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  • 1
    ISSN: 1432-0738
    Keywords: Breathing pattern ; Mice ; Airborne chemicals ; Respiratory tract
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A system was developed for exposure of unanesthetized mice to airborne chemicals and for continuous measurement of their breathing pattern prior to, during and following exposure. By measuring inspiratory and expiratory airflows (VI and VE), and integration with time to yield tidal volume (VT), we obtained characteristic modifications to the normal breathing pattern. These permitted recognition that a specific portion of the respiratory tract was affected by the selected airborne chemicals. Following recognition, we also quantitated the degree of effect using one specific measurement in each case. An effect on the upper respiratory tract, induced by the sensory irritant, 2-chlorobenzylchloride, was quantitated by measuring a decrease in respiratory frequency. An effect on the conducting airways, induced by the airway constrictor, carbamylcholine, was quantitated by a decrease in VE at the mid-point of VT. An effect at the alveolar level, induced either by the vagal nerve ending stimulant, propranolol, or by the pulmonary irritant, machining fluid G, was quantitated by an increase in the length of a pause induced at the end of expiration. The system is easy to construct and operate and can be used to rapidly evaluate the effects of airborne chemicals on the respiratory tract.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2011-03-11
    Description: Anxiety--a sustained state of heightened apprehension in the absence of immediate threat--becomes severely debilitating in disease states. Anxiety disorders represent the most common of psychiatric diseases (28% lifetime prevalence) and contribute to the aetiology of major depression and substance abuse. Although it has been proposed that the amygdala, a brain region important for emotional processing, has a role in anxiety, the neural mechanisms that control anxiety remain unclear. Here we explore the neural circuits underlying anxiety-related behaviours by using optogenetics with two-photon microscopy, anxiety assays in freely moving mice, and electrophysiology. With the capability of optogenetics to control not only cell types but also specific connections between cells, we observed that temporally precise optogenetic stimulation of basolateral amygdala (BLA) terminals in the central nucleus of the amygdala (CeA)--achieved by viral transduction of the BLA with a codon-optimized channelrhodopsin followed by restricted illumination in the downstream CeA--exerted an acute, reversible anxiolytic effect. Conversely, selective optogenetic inhibition of the same projection with a third-generation halorhodopsin (eNpHR3.0) increased anxiety-related behaviours. Importantly, these effects were not observed with direct optogenetic control of BLA somata, possibly owing to recruitment of antagonistic downstream structures. Together, these results implicate specific BLA-CeA projections as critical circuit elements for acute anxiety control in the mammalian brain, and demonstrate the importance of optogenetically targeting defined projections, beyond simply targeting cell types, in the study of circuit function relevant to neuropsychiatric disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154022/" 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/PMC3154022/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tye, Kay M -- Prakash, Rohit -- Kim, Sung-Yon -- Fenno, Lief E -- Grosenick, Logan -- Zarabi, Hosniya -- Thompson, Kimberly R -- Gradinaru, Viviana -- Ramakrishnan, Charu -- Deisseroth, Karl -- 1F32MH088010-01/MH/NIMH NIH HHS/ -- DP1 OD000616/OD/NIH HHS/ -- DP1 OD000616-01/OD/NIH HHS/ -- R01 DA020794/DA/NIDA NIH HHS/ -- R01 DA020794-01/DA/NIDA NIH HHS/ -- R01 MH075957/MH/NIMH NIH HHS/ -- R01 MH075957-01A2/MH/NIMH NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):358-62. doi: 10.1038/nature09820. Epub 2011 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21389985" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/*physiology/radiation effects ; Animals ; Anxiety/*physiopathology ; Anxiety Disorders/physiopathology ; Halorhodopsins/metabolism ; Light ; Mice ; Models, Neurological ; Neural Pathways/physiology/radiation effects ; Neurons/physiology/radiation effects ; Stress, Physiological/physiology ; Synapses/physiology/radiation effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2015-12-15
    Description: Vertebrate corpse decomposition provides an important stage in nutrient cycling in most terrestrial habitats, yet microbially mediated processes are poorly understood. Here we combine deep microbial community characterization, community-level metabolic reconstruction, and soil biogeochemical assessment to understand the principles governing microbial community assembly during decomposition of mouse and human corpses on different soil substrates. We find a suite of bacterial and fungal groups that contribute to nitrogen cycling and a reproducible network of decomposers that emerge on predictable time scales. Our results show that this decomposer community is derived primarily from bulk soil, but key decomposers are ubiquitous in low abundance. Soil type was not a dominant factor driving community development, and the process of decomposition is sufficiently reproducible to offer new opportunities for forensic investigations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, Jessica L -- Xu, Zhenjiang Zech -- Weiss, Sophie -- Lax, Simon -- Van Treuren, Will -- Hyde, Embriette R -- Song, Se Jin -- Amir, Amnon -- Larsen, Peter -- Sangwan, Naseer -- Haarmann, Daniel -- Humphrey, Greg C -- Ackermann, Gail -- Thompson, Luke R -- Lauber, Christian -- Bibat, Alexander -- Nicholas, Catherine -- Gebert, Matthew J -- Petrosino, Joseph F -- Reed, Sasha C -- Gilbert, Jack A -- Lynne, Aaron M -- Bucheli, Sibyl R -- Carter, David O -- Knight, Rob -- 3 R01 HG004872-03S2/HG/NHGRI NIH HHS/ -- 5 U01 HG004866-04/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):158-62. doi: 10.1126/science.aad2646. Epub 2015 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Colorado, Boulder, CO 80309, USA. Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. robknight@ucsd.edu jessica.metcalf@colorado.edu. ; Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. ; Department of Chemical and Biological Engineering, University of Colorado, Boulder, CO 80303, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Institute for Genomic and Systems Biology, University of Chicago, 900 East 57th Street, Chicago, IL 606037, USA. ; Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA. ; Department of Ecology and Evolutionary Biology, University of Colorado, Boulder, CO 80309, USA. Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. Department of Surgery, University of Chicago, A27 South Maryland Avenue, Chicago, IL 60637, USA. ; Department of Biological Sciences, Sam Houston State University, Huntsville, TX 77340, USA. ; Nestle Institute of Health Sciences, Ecole Polytechnique Federale Lausanne, Batiment H, 1015 Lausanne, Switzerland. ; BioFrontiers Institute, University of Colorado, Boulder, CO 80303, USA. ; Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA. ; U.S. Geological Survey, Southwest Biological Science Center, Moab, UT 84532, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Institute for Genomic and Systems Biology, University of Chicago, 900 East 57th Street, Chicago, IL 606037, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. Department of Surgery, University of Chicago, A27 South Maryland Avenue, Chicago, IL 60637, USA. Marine Biological Laboratory, 7 MBL St, Woods Hole, MA 02543, USA. ; Laboratory of Forensic Taphonomy, Forensic Sciences Unit, Division of Natural Sciences and Mathematics, Chaminade University of Honolulu, Honolulu, HI 96816, USA. ; Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. Department of Computer Science and Engineering, University of California, San Diego, San Diego, CA 92037, USA. robknight@ucsd.edu jessica.metcalf@colorado.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26657285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/*metabolism ; Biodegradation, Environmental ; *Cadaver ; Ecosystem ; Fungi/classification/*metabolism ; Mice ; *Microbial Consortia ; Nitrogen Cycle ; Soil/chemistry/classification ; *Soil Microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2013-05-15
    Description: Macropinocytosis is a highly conserved endocytic process by which extracellular fluid and its contents are internalized into cells through large, heterogeneous vesicles known as macropinosomes. Oncogenic Ras proteins have been shown to stimulate macropinocytosis but the functional contribution of this uptake mechanism to the transformed phenotype remains unknown. Here we show that Ras-transformed cells use macropinocytosis to transport extracellular protein into the cell. The internalized protein undergoes proteolytic degradation, yielding amino acids including glutamine that can enter central carbon metabolism. Accordingly, the dependence of Ras-transformed cells on free extracellular glutamine for growth can be suppressed by the macropinocytic uptake of protein. Consistent with macropinocytosis representing an important route of nutrient uptake in tumours, its pharmacological inhibition compromises the growth of Ras-transformed pancreatic tumour xenografts. These results identify macropinocytosis as a mechanism by which cancer cells support their unique metabolic needs and point to the possible exploitation of this process in the design of anticancer therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810415/" 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/PMC3810415/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Commisso, Cosimo -- Davidson, Shawn M -- Soydaner-Azeloglu, Rengin G -- Parker, Seth J -- Kamphorst, Jurre J -- Hackett, Sean -- Grabocka, Elda -- Nofal, Michel -- Drebin, Jeffrey A -- Thompson, Craig B -- Rabinowitz, Joshua D -- Metallo, Christian M -- Vander Heiden, Matthew G -- Bar-Sagi, Dafna -- 5 P30CA016087-32/CA/NCI NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- P01-CA117969/CA/NCI NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30-CA14051-39/CA/NCI NIH HHS/ -- R01 CA055360/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- R01 CA163591/CA/NCI NIH HHS/ -- R01CA055360/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 May 30;497(7451):633-7. doi: 10.1038/nature12138. Epub 2013 May 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23665962" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*metabolism ; Animals ; Biological Transport ; Carbon/metabolism ; Cell Line, Transformed ; Cell Line, Tumor ; Cell Proliferation ; *Cell Transformation, Neoplastic/genetics ; Disease Models, Animal ; Female ; Glutamine/metabolism ; Mice ; Mice, Nude ; NIH 3T3 Cells ; Oncogene Protein p21(ras)/genetics/*metabolism ; Pancreatic Neoplasms/genetics/*metabolism/*pathology ; *Pinocytosis ; Proteolysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-11-26
    Description: To achieve its precise neural connectivity, the developing mammalian nervous system undergoes extensive activity-dependent synapse remodelling. Recently, microglial cells have been shown to be responsible for a portion of synaptic pruning, but the remaining mechanisms remain unknown. Here we report a new role for astrocytes in actively engulfing central nervous system synapses. This process helps to mediate synapse elimination, requires the MEGF10 and MERTK phagocytic pathways, and is strongly dependent on neuronal activity. Developing mice deficient in both astrocyte pathways fail to refine their retinogeniculate connections normally and retain excess functional synapses. Finally, we show that in the adult mouse brain, astrocytes continuously engulf both excitatory and inhibitory synapses. These studies reveal a novel role for astrocytes in mediating synapse elimination in the developing and adult brain, identify MEGF10 and MERTK as critical proteins in the synapse remodelling underlying neural circuit refinement, and have important implications for understanding learning and memory as well as neurological disease processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969024/" 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/PMC3969024/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Won-Suk -- Clarke, Laura E -- Wang, Gordon X -- Stafford, Benjamin K -- Sher, Alexander -- Chakraborty, Chandrani -- Joung, Julia -- Foo, Lynette C -- Thompson, Andrew -- Chen, Chinfei -- Smith, Stephen J -- Barres, Ben A -- 5 R21NS072556/NS/NINDS NIH HHS/ -- NS069375/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- R01 EY013613/EY/NEI NIH HHS/ -- R01 NS075252/NS/NINDS NIH HHS/ -- R21 NS072556/NS/NINDS NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- England -- Nature. 2013 Dec 19;504(7480):394-400. doi: 10.1038/nature12776. Epub 2013 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University, School of Medicine, Stanford, California 94305, USA. ; 1] Department of Neurobiology, Stanford University, School of Medicine, Stanford, California 94305, USA [2]. ; 1] Department of Molecular and Cellular Physiology, Stanford University, School of Medicine, Stanford, California 94305, USA [2]. ; Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, Michigan 48105, USA. ; Santa Cruz Institute of Particle Physic and Department of Physics, University of California, Santa Cruz, California 95064, USA. ; Institute of Molecular and Cell Biology, A *Star, 61 Biopolis Drive, Proteos Building, 138673 Singapore. ; Children's Hospital, Harvard Medical School, 300 Longwood Avenue, CLS12250, Boston, Massachusetts 02115, USA. ; Department of Molecular and Cellular Physiology, 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/24270812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/*metabolism ; Brain/cytology ; In Vitro Techniques ; Lateral Thalamic Nuclei/cytology/metabolism ; Learning/physiology ; Membrane Proteins/deficiency/genetics/*metabolism ; Mice ; Mice, Transgenic ; Neural Pathways/cytology/*metabolism ; *Phagocytosis ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Receptor Protein-Tyrosine Kinases/deficiency/genetics/*metabolism ; Retina/physiology ; Synapses/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-12-14
    Description: Major depression is characterized by diverse debilitating symptoms that include hopelessness and anhedonia. Dopamine neurons involved in reward and motivation are among many neural populations that have been hypothesized to be relevant, and certain antidepressant treatments, including medications and brain stimulation therapies, can influence the complex dopamine system. Until now it has not been possible to test this hypothesis directly, even in animal models, as existing therapeutic interventions are unable to specifically target dopamine neurons. Here we investigated directly the causal contributions of defined dopamine neurons to multidimensional depression-like phenotypes induced by chronic mild stress, by integrating behavioural, pharmacological, optogenetic and electrophysiological methods in freely moving rodents. We found that bidirectional control (inhibition or excitation) of specified midbrain dopamine neurons immediately and bidirectionally modulates (induces or relieves) multiple independent depression symptoms caused by chronic stress. By probing the circuit implementation of these effects, we observed that optogenetic recruitment of these dopamine neurons potently alters the neural encoding of depression-related behaviours in the downstream nucleus accumbens of freely moving rodents, suggesting that processes affecting depression symptoms may involve alterations in the neural encoding of action in limbic circuitry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160519/" 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/PMC4160519/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tye, Kay M -- Mirzabekov, Julie J -- Warden, Melissa R -- Ferenczi, Emily A -- Tsai, Hsing-Chen -- Finkelstein, Joel -- Kim, Sung-Yon -- Adhikari, Avishek -- Thompson, Kimberly R -- Andalman, Aaron S -- Gunaydin, Lisa A -- Witten, Ilana B -- Deisseroth, Karl -- DP2 DA035149/DA/NIDA NIH HHS/ -- F32 MH880102/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jan 24;493(7433):537-41. doi: 10.1038/nature11740. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. kaytye@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Depression/chemically induced/*physiopathology ; Dopamine/metabolism ; Dopaminergic Neurons/drug effects/*metabolism/radiation effects ; Female ; Male ; Mice ; Models, Neurological ; Nucleus Accumbens/metabolism ; Optogenetics ; Phenotype ; Rats ; Rats, Long-Evans ; Stress, Psychological/physiopathology ; Time Factors ; Ventral Tegmental Area/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2015-05-20
    Description: Mutations or amplification of the MET proto-oncogene are involved in the pathogenesis of several tumours, which rely on the constitutive engagement of this pathway for their growth and survival. However, MET is expressed not only by cancer cells but also by tumour-associated stromal cells, although its precise role in this compartment is not well characterized. Here we show that MET is required for neutrophil chemoattraction and cytotoxicity in response to its ligand hepatocyte growth factor (HGF). Met deletion in mouse neutrophils enhances tumour growth and metastasis. This phenotype correlates with reduced neutrophil infiltration to both the primary tumour and metastatic sites. Similarly, Met is necessary for neutrophil transudation during colitis, skin rash or peritonitis. Mechanistically, Met is induced by tumour-derived tumour necrosis factor (TNF)-alpha or other inflammatory stimuli in both mouse and human neutrophils. This induction is instrumental for neutrophil transmigration across an activated endothelium and for inducible nitric oxide synthase production upon HGF stimulation. Consequently, HGF/MET-dependent nitric oxide release by neutrophils promotes cancer cell killing, which abates tumour growth and metastasis. After systemic administration of a MET kinase inhibitor, we prove that the therapeutic benefit of MET targeting in cancer cells is partly countered by the pro-tumoural effect arising from MET blockade in neutrophils. Our work identifies an unprecedented role of MET in neutrophils, suggests a potential 'Achilles' heel' of MET-targeted therapies in cancer, and supports the rationale for evaluating anti-MET drugs in certain inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594765/" 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/PMC4594765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finisguerra, Veronica -- Di Conza, Giusy -- Di Matteo, Mario -- Serneels, Jens -- Costa, Sandra -- Thompson, A A Roger -- Wauters, Els -- Walmsley, Sarah -- Prenen, Hans -- Granot, Zvi -- Casazza, Andrea -- Mazzone, Massimiliano -- 098516/Wellcome Trust/United Kingdom -- 308459/European Research Council/International -- G0802255/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jun 18;522(7556):349-53. doi: 10.1038/nature14407. Epub 2015 May 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; 1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium [3] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal [4] ICVS/3B's - PT Government Associate Laboratory, 4710-057 Braga/Guimaraes, Portugal. ; Department of Infection and Immunity, University of Sheffield, Sheffield S10 2RX, UK. ; 1] Respiratory Division, University Hospital Gasthuisberg, Leuven B3000, Belgium [2] Laboratory of Translational Genetics, Vesalius Research Center, VIB, Leuven B3000, Belgium [3] Laboratory of Translational Genetics, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Digestive Oncology Unit, University Hospital Gasthuisberg, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University, Jerusalem 91120, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25985180" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Animals ; Antineoplastic Agents/*adverse effects/*pharmacology ; Disease Models, Animal ; Disease Progression ; Female ; Gene Deletion ; Hepatocyte Growth Factor ; Humans ; Inflammation/immunology/pathology ; Male ; Mice ; Middle Aged ; Neoplasm Metastasis ; Neoplasms/drug therapy/*immunology/*metabolism/pathology ; Neutrophils/drug effects/*immunology/secretion ; Nitric Oxide/secretion ; Proto-Oncogene Proteins c-met/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Solubility ; Transendothelial and Transepithelial Migration ; Tumor Necrosis Factor-alpha/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-06-11
    Description: Oxygen (O(2)) is a critical constraint on marine ecosystems. As oceanic O(2) falls to hypoxic concentrations, habitability for aerobic organisms decreases rapidly. We show that the spatial extent of hypoxia is highly sensitive to small changes in the ocean's O(2) content, with maximum responses at suboxic concentrations where anaerobic metabolisms predominate. In model-based reconstructions of historical oxygen changes, the world's largest suboxic zone, in the Pacific Ocean, varies in size by a factor of 2. This is attributable to climate-driven changes in the depth of the tropical and subtropical thermocline that have multiplicative effects on respiration rates in low-O(2) water. The same mechanism yields even larger fluctuations in the rate of nitrogen removal by denitrification, creating a link between decadal climate oscillations and the nutrient limitation of marine photosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deutsch, Curtis -- Brix, Holger -- Ito, Taka -- Frenzel, Hartmut -- Thompson, LuAnne -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):336-9. doi: 10.1126/science.1202422. Epub 2011 Jun 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Atmospheric and Oceanic Sciences, University of California, Los Angeles, CA 90095, USA. cdeutsch@atmos.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21659566" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis ; *Climate Change ; Computer Simulation ; Denitrification ; *Ecosystem ; Nitrogen/metabolism ; Oceans and Seas ; Oxygen/*analysis/metabolism ; Pacific Ocean ; Seawater/*chemistry ; Temperature ; Time Factors ; Water Movements
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-03-23
    Description: The air-filled cavity and ossicles of the mammalian middle ear conduct sound to the cochlea. Using transgenic mice, we show that the mammalian middle ear develops through cavitation of a neural crest mass. These cells, which previously underwent an epithelial-to-mesenchymal transformation upon leaving the neural tube, undergo a mesenchymal-to-epithelial transformation to form a lining continuous with the endodermally derived auditory tube. The epithelium derived from endodermal cells, which surrounds the auditory tube and eardrum, develops cilia, whereas the neural crest-derived epithelium does not. Thus, the cilia critical to clearing pathogenic infections from the middle ear are distributed according to developmental derivations. A different process of cavitation appears evident in birds and reptiles, indicating that this dual epithelium may be unique to mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Hannah -- Tucker, Abigail S -- G1001232/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1453-6. doi: 10.1126/science.1232862.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Craniofacial Development and Stem Cell Biology, King's College London, Guy's Hospital, London, UK, SE1 9RT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23520114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chick Embryo ; Cilia/ultrastructure ; Ear, Middle/anatomy & histology/*cytology/*embryology ; Embryonic Development ; Endoderm/*cytology/embryology ; Epithelial Cells/ultrastructure ; Epithelial-Mesenchymal Transition ; Epithelium/*embryology/ultrastructure ; Female ; Lizards/anatomy & histology/embryology ; Male ; Mammals/anatomy & histology/embryology ; Mesoderm/embryology ; Mice ; Mice, Transgenic ; Neural Crest/*cytology/embryology ; Shrews/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2012-11-20
    Description: The prefrontal cortex (PFC) is thought to participate in high-level control of the generation of behaviours (including the decision to execute actions); indeed, imaging and lesion studies in human beings have revealed that PFC dysfunction can lead to either impulsive states with increased tendency to initiate action, or to amotivational states characterized by symptoms such as reduced activity, hopelessness and depressed mood. Considering the opposite valence of these two phenotypes as well as the broad complexity of other tasks attributed to PFC, we sought to elucidate the PFC circuitry that favours effortful behavioural responses to challenging situations. Here we develop and use a quantitative method for the continuous assessment and control of active response to a behavioural challenge, synchronized with single-unit electrophysiology and optogenetics in freely moving rats. In recording from the medial PFC (mPFC), we observed that many neurons were not simply movement-related in their spike-firing patterns but instead were selectively modulated from moment to moment, according to the animal's decision to act in a challenging situation. Surprisingly, we next found that direct activation of principal neurons in the mPFC had no detectable causal effect on this behaviour. We tested whether this behaviour could be causally mediated by only a subclass of mPFC cells defined by specific downstream wiring. Indeed, by leveraging optogenetic projection-targeting to control cells with specific efferent wiring patterns, we found that selective activation of those mPFC cells projecting to the brainstem dorsal raphe nucleus (DRN), a serotonergic nucleus implicated in major depressive disorder, induced a profound, rapid and reversible effect on selection of the active behavioural state. These results may be of importance in understanding the neural circuitry underlying normal and pathological patterns of action selection and motivation in behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warden, Melissa R -- Selimbeyoglu, Aslihan -- Mirzabekov, Julie J -- Lo, Maisie -- Thompson, Kimberly R -- Kim, Sung-Yon -- Adhikari, Avishek -- Tye, Kay M -- Frank, Loren M -- Deisseroth, Karl -- 1F32MH088010-01/MH/NIMH NIH HHS/ -- F32 MH088010/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 20;492(7429):428-32. doi: 10.1038/nature11617.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, California 94305, USA. mwarden@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23160494" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Behavior, Animal/*physiology ; Depression/psychology ; Electrophysiology ; Locomotion/physiology ; Male ; Motivation/*physiology ; Neurons/*physiology ; Optogenetics ; Prefrontal Cortex/*physiology ; Raphe Nuclei/*physiology ; Rats ; Rats, Long-Evans ; Swimming/*physiology ; Synapses/physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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