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  • Animals  (233)
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  • Nature Publishing Group (NPG)  (233)
  • 2015-2019  (233)
  • 2016  (233)
  • 1
    Publication Date: 2016-02-06
    Description: The position of Xenacoelomorpha in the tree of life remains a major unresolved question in the study of deep animal relationships. Xenacoelomorpha, comprising Acoela, Nemertodermatida, and Xenoturbella, are bilaterally symmetrical marine worms that lack several features common to most other bilaterians, for example an anus, nephridia, and a circulatory system. Two conflicting hypotheses are under debate: Xenacoelomorpha is the sister group to all remaining Bilateria (= Nephrozoa, namely protostomes and deuterostomes) or is a clade inside Deuterostomia. Thus, determining the phylogenetic position of this clade is pivotal for understanding the early evolution of bilaterian features, or as a case of drastic secondary loss of complexity. Here we show robust phylogenomic support for Xenacoelomorpha as the sister taxon of Nephrozoa. Our phylogenetic analyses, based on 11 novel xenacoelomorph transcriptomes and using different models of evolution under maximum likelihood and Bayesian inference analyses, strongly corroborate this result. Rigorous testing of 25 experimental data sets designed to exclude data partitions and taxa potentially prone to reconstruction biases indicates that long-branch attraction, saturation, and missing data do not influence these results. The sister group relationship between Nephrozoa and Xenacoelomorpha supported by our phylogenomic analyses implies that the last common ancestor of bilaterians was probably a benthic, ciliated acoelomate worm with a single opening into an epithelial gut, and that excretory organs, coelomic cavities, and nerve cords evolved after xenacoelomorphs separated from the stem lineage of Nephrozoa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon, Johanna Taylor -- Vellutini, Bruno Cossermelli -- Smith, Julian 3rd -- Ronquist, Fredrik -- Jondelius, Ulf -- Hejnol, Andreas -- England -- Nature. 2016 Feb 4;530(7588):89-93. doi: 10.1038/nature16520.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Naturhistoriska Riksmuseet, PO Box 50007, SE-104 05 Stockholm, Sweden. ; Sars International Centre for Marine Molecular Biology, University of Bergen, Thormohlensgate 55, 5008 Bergen, Norway. ; Department of Biology, Winthrop University, 701 Oakland Avenue, Rock Hill, South Carolina 29733, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842059" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Structures/anatomy & histology ; Animals ; Aquatic Organisms/*classification/genetics ; Bayes Theorem ; Genes ; Likelihood Functions ; Male ; Models, Biological ; *Phylogeny ; Transcriptome
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  • 2
    Publication Date: 2016-01-21
    Description: Bacteria express many small RNAs for which the regulatory roles in pathogenesis have remained poorly understood due to a paucity of robust phenotypes in standard virulence assays. Here we use a generic 'dual RNA-seq' approach to profile RNA expression simultaneously in pathogen and host during Salmonella enterica serovar Typhimurium infection and reveal the molecular impact of bacterial riboregulators. We identify a PhoP-activated small RNA, PinT, which upon bacterial internalization temporally controls the expression of both invasion-associated effectors and virulence genes required for intracellular survival. This riboregulatory activity causes pervasive changes in coding and noncoding transcripts of the host. Interspecies correlation analysis links PinT to host cell JAK-STAT signalling, and we identify infection-specific alterations in multiple long noncoding RNAs. Our study provides a paradigm for a sensitive RNA-based analysis of intracellular bacterial pathogens and their hosts without physical separation, as well as a new discovery route for hidden functions of pathogen genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westermann, Alexander J -- Forstner, Konrad U -- Amman, Fabian -- Barquist, Lars -- Chao, Yanjie -- Schulte, Leon N -- Muller, Lydia -- Reinhardt, Richard -- Stadler, Peter F -- Vogel, Jorg -- England -- Nature. 2016 Jan 28;529(7587):496-501. doi: 10.1038/nature16547. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Wurzburg, RNA Biology Group, Institute for Molecular Infection Biology, Josef-Schneider-Strasse 2/D15, D-97080 Wurzburg, Germany. ; University of Wurzburg, Core Unit Systems Medicine, Josef-Schneider-Strasse 2/D15, D-97080 Wurzburg, Germany. ; University of Leipzig, Department of Computer Science and Interdisciplinary Center for Bioinformatics, Hartelstrasse 16-18, D-04107 Leipzig, Germany. ; University of Vienna, Theoretical Biochemistry Group, Institute for Theoretical Chemistry, Wahringer Strasse 17, A-1090 Vienna, Austria. ; Max Planck Genome Centre Cologne, Max Planck Institute for Plant Breeding Research, Carl-von-Linne-Weg 10, D-50829 Cologne, Germany. ; Max Planck Institute for Mathematics in the Sciences, Inselstrasse 22, D-04103 Leipzig, Germany. ; Santa Fe Institute, 1399 Hyde Park Rd, Santa Fe, New Mexico 87501, USA. ; Research Centre for Infectious Diseases (ZINF), University of Wurzburg, D-97070 Wurzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/metabolism ; Female ; Gene Expression Regulation/*genetics ; Genes, Bacterial/genetics ; HeLa Cells ; Host-Pathogen Interactions/*genetics ; Humans ; Janus Kinases/metabolism ; Mice ; Microbial Viability/genetics ; RNA, Bacterial/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; STAT Transcription Factors/metabolism ; Salmonella typhimurium/cytology/*genetics/pathogenicity ; Signal Transduction/genetics ; Transcriptome/genetics ; Virulence/genetics
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  • 3
    Publication Date: 2016-02-19
    Description: Sex differences in physiology and disease susceptibility are commonly attributed to developmental and/or hormonal factors, but there is increasing realization that cell-intrinsic mechanisms play important and persistent roles. Here we use the Drosophila melanogaster intestine to investigate the nature and importance of cellular sex in an adult somatic organ in vivo. We find that the adult intestinal epithelium is a cellular mosaic of different sex differentiation pathways, and displays extensive sex differences in expression of genes with roles in growth and metabolism. Cell-specific reversals of the sexual identity of adult intestinal stem cells uncovers the key role this identity has in controlling organ size, reproductive plasticity and response to genetically induced tumours. Unlike previous examples of sexually dimorphic somatic stem cell activity, the sex differences in intestinal stem cell behaviour arise from intrinsic mechanisms that control cell cycle duration and involve a new doublesex- and fruitless-independent branch of the sex differentiation pathway downstream of transformer. Together, our findings indicate that the plasticity of an adult somatic organ is reversibly controlled by its sexual identity, imparted by a new mechanism that may be active in more tissues than previously recognized.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hudry, Bruno -- Khadayate, Sanjay -- Miguel-Aliaga, Irene -- Medical Research Council/United Kingdom -- England -- Nature. 2016 Feb 18;530(7590):344-8. doi: 10.1038/nature16953.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Clinical Sciences Centre, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26887495" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology ; Animals ; Cell Cycle ; Cell Proliferation ; Cell Transformation, Neoplastic ; Dosage Compensation, Genetic ; Drosophila Proteins/metabolism ; Drosophila melanogaster/*anatomy & histology/*cytology/genetics/growth & ; development ; Female ; Intestines/*cytology ; Male ; Nuclear Proteins/metabolism ; *Organ Size ; RNA-Binding Proteins/metabolism ; Reproduction ; Ribonucleoproteins/metabolism ; *Sex Characteristics ; Sex Differentiation/genetics
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  • 4
    Publication Date: 2016-03-24
    Description: Developmental disabilities, including attention-deficit hyperactivity disorder (ADHD), intellectual disability (ID), and autism spectrum disorders (ASD), affect one in six children in the USA. Recently, gene mutations in patched domain containing 1 (PTCHD1) have been found in ~1% of patients with ID and ASD. Individuals with PTCHD1 deletion show symptoms of ADHD, sleep disruption, hypotonia, aggression, ASD, and ID. Although PTCHD1 is probably critical for normal development, the connection between its deletion and the ensuing behavioural defects is poorly understood. Here we report that during early post-natal development, mouse Ptchd1 is selectively expressed in the thalamic reticular nucleus (TRN), a group of GABAergic neurons that regulate thalamocortical transmission, sleep rhythms, and attention. Ptchd1 deletion attenuates TRN activity through mechanisms involving small conductance calcium-dependent potassium currents (SK). TRN-restricted deletion of Ptchd1 leads to attention deficits and hyperactivity, both of which are rescued by pharmacological augmentation of SK channel activity. Global Ptchd1 deletion recapitulates learning impairment, hyper-aggression, and motor defects, all of which are insensitive to SK pharmacological targeting and not found in the TRN-restricted deletion mouse. This study maps clinically relevant behavioural phenotypes onto TRN dysfunction in a human disease model, while also identifying molecular and circuit targets for intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4875756/" 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/PMC4875756/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wells, Michael F -- Wimmer, Ralf D -- Schmitt, L Ian -- Feng, Guoping -- Halassa, Michael M -- F31 MH098641/MH/NIMH NIH HHS/ -- R00 NS078115/NS/NINDS NIH HHS/ -- R01 MH097104/MH/NIMH NIH HHS/ -- R01 MH107680/MH/NIMH NIH HHS/ -- R01MH097104/MH/NIMH NIH HHS/ -- R01MH10768/MH/NIMH NIH HHS/ -- England -- Nature. 2016 Apr 7;532(7597):58-63. doi: 10.1038/nature17427. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. ; Neuroscience Institute, New York University Langone Medical Center, New York, New York 10016, USA. ; Department of Neuroscience and Physiology, New York University Langone Medical Center, New York, New York 10016, USA. ; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; Department of Psychiatry, New York University Langone Medical Center, New York, New York 10016, USA. ; Center for Neural Science, New York University, New York, New York 1003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007844" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; Animals, Newborn ; Attention ; Attention Deficit Disorder with ; Hyperactivity/genetics/*physiopathology/*psychology ; Behavior, Animal ; Disease Models, Animal ; Electric Conductivity ; Female ; GABAergic Neurons/metabolism/pathology ; *Gene Deletion ; Humans ; Learning Disorders/genetics/physiopathology ; Male ; Membrane Proteins/*deficiency/*genetics/metabolism ; Mice ; Mice, Knockout ; Motor Disorders/genetics/physiopathology ; Neural Inhibition ; Potassium Channels, Calcium-Activated/metabolism ; Sleep ; Sleep Deprivation/genetics/physiopathology ; Thalamic Nuclei/pathology/*physiopathology
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  • 5
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    Nature Publishing Group (NPG)
    Publication Date: 2016-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owens, Brian -- England -- Nature. 2016 May 11;533(7602):S71-2. doi: 10.1038/533S71a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27167398" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics ; *Access to Information ; Animals ; *Diffusion of Innovation ; Drug Industry/economics/methods ; Humans ; *Information Dissemination ; Mice ; Neurosciences/economics/manpower/*methods/organization & administration ; Patents as Topic ; Public Sector/economics ; Public-Private Sector Partnerships ; Quebec
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caron, David A -- England -- Nature. 2016 Apr 28;532(7600):444-5. doi: 10.1038/nature17892. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California, Los Angeles, California 90089-0371, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096370" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms/*metabolism ; *Biomass ; *Biota ; Carbon/*metabolism ; *Ecosystem ; *Oceans and Seas ; Plankton/*metabolism ; Rhizaria/*isolation & purification ; Seawater/*chemistry ; Zooplankton/*isolation & purification
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  • 7
    Publication Date: 2016-01-07
    Description: Endothelial cells (ECs) are plastic cells that can switch between growth states with different bioenergetic and biosynthetic requirements. Although quiescent in most healthy tissues, ECs divide and migrate rapidly upon proangiogenic stimulation. Adjusting endothelial metabolism to the growth state is central to normal vessel growth and function, yet it is poorly understood at the molecular level. Here we report that the forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that couples metabolic and proliferative activities in ECs. Endothelial-restricted deletion of FOXO1 in mice induces a profound increase in EC proliferation that interferes with coordinated sprouting, thereby causing hyperplasia and vessel enlargement. Conversely, forced expression of FOXO1 restricts vascular expansion and leads to vessel thinning and hypobranching. We find that FOXO1 acts as a gatekeeper of endothelial quiescence, which decelerates metabolic activity by reducing glycolysis and mitochondrial respiration. Mechanistically, FOXO1 suppresses signalling by MYC (also known as c-MYC), a powerful driver of anabolic metabolism and growth. MYC ablation impairs glycolysis, mitochondrial function and proliferation of ECs while its EC-specific overexpression fuels these processes. Moreover, restoration of MYC signalling in FOXO1-overexpressing endothelium normalizes metabolic activity and branching behaviour. Our findings identify FOXO1 as a critical rheostat of vascular expansion and define the FOXO1-MYC transcriptional network as a novel metabolic checkpoint during endothelial growth and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Kerstin -- Happel, Katharina -- Eelen, Guy -- Schoors, Sandra -- Oellerich, Mark F -- Lim, Radiance -- Zimmermann, Barbara -- Aspalter, Irene M -- Franco, Claudio A -- Boettger, Thomas -- Braun, Thomas -- Fruttiger, Marcus -- Rajewsky, Klaus -- Keller, Charles -- Bruning, Jens C -- Gerhardt, Holger -- Carmeliet, Peter -- Potente, Michael -- K08CA090438/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2016 Jan 14;529(7585):216-20. doi: 10.1038/nature16498. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Angiogenesis &Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven 3000, Belgium. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven 3000, Belgium. ; Vascular Biology Laboratory, London Research Institute, Cancer Research UK, London WC2A 3LY, UK. ; Vascular Morphogenesis Laboratory, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon 1649-028, Portugal. ; Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; UCL Institute of Ophthalmology, University College London, London EC1V 9EL, UK. ; Max Delbruck Center for Molecular Medicine (MDC), D-13125 Berlin, Germany. ; Children's Cancer Therapy Development Institute, Beaverton, Oregon 97005, USA. ; Max Planck Institute for Metabolism Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University of Cologne, D-50931 Cologne, Germany. ; Vascular Patterning Laboratory, Vesalius Research Center, VIB and University of Leuven, Leuven 3000, Belgium. ; DZHK (German Center for Cardiovascular Research), partner site Berlin, D-13347 Berlin, Germany. ; Berlin Institute of Health (BIH), D-10117 Berlin, Germany. ; International Institute of Molecular and Cell Biology, 02-109 Warsaw, Poland. ; DZHK (German Center for Cardiovascular Research), partner site Frankfurt Rhine-Main, D-13347 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Respiration ; Endothelium, Vascular/cytology/*growth & development/*metabolism ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Glycolysis ; Human Umbilical Vein Endothelial Cells/cytology/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-myc/deficiency/genetics/metabolism ; Signal Transduction
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  • 8
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    Nature Publishing Group (NPG)
    Publication Date: 2016-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willyard, Cassandra -- England -- Nature. 2016 Apr 14;532(7598):166-8. doi: 10.1038/532166a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27075079" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/economics/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/economics/*therapeutic use ; Clinical Trials as Topic ; DNA Mutational Analysis ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm/*drug effects/genetics ; *Evolution, Molecular ; Female ; Humans ; Immunotherapy, Adoptive/economics/trends ; Mice ; Molecular Targeted Therapy/economics/*methods/trends ; Mutation/*genetics ; Neoplasm Metastasis/drug therapy/genetics/pathology ; Neoplasm Recurrence, Local/chemically induced/genetics/prevention & control ; Neoplasms/*drug therapy/*genetics/pathology ; Selection, Genetic/*drug effects/genetics ; Tumor Microenvironment/drug effects
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  • 9
    Publication Date: 2016-04-14
    Description: Bone marrow endothelial cells (BMECs) form a network of blood vessels that regulate both leukocyte trafficking and haematopoietic stem and progenitor cell (HSPC) maintenance. However, it is not clear how BMECs balance these dual roles, and whether these events occur at the same vascular site. We found that mammalian bone marrow stem cell maintenance and leukocyte trafficking are regulated by distinct blood vessel types with different permeability properties. Less permeable arterial blood vessels maintain haematopoietic stem cells in a low reactive oxygen species (ROS) state, whereas the more permeable sinusoids promote HSPC activation and are the exclusive site for immature and mature leukocyte trafficking to and from the bone marrow. A functional consequence of high permeability of blood vessels is that exposure to blood plasma increases bone marrow HSPC ROS levels, augmenting their migration and differentiation, while compromising their long-term repopulation and survival. These findings may have relevance for clinical haematopoietic stem cell transplantation and mobilization protocols.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Itkin, Tomer -- Gur-Cohen, Shiri -- Spencer, Joel A -- Schajnovitz, Amir -- Ramasamy, Saravana K -- Kusumbe, Anjali P -- Ledergor, Guy -- Jung, Yookyung -- Milo, Idan -- Poulos, Michael G -- Kalinkovich, Alexander -- Ludin, Aya -- Kollet, Orit -- Shakhar, Guy -- Butler, Jason M -- Rafii, Shahin -- Adams, Ralf H -- Scadden, David T -- Lin, Charles P -- Lapidot, Tsvee -- EB017274/EB/NIBIB NIH HHS/ -- HL100402/HL/NHLBI NIH HHS/ -- R01 EB017274/EB/NIBIB NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- England -- Nature. 2016 Apr 21;532(7599):323-8. doi: 10.1038/nature17624. Epub 2016 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. ; Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Harvard Stem Cell Institute, Cambridge, Massachusetts 02114, USA. ; Center for Regenerative Medicine and Cancer Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. ; Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and Faculty of Medicine, University of Munster, D-48149 Munster, Germany. ; Internal Medicine Department, Tel-Aviv Sourasky Medical Center, Tel-Aviv 64239, Israel. ; Department of Genetic Medicine, Weill Cornell Medical College, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27074509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/metabolism ; Arteries/cytology/physiology ; Blood Vessels/*cytology/*physiology ; Bone Marrow/*blood supply ; Bone Marrow Cells/cytology ; Cell Differentiation ; Cell Movement ; Cell Self Renewal ; Cell Survival ; Chemokine CXCL12/metabolism ; Endothelial Cells/physiology ; Female ; *Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Leukocytes/cytology ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Nestin/metabolism ; Pericytes/physiology ; Permeability ; Plasma/metabolism ; Reactive Oxygen Species/metabolism ; Receptors, CXCR4/metabolism
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  • 10
    Publication Date: 2016-01-19
    Description: Many procedures in modern clinical medicine rely on the use of electronic implants in treating conditions that range from acute coronary events to traumatic injury. However, standard permanent electronic hardware acts as a nidus for infection: bacteria form biofilms along percutaneous wires, or seed haematogenously, with the potential to migrate within the body and to provoke immune-mediated pathological tissue reactions. The associated surgical retrieval procedures, meanwhile, subject patients to the distress associated with re-operation and expose them to additional complications. Here, we report materials, device architectures, integration strategies, and in vivo demonstrations in rats of implantable, multifunctional silicon sensors for the brain, for which all of the constituent materials naturally resorb via hydrolysis and/or metabolic action, eliminating the need for extraction. Continuous monitoring of intracranial pressure and temperature illustrates functionality essential to the treatment of traumatic brain injury; the measurement performance of our resorbable devices compares favourably with that of non-resorbable clinical standards. In our experiments, insulated percutaneous wires connect to an externally mounted, miniaturized wireless potentiostat for data transmission. In a separate set-up, we connect a sensor to an implanted (but only partially resorbable) data-communication system, proving the principle that there is no need for any percutaneous wiring. The devices can be adapted to sense fluid flow, motion, pH or thermal characteristics, in formats that are compatible with the body's abdomen and extremities, as well as the deep brain, suggesting that the sensors might meet many needs in clinical medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Seung-Kyun -- Murphy, Rory K J -- Hwang, Suk-Won -- Lee, Seung Min -- Harburg, Daniel V -- Krueger, Neil A -- Shin, Jiho -- Gamble, Paul -- Cheng, Huanyu -- Yu, Sooyoun -- Liu, Zhuangjian -- McCall, Jordan G -- Stephen, Manu -- Ying, Hanze -- Kim, Jeonghyun -- Park, Gayoung -- Webb, R Chad -- Lee, Chi Hwan -- Chung, Sangjin -- Wie, Dae Seung -- Gujar, Amit D -- Vemulapalli, Bharat -- Kim, Albert H -- Lee, Kyung-Mi -- Cheng, Jianjun -- Huang, Younggang -- Lee, Sang Hoon -- Braun, Paul V -- Ray, Wilson Z -- Rogers, John A -- F31MH101956/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Feb 4;530(7588):71-6. doi: 10.1038/nature16492. Epub 2016 Jan 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Frederick Seitz Materials Research Laboratory, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Department of Neurological Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 136-701, Republic of Korea. ; Department of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Department of Engineering Science and Mechanics, Materials Research Institute, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Institute of High Performance Computing, Singapore 138632, Singapore. ; Department of Anesthesiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Biomicrosystem Technology, Korea University, Seoul 136-701, South Korea. ; Department of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul 136-713, South Korea. ; Weldon School of Biomedical Engineering, School of Mechanical Engineering, The Center for Implantable Devices, Birck Nanotechnology Center, Purdue University, West Lafayette, Indiana 47907, USA. ; School of Mechanical Engineering, Purdue University, West Lafayette, Indiana 47907, USA. ; Department of Mechanical Engineering, Civil and Environmental Engineering, Materials Science and Engineering, and Skin Disease Research Center, Northwestern University, Evanston, Illinois 60208, USA. ; Department of Biomedical Engineering, College of Health Science, Korea University, Seoul 136-703, South Korea. ; Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26779949" target="_blank"〉PubMed〈/a〉
    Keywords: *Absorbable Implants/adverse effects ; Administration, Cutaneous ; Animals ; Body Temperature ; Brain/*metabolism/surgery ; Electronics/*instrumentation ; Equipment Design ; Hydrolysis ; Male ; Monitoring, Physiologic/adverse effects/*instrumentation ; Organ Specificity ; Pressure ; *Prostheses and Implants/adverse effects ; Rats ; Rats, Inbred Lew ; *Silicon ; Telemetry/instrumentation ; Wireless Technology/instrumentation
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