; Mice, Inbred C3H ; Molecular Sequence Data ; Mutation/genetics ; Salmonella Infections/mortality/pathology ; Salmonella typhimurium/genetics/metabolism/*pathogenicity ; Sequence Alignment ; Virulence/*genetics
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    Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-14
    Description: The largest mucosal surface in the body is in the gastrointestinal tract, a location that is heavily colonized by microbes that are normally harmless. A key mechanism required for maintaining a homeostatic balance between this microbial burden and the lymphocytes that densely populate the gastrointestinal tract is the production and transepithelial transport of poly-reactive IgA (ref. 1). Within the mucosal tissues, B cells respond to cytokines, sometimes in the absence of T-cell help, undergo class switch recombination of their immunoglobulin receptor to IgA, and differentiate to become plasma cells. However, IgA-secreting plasma cells probably have additional attributes that are needed for coping with the tremendous bacterial load in the gastrointestinal tract. Here we report that mouse IgA(+) plasma cells also produce the antimicrobial mediators tumour-necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS), and express many molecules that are commonly associated with monocyte/granulocytic cell types. The development of iNOS-producing IgA(+) plasma cells can be recapitulated in vitro in the presence of gut stroma, and the acquisition of this multifunctional phenotype in vivo and in vitro relies on microbial co-stimulation. Deletion of TNF-alpha and iNOS in B-lineage cells resulted in a reduction in IgA production, altered diversification of the gut microbiota and poor clearance of a gut-tropic pathogen. These findings reveal a novel adaptation to maintaining homeostasis in the gut, and extend the repertoire of protective responses exhibited by some B-lineage cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3487691/" 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/PMC3487691/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fritz, Jorg H -- Rojas, Olga Lucia -- Simard, Nathalie -- McCarthy, Douglas D -- Hapfelmeier, Siegfried -- Rubino, Stephen -- Robertson, Susan J -- Larijani, Mani -- Gosselin, Jean -- Ivanov, Ivaylo I -- Martin, Alberto -- Casellas, Rafael -- Philpott, Dana J -- Girardin, Stephen E -- McCoy, Kathy D -- Macpherson, Andrew J -- Paige, Christopher J -- Gommerman, Jennifer L -- 67157-3/Canadian Institutes of Health Research/Canada -- 89783-2/Canadian Institutes of Health Research/Canada -- MOP 114972/Canadian Institutes of Health Research/Canada -- MOP 67157/Canadian Institutes of Health Research/Canada -- MOP 89783/Canadian Institutes of Health Research/Canada -- MOP 9862/Canadian Institutes of Health Research/Canada -- R00 DK085329/DK/NIDDK NIH HHS/ -- R00 DK085329-02/DK/NIDDK NIH HHS/ -- Z01 AR041148-03/Intramural NIH HHS/ -- ZIA AR041148-08/Intramural NIH HHS/ -- England -- Nature. 2011 Dec 11;481(7380):199-203. doi: 10.1038/nature10698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Toronto, Toronto M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158124" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology ; Cell Lineage ; Cells, Cultured ; Chimera/immunology ; Citrobacter rodentium/immunology ; Coculture Techniques ; Female ; Germ-Free Life ; Granulocytes/cytology/metabolism ; Immunity, Innate/immunology ; Immunoglobulin A/biosynthesis/*immunology ; Intestinal Mucosa/cytology/immunology ; Intestine, Small/*cytology/*immunology/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocytes/cytology/metabolism ; Nitric Oxide Synthase Type II/biosynthesis/deficiency/metabolism ; Phenotype ; Plasma Cells/*cytology/*immunology/metabolism ; Spleen/cytology ; Stromal Cells/cytology ; Tumor Necrosis Factor-alpha/biosynthesis/deficiency/immunology/metabolism
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    Hsp72 preserves muscle function and slows progression of severe muscular dystrophy (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-04-13
    Description: Duchenne muscular dystrophy (DMD) is a severe and progressive muscle wasting disorder caused by mutations in the dystrophin gene that result in the absence of the membrane-stabilizing protein dystrophin. Dystrophin-deficient muscle fibres are fragile and susceptible to an influx of Ca(2+), which activates inflammatory and muscle degenerative pathways. At present there is no cure for DMD, and existing therapies are ineffective. Here we show that increasing the expression of intramuscular heat shock protein 72 (Hsp72) preserves muscle strength and ameliorates the dystrophic pathology in two mouse models of muscular dystrophy. Treatment with BGP-15 (a pharmacological inducer of Hsp72 currently in clinical trials for diabetes) improved muscle architecture, strength and contractile function in severely affected diaphragm muscles in mdx dystrophic mice. In dko mice, a phenocopy of DMD that results in severe spinal curvature (kyphosis), muscle weakness and premature death, BGP-15 decreased kyphosis, improved the dystrophic pathophysiology in limb and diaphragm muscles and extended lifespan. We found that the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA, the main protein responsible for the removal of intracellular Ca(2+)) is dysfunctional in severely affected muscles of mdx and dko mice, and that Hsp72 interacts with SERCA to preserve its function under conditions of stress, ultimately contributing to the decreased muscle degeneration seen with Hsp72 upregulation. Treatment with BGP-15 similarly increased SERCA activity in dystrophic skeletal muscles. Our results provide evidence that increasing the expression of Hsp72 in muscle (through the administration of BGP-15) has significant therapeutic potential for DMD and related conditions, either as a self-contained therapy or as an adjuvant with other potential treatments, including gene, cell and pharmacological therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gehrig, Stefan M -- van der Poel, Chris -- Sayer, Timothy A -- Schertzer, Jonathan D -- Henstridge, Darren C -- Church, Jarrod E -- Lamon, Severine -- Russell, Aaron P -- Davies, Kay E -- Febbraio, Mark A -- Lynch, Gordon S -- GTB07001/Telethon/Italy -- MC_U137761449/Medical Research Council/United Kingdom -- England -- Nature. 2012 Apr 4;484(7394):394-8. doi: 10.1038/nature10980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic and Clinical Myology Laboratory, Department of Physiology, University of Melbourne, Victoria, 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Transporting ATPases/metabolism ; Diaphragm/drug effects/physiology ; Disease Models, Animal ; *Disease Progression ; Female ; Gene Expression Regulation/drug effects ; HSP72 Heat-Shock Proteins/biosynthesis/genetics/*metabolism ; Kyphosis/drug therapy ; Longevity/drug effects ; Male ; Mice ; Mice, Inbred mdx ; Mice, Transgenic ; Muscle, Skeletal/drug effects/*physiology/physiopathology ; Muscular Dystrophy, Duchenne/genetics/*metabolism/pathology/*physiopathology ; Oximes/pharmacology ; Piperidines/pharmacology ; Rats
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    Prenatal diagnostics: Fetal genes in mother's blood (2012)
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    Publication Date: 2012-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bianchi, Diana W -- England -- Nature. 2012 Jul 18;487(7407):304-5. doi: 10.1038/487304a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810690" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*analysis ; Female ; *Genome, Human ; Humans ; Male ; Pregnancy ; Prenatal Diagnosis/*methods
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    Neuroscience: Genes and human brain evolution (2012)
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    Publication Date: 2012-06-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636765/" 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/PMC3636765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geschwind, Daniel H -- Konopka, Genevieve -- R00 MH090238/MH/NIMH NIH HHS/ -- R37 MH060233/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Jun 28;486(7404):481-2. doi: 10.1038/nature11380.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722844" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Brain/*anatomy & histology/*metabolism ; Evolution, Molecular ; Female ; GTPase-Activating Proteins/*genetics ; Gene Duplication/genetics ; Genes, Duplicate/*genetics ; Humans ; Hydatidiform Mole/genetics ; Male ; Pregnancy
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    Translational medicine: Double protection for weakened bones (2012)
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    Publication Date: 2012-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaidi, Mone -- Iqbal, Jameel -- England -- Nature. 2012 May 2;485(7396):47-8. doi: 10.1038/485047a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22552091" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; *Cytoprotection ; Female ; Male ; Osteoblasts/*cytology ; Osteoclasts/*cytology ; *Osteogenesis ; Semaphorin-3A/*metabolism
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    The let-7-Imp axis regulates ageing of the Drosophila testis stem-cell niche (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-06-05
    Description: Adult stem cells support tissue homeostasis and repair throughout the life of an individual. During ageing, numerous intrinsic and extrinsic changes occur that result in altered stem-cell behaviour and reduced tissue maintenance and regeneration. In the Drosophila testis, ageing results in a marked decrease in the self-renewal factor Unpaired (Upd), leading to a concomitant loss of germline stem cells. Here we demonstrate that IGF-II messenger RNA binding protein (Imp) counteracts endogenous small interfering RNAs to stabilize upd (also known as os) RNA. However, similar to upd, Imp expression decreases in the hub cells of older males, which is due to the targeting of Imp by the heterochronic microRNA let-7. In the absence of Imp, upd mRNA therefore becomes unprotected and susceptible to degradation. Understanding the mechanistic basis for ageing-related changes in stem-cell behaviour will lead to the development of strategies to treat age-onset diseases and facilitate stem-cell-based therapies in older individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toledano, Hila -- D'Alterio, Cecilia -- Czech, Benjamin -- Levine, Erel -- Jones, D Leanne -- R01 AG028092/AG/NIA NIH HHS/ -- R01 AG040288/AG/NIA NIH HHS/ -- England -- Nature. 2012 May 23;485(7400):605-10. doi: 10.1038/nature11061.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22660319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins/metabolism ; Base Sequence ; Cell Aging/*physiology ; Drosophila Proteins/biosynthesis/genetics/*metabolism ; Drosophila melanogaster/*cytology/genetics/*metabolism ; Female ; Male ; MicroRNAs/*genetics ; Organ Specificity ; RNA Helicases/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Small Interfering/antagonists & inhibitors/genetics/metabolism ; RNA-Binding Proteins/biosynthesis/genetics/*metabolism ; Ribonuclease III/metabolism ; Stem Cell Niche/genetics/*physiology ; Testis/*cytology ; Transcription Factors/genetics/metabolism
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    Keith H. Campbell (1954-2012) (2012)
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    Publication Date: 2012-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trounson, Alan -- England -- Nature. 2012 Nov 8;491(7423):193. doi: 10.1038/491193a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute for Regenerative Medicine, San Francisco, California 94107, USA. atrounson@cirm.ca.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135461" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Awards and Prizes ; Cellular Reprogramming ; Cloning, Organism/*history ; Embryonic Stem Cells/physiology ; Female ; Great Britain ; History, 20th Century ; Induced Pluripotent Stem Cells/physiology ; Sheep ; Swine
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