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  • 1
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    Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-02-19
    Description: Understanding the neuropathology of multiple sclerosis (MS) is essential for improved therapies. Therefore, identification of targets specific to pathological types of MS may have therapeutic benefits. Here we identify, by laser-capture microdissection and proteomics, proteins unique to three major types of MS lesions: acute plaque, chronic active plaque and chronic plaque. Comparative proteomic profiles identified tissue factor and protein C inhibitor within chronic active plaque samples, suggesting dysregulation of molecules associated with coagulation. In vivo administration of hirudin or recombinant activated protein C reduced disease severity in experimental autoimmune encephalomyelitis and suppressed Th1 and Th17 cytokines in astrocytes and immune cells. Administration of mutant forms of recombinant activated protein C showed that both its anticoagulant and its signalling functions were essential for optimal amelioration of experimental autoimmune encephalomyelitis. A proteomic approach illuminated potential therapeutic targets selective for specific pathological stages of MS and implicated participation of the coagulation cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, May H -- Hwang, Sun-Il -- Roy, Dolly B -- Lundgren, Deborah H -- Price, Jordan V -- Ousman, Shalina S -- Fernald, Guy Haskin -- Gerlitz, Bruce -- Robinson, William H -- Baranzini, Sergio E -- Grinnell, Brian W -- Raine, Cedric S -- Sobel, Raymond A -- Han, David K -- Steinman, Lawrence -- T32 AI007290/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Feb 28;451(7182):1076-81. doi: 10.1038/nature06559. Epub 2008 Feb 17.〈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/18278032" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Blood Coagulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/metabolism/pathology ; Female ; *Gene Expression Profiling ; Humans ; Inflammation/metabolism/pathology ; Male ; Mice ; Middle Aged ; Multiple Sclerosis/classification/drug therapy/*metabolism/*pathology ; Protein C/genetics/metabolism/pharmacology ; *Proteomics ; Th1 Cells/immunology ; Th2 Cells/immunology ; Thrombin/antagonists & inhibitors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Cell type-specific loss of BDNF signaling mimics optogenetic control of cocaine reward (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: The nucleus accumbens is a key mediator of cocaine reward, but the distinct roles of the two subpopulations of nucleus accumbens projection neurons, those expressing dopamine D1 versus D2 receptors, are poorly understood. We show that deletion of TrkB, the brain-derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine reward. Because loss of TrkB in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on cocaine reward. Activation of D2+ neurons, mimicking the loss of TrkB, suppresses cocaine reward, with opposite effects induced by activation of D1+ neurons. These results provide insight into the molecular control of D1+ and D2+ neuronal activity as well as the circuit-level contribution of these cell types to cocaine reward.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011229/" 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/PMC3011229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobo, Mary Kay -- Covington, Herbert E 3rd -- Chaudhury, Dipesh -- Friedman, Allyson K -- Sun, HaoSheng -- Damez-Werno, Diane -- Dietz, David M -- Zaman, Samir -- Koo, Ja Wook -- Kennedy, Pamela J -- Mouzon, Ezekiell -- Mogri, Murtaza -- Neve, Rachael L -- Deisseroth, Karl -- Han, Ming-Hu -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-20/DA/NIDA NIH HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA014133-10/DA/NIDA NIH HHS/ -- R01 DA014133-11/DA/NIDA NIH HHS/ -- R01 DA014133-12/DA/NIDA NIH HHS/ -- R01 MH051399/MH/NIMH NIH HHS/ -- R01 MH051399-19/MH/NIMH NIH HHS/ -- R01 MH051399-20/MH/NIMH NIH HHS/ -- T32 DA007135-26A2/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):385-90. doi: 10.1126/science.1188472.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/*metabolism ; Cocaine/*pharmacology ; Cocaine-Related Disorders/*metabolism ; Conditioning (Psychology) ; Light ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Models, Biological ; Motor Activity/drug effects ; Neurons/*metabolism ; Nucleus Accumbens/cytology/*metabolism ; RNA, Messenger/genetics/metabolism ; Receptor, trkB/genetics/*metabolism ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; *Reward ; Rhodopsin/genetics/metabolism ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-14
    Description: Ventral tegmental area (VTA) dopamine neurons in the brain's reward circuit have a crucial role in mediating stress responses, including determining susceptibility versus resilience to social-stress-induced behavioural abnormalities. VTA dopamine neurons show two in vivo patterns of firing: low frequency tonic firing and high frequency phasic firing. Phasic firing of the neurons, which is well known to encode reward signals, is upregulated by repeated social-defeat stress, a highly validated mouse model of depression. Surprisingly, this pathophysiological effect is seen in susceptible mice only, with no apparent change in firing rate in resilient individuals. However, direct evidence--in real time--linking dopamine neuron phasic firing in promoting the susceptible (depression-like) phenotype is lacking. Here we took advantage of the temporal precision and cell-type and projection-pathway specificity of optogenetics to show that enhanced phasic firing of these neurons mediates susceptibility to social-defeat stress in freely behaving mice. We show that optogenetic induction of phasic, but not tonic, firing in VTA dopamine neurons of mice undergoing a subthreshold social-defeat paradigm rapidly induced a susceptible phenotype as measured by social avoidance and decreased sucrose preference. Optogenetic phasic stimulation of these neurons also quickly induced a susceptible phenotype in previously resilient mice that had been subjected to repeated social-defeat stress. Furthermore, we show differences in projection-pathway specificity in promoting stress susceptibility: phasic activation of VTA neurons projecting to the nucleus accumbens (NAc), but not to the medial prefrontal cortex (mPFC), induced susceptibility to social-defeat stress. Conversely, optogenetic inhibition of the VTA-NAc projection induced resilience, whereas inhibition of the VTA-mPFC projection promoted susceptibility. Overall, these studies reveal novel firing-pattern- and neural-circuit-specific mechanisms of depression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554860/" 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/PMC3554860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhury, Dipesh -- Walsh, Jessica J -- Friedman, Allyson K -- Juarez, Barbara -- Ku, Stacy M -- Koo, Ja Wook -- Ferguson, Deveroux -- Tsai, Hsing-Chen -- Pomeranz, Lisa -- Christoffel, Daniel J -- Nectow, Alexander R -- Ekstrand, Mats -- Domingos, Ana -- Mazei-Robison, Michelle S -- Mouzon, Ezekiell -- Lobo, Mary Kay -- Neve, Rachael L -- Friedman, Jeffrey M -- Russo, Scott J -- Deisseroth, Karl -- Nestler, Eric J -- Han, Ming-Hu -- F31 MH095425/MH/NIMH NIH HHS/ -- F32 MH096464/MH/NIMH NIH HHS/ -- K99 MH094405/MH/NIMH NIH HHS/ -- R01 MH092306/MH/NIMH NIH HHS/ -- R25 GM064118/GM/NIGMS NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- T32 MH087004/MH/NIMH NIH HHS/ -- T32 MH096678/MH/NIMH NIH HHS/ -- England -- Nature. 2013 Jan 24;493(7433):532-6. doi: 10.1038/nature11713. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Friedman Brain Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Depression/etiology/*physiopathology ; Dopaminergic Neurons/*metabolism ; Food Preferences ; Male ; Mesencephalon/*cytology ; Mice ; Neural Pathways ; Nucleus Accumbens/physiology ; Optogenetics ; Phenotype ; Prefrontal Cortex/physiology ; *Social Behavior ; Stress, Psychological/complications/*physiopathology ; Sucrose/administration & dosage ; Time Factors ; Ventral Tegmental Area/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    BDNF is a negative modulator of morphine action (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: Brain-derived neurotrophic factor (BDNF) is a key positive regulator of neural plasticity, promoting, for example, the actions of stimulant drugs of abuse such as cocaine. We discovered a surprising opposite role for BDNF in countering responses to chronic morphine exposure. The suppression of BDNF in the ventral tegmental area (VTA) enhanced the ability of morphine to increase dopamine (DA) neuron excitability and promote reward. In contrast, optical stimulation of VTA DA terminals in nucleus accumbens (NAc) completely reversed the suppressive effect of BDNF on morphine reward. Furthermore, we identified numerous genes in the NAc, a major target region of VTA DA neurons, whose regulation by BDNF in the context of chronic morphine exposure mediated this counteractive function. These findings provide insight into the molecular basis of morphine-induced neuroadaptations in the brain's reward circuitry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547365/" 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/PMC3547365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koo, Ja Wook -- Mazei-Robison, Michelle S -- Chaudhury, Dipesh -- Juarez, Barbara -- LaPlant, Quincey -- Ferguson, Deveroux -- Feng, Jian -- Sun, Haosheng -- Scobie, Kimberly N -- Damez-Werno, Diane -- Crumiller, Marshall -- Ohnishi, Yoshinori N -- Ohnishi, Yoko H -- Mouzon, Ezekiell -- Dietz, David M -- Lobo, Mary Kay -- Neve, Rachael L -- Russo, Scott J -- Han, Ming-Hu -- Nestler, Eric J -- K99 MH094405/MH/NIMH NIH HHS/ -- P01 DA008227/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 MH092306/MH/NIMH NIH HHS/ -- T32 MH087004/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):124-8. doi: 10.1126/science.1222265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042896" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/genetics/*physiology ; Dopamine/metabolism ; Dopaminergic Neurons/*drug effects/physiology ; Gene Expression Regulation ; Gene Knockdown Techniques ; Gene Knockout Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Morphine/*pharmacology ; Morphine Dependence/genetics/*physiopathology ; Nucleus Accumbens/drug effects/physiopathology ; Photic Stimulation ; Receptor, trkB/genetics/physiology ; Ventral Tegmental Area/*drug effects/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Enhancing depression mechanisms in midbrain dopamine neurons achieves homeostatic resilience (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-04-20
    Description: Typical therapies try to reverse pathogenic mechanisms. Here, we describe treatment effects achieved by enhancing depression-causing mechanisms in ventral tegmental area (VTA) dopamine (DA) neurons. In a social defeat stress model of depression, depressed (susceptible) mice display hyperactivity of VTA DA neurons, caused by an up-regulated hyperpolarization-activated current (I(h)). Mice resilient to social defeat stress, however, exhibit stable normal firing of these neurons. Unexpectedly, resilient mice had an even larger I(h), which was observed in parallel with increased potassium (K(+)) channel currents. Experimentally further enhancing Ih or optogenetically increasing the hyperactivity of VTA DA neurons in susceptible mice completely reversed depression-related behaviors, an antidepressant effect achieved through resilience-like, projection-specific homeostatic plasticity. These results indicate a potential therapeutic path of promoting natural resilience for depression treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334447/" 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/PMC4334447/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedman, Allyson K -- Walsh, Jessica J -- Juarez, Barbara -- Ku, Stacy M -- Chaudhury, Dipesh -- Wang, Jing -- Li, Xianting -- Dietz, David M -- Pan, Nina -- Vialou, Vincent F -- Neve, Rachael L -- Yue, Zhenyu -- Han, Ming-Hu -- F31 MH095425/MH/NIMH NIH HHS/ -- F32 MH096464/MH/NIMH NIH HHS/ -- R01 MH092306/MH/NIMH NIH HHS/ -- R01 NS060123/NS/NINDS NIH HHS/ -- T32 MH 087004/MH/NIMH NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- T32 MH087004/MH/NIMH NIH HHS/ -- T32 MH096678/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 18;344(6181):313-9. doi: 10.1126/science.1249240.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24744379" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Depression/*physiopathology ; Dopaminergic Neurons/*physiology ; Electrophysiological Phenomena ; Homeostasis ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels ; Male ; Membrane Potentials/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Optogenetics ; Patch-Clamp Techniques ; Potassium Channels/metabolism ; *Resilience, Psychological ; Social Behavior ; Stress, Psychological/*physiopathology ; Triazines/pharmacology ; Ventral Tegmental Area/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    HDL-bound sphingosine-1-phosphate restrains lymphopoiesis and neuroinflammation (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-06-09
    Description: Lipid mediators influence immunity in myriad ways. For example, circulating sphingosine-1-phosphate (S1P) is a key regulator of lymphocyte egress. Although the majority of plasma S1P is bound to apolipoprotein M (ApoM) in the high-density lipoprotein (HDL) particle, the immunological functions of the ApoM-S1P complex are unknown. Here we show that ApoM-S1P is dispensable for lymphocyte trafficking yet restrains lymphopoiesis by activating the S1P1 receptor on bone marrow lymphocyte progenitors. Mice that lacked ApoM (Apom(-/-)) had increased proliferation of Lin(-) Sca-1(+) cKit(+) haematopoietic progenitor cells (LSKs) and common lymphoid progenitors (CLPs) in bone marrow. Pharmacological activation or genetic overexpression of S1P1 suppressed LSK and CLP cell proliferation in vivo. ApoM was stably associated with bone marrow CLPs, which showed active S1P1 signalling in vivo. Moreover, ApoM-bound S1P, but not albumin-bound S1P, inhibited lymphopoiesis in vitro. Upon immune stimulation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier. Thus, the ApoM-S1P-S1P1 signalling axis restrains the lymphocyte compartment and, subsequently, adaptive immune responses. Unique biological functions imparted by specific S1P chaperones could be exploited for novel therapeutic opportunities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506268/" 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/PMC4506268/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blaho, Victoria A -- Galvani, Sylvain -- Engelbrecht, Eric -- Liu, Catherine -- Swendeman, Steven L -- Kono, Mari -- Proia, Richard L -- Steinman, Lawrence -- Han, May H -- Hla, Timothy -- F32 CA14211/CA/NCI NIH HHS/ -- F32 CA142117/CA/NCI NIH HHS/ -- HL67330/HL/NHLBI NIH HHS/ -- HL70694/HL/NHLBI NIH HHS/ -- HL89934/HL/NHLBI NIH HHS/ -- P01 HL070694/HL/NHLBI NIH HHS/ -- P20 RR017677/RR/NCRR NIH HHS/ -- P30 CA138313/CA/NCI NIH HHS/ -- R01 HL089934/HL/NHLBI NIH HHS/ -- R37 HL067330/HL/NHLBI NIH HHS/ -- Z01 DK056014-02/Intramural NIH HHS/ -- Z01 DK056015-01/Intramural NIH HHS/ -- England -- Nature. 2015 Jul 16;523(7560):342-6. doi: 10.1038/nature14462. Epub 2015 Jun 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York 10065, USA [2] Brain and Mind Research Institute, Weill Medical College of Cornell University, New York, New York 10065, USA. ; Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York 10065, USA. ; Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA. ; Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26053123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins/deficiency/genetics/*metabolism ; Blood-Brain Barrier/pathology ; Cell Movement ; Cell Proliferation/genetics ; Central Nervous System/immunology/metabolism/*pathology ; Encephalomyelitis, Autoimmune, ; Experimental/genetics/immunology/metabolism/pathology ; Female ; Fingolimod Hydrochloride/pharmacology ; Hematopoietic Stem Cells/cytology/metabolism ; Inflammation/immunology/metabolism/pathology ; Lipoproteins, HDL/*metabolism ; Lymphocytes/*cytology/immunology/*metabolism ; Lymphoid Progenitor Cells/cytology/metabolism ; *Lymphopoiesis ; Lysophospholipids/agonists/blood/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Protein Binding ; Receptors, Lysosphingolipid/metabolism ; Signal Transduction ; Sphingosine/agonists/*analogs & derivatives/blood/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Electronic Resource
    Electronic Resource
    Synthesis of yttrium iron garnet precursor particles by homogeneous precipitation (1996)
    Springer
    Journal of materials science 31 (1996), S. 4233-4240 
    Details
    ISSN: 1573-4803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract Yttrium iron garnet (YIG) precursor particles were obtained by homogeneous precipitation in a nitrate salt solution by a reaction involving the thermal decomposition of urea. Chemical analysis indicated that solid phases were initially precipitated with sequential iron ion content. The precipitate formed was an amorphous mixed iron oxide phase. The complex composition and the thermal decomposition of the precipitate were studied by thermogravimetry-differential thermal analysis, differential scanning calorimetry, X-ray diffraction, and Fourier transform-infrared spectroscopy. Precipitate morphology was observed by SEM and TEM. Fine-grained single-phase yttrium iron garnet (YIG:Y3Fe5O12) powders were obtained by calcination of the precipitate at 1200 °C. YFeO3 intermediate compound was formed at 600 °C prior to the final crystallization of YIG.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00356444
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  • 8
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    Blocking angiotensin-converting enzyme induces potent regulatory T cells and modulates TH1- and TH17-mediated autoimmunity (2009)
    National Academy of Sciences
    Details
    Publication Date: 2009-08-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Nonlinear partial differential equations and applications: Mitogen-activated protein kinase signaling in postgermination arrest of development by abscisic acid (2002)
    National Academy of Sciences
    Details
    Publication Date: 2002-11-14
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Essential role of the cAMP-cAMP response-element binding protein pathway in opiate-induced homeostatic adaptations of locus coeruleus neurons (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-09-13
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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