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  • 1
    Publication Date: 2000-01-11
    Description: The quantum cascade laser, which uses electronic transitions within a single band of a semiconductor, constitutes a possible way to integrate active optical components into silicon-based technology. This concept necessitates a transition with a narrow linewidth and an upper state with a sufficiently long lifetime. We report the observation of intersubband electroluminescence from a p-type silicon/silicon-germanium quantum cascade structure, centered at 130 millielectron volts with a width of 22 millielectron volts, with the expected polarization, and discernible up to 180 kelvin. The nonradiative lifetime is found to depend strongly on the design of the quantum well structure, and is shown to reach values comparable to that of an equivalent GaInAs/AlInAs laser structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dehlinger, G -- Diehl, L -- Gennser, U -- Sigg, H -- Faist, J -- Ensslin, K -- Grutzmacher, D -- Muller, E -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2277-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Micro- and Nanotechnology, Paul Scherrer Institut, CH-5232 Villigen, Switzerland. gabriel.dehlinger@psi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125134" target="_blank"〉PubMed〈/a〉
    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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  • 2
    Publication Date: 2014-12-04
    Description: T-helper type 17 (TH17) cells that produce the cytokines interleukin-17A (IL-17A) and IL-17F are implicated in the pathogenesis of several autoimmune diseases. The differentiation of TH17 cells is regulated by transcription factors such as RORgammat, but post-translational mechanisms preventing the rampant production of pro-inflammatory IL-17A have received less attention. Here we show that the deubiquitylating enzyme DUBA is a negative regulator of IL-17A production in T cells. Mice with DUBA-deficient T cells developed exacerbated inflammation in the small intestine after challenge with anti-CD3 antibodies. DUBA interacted with the ubiquitin ligase UBR5, which suppressed DUBA abundance in naive T cells. DUBA accumulated in activated T cells and stabilized UBR5, which then ubiquitylated RORgammat in response to TGF-beta signalling. Our data identify DUBA as a cell-intrinsic suppressor of IL-17 production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rutz, Sascha -- Kayagaki, Nobuhiko -- Phung, Qui T -- Eidenschenk, Celine -- Noubade, Rajkumar -- Wang, Xiaoting -- Lesch, Justin -- Lu, Rongze -- Newton, Kim -- Huang, Oscar W -- Cochran, Andrea G -- Vasser, Mark -- Fauber, Benjamin P -- DeVoss, Jason -- Webster, Joshua -- Diehl, Lauri -- Modrusan, Zora -- Kirkpatrick, Donald S -- Lill, Jennie R -- Ouyang, Wenjun -- Dixit, Vishva M -- England -- Nature. 2015 Feb 19;518(7539):417-21. doi: 10.1038/nature13979. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Protein Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Early Discovery Biochemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Discovery Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Stability ; Female ; Inflammation/genetics/pathology ; Interleukin-17/*biosynthesis ; Intestine, Small/metabolism/pathology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; *Protein Biosynthesis ; Signal Transduction ; Substrate Specificity ; Th17 Cells/*metabolism ; Transforming Growth Factor beta/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin-Specific Proteases/biosynthesis/deficiency/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/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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  • 4
    Publication Date: 2004-01-31
    Description: Protein tyrosine kinases and phosphatases cooperate to regulate normal immune cell function. We examined the role of PEST domain-enriched tyrosine phosphatase (PEP) in regulating T cell antigen-receptor function during thymocyte development and peripheral T cell differentiation. Although normal naive T cell functions were retained in pep-deficient mice, effector/memory T cells demonstrated enhanced activation of Lck. In turn, this resulted in increased expansion and function of the effector/memory T cell pool, which was also associated with spontaneous development of germinal centers and elevated serum antibody levels. These results revealed a central role for PEP in negatively regulating specific aspects of T cell development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasegawa, Kiminori -- Martin, Flavius -- Huang, Guangming -- Tumas, Dan -- Diehl, Lauri -- Chan, Andrew C -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):685-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, Inc., One DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; B-Lymphocytes/physiology ; CD4-Positive T-Lymphocytes/immunology/physiology ; CD8-Positive T-Lymphocytes/immunology/physiology ; Cell Cycle ; Gene Targeting ; Germinal Center/physiology ; Hydrogen-Ion Concentration ; Immunoglobulins/blood ; *Immunologic Memory ; Lymphocyte Activation ; Lymphocyte Count ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 12 ; Protein Tyrosine Phosphatases/genetics/*metabolism ; Receptors, Antigen, T-Cell/genetics/immunology ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/*immunology/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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  • 5
    Publication Date: 2014-08-15
    Description: The connection between an altered gut microbiota and metabolic disorders such as obesity, diabetes, and cardiovascular disease is well established. Defects in preserving the integrity of the mucosal barriers can result in systemic endotoxaemia that contributes to chronic low-grade inflammation, which further promotes the development of metabolic syndrome. Interleukin (IL)-22 exerts essential roles in eliciting antimicrobial immunity and maintaining mucosal barrier integrity within the intestine. Here we investigate the connection between IL-22 and metabolic disorders. We find that the induction of IL-22 from innate lymphoid cells and CD4(+) T cells is impaired in obese mice under various immune challenges, especially in the colon during infection with Citrobacter rodentium. While innate lymphoid cell populations are largely intact in obese mice, the upregulation of IL-23, a cytokine upstream of IL-22, is compromised during the infection. Consequently, these mice are susceptible to C. rodentium infection, and both exogenous IL-22 and IL-23 are able to restore the mucosal host defence. Importantly, we further unveil unexpected functions of IL-22 in regulating metabolism. Mice deficient in IL-22 receptor and fed with high-fat diet are prone to developing metabolic disorders. Strikingly, administration of exogenous IL-22 in genetically obese leptin-receptor-deficient (db/db) mice and mice fed with high-fat diet reverses many of the metabolic symptoms, including hyperglycaemia and insulin resistance. IL-22 shows diverse metabolic benefits, as it improves insulin sensitivity, preserves gut mucosal barrier and endocrine functions, decreases endotoxaemia and chronic inflammation, and regulates lipid metabolism in liver and adipose tissues. In summary, we identify the IL-22 pathway as a novel target for therapeutic intervention in metabolic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiaoting -- Ota, Naruhisa -- Manzanillo, Paolo -- Kates, Lance -- Zavala-Solorio, Jose -- Eidenschenk, Celine -- Zhang, Juan -- Lesch, Justin -- Lee, Wyne P -- Ross, Jed -- Diehl, Lauri -- van Bruggen, Nicholas -- Kolumam, Ganesh -- Ouyang, Wenjun -- England -- Nature. 2014 Oct 9;514(7521):237-41. doi: 10.1038/nature13564. Epub 2014 Aug 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Immunology, Genentech, South San Francisco, California 94080, USA [2]. ; Department of Immunology, Genentech, South San Francisco, California 94080, USA. ; Department of Biomedical Imaging, Genentech, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, South San Francisco, California 94080, USA. ; 1] Department of Biomedical Imaging, Genentech, South San Francisco, California 94080, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25119041" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/drug effects/metabolism ; Animals ; CD4-Positive T-Lymphocytes/immunology/secretion ; Chronic Disease ; Citrobacter rodentium/drug effects/immunology/physiology ; Colon/drug effects/immunology/microbiology ; Diabetes Mellitus/*immunology/*metabolism/pathology ; Diet, High-Fat ; Female ; Hyperglycemia/diet therapy/drug therapy/metabolism ; *Immunity, Mucosal/drug effects ; Inflammation/drug therapy/metabolism/pathology ; Insulin/metabolism ; Insulin Resistance ; Interleukin-23/immunology/metabolism/pharmacology ; Interleukins/*immunology/*metabolism/pharmacology/therapeutic use ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Male ; Metabolic Diseases/diet therapy/drug therapy/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/metabolism ; Receptors, Interleukin/deficiency/metabolism ; Receptors, Leptin/deficiency/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: 2014-02-21
    Description: Crohn's disease is a debilitating inflammatory bowel disease (IBD) that can involve the entire digestive tract. A single-nucleotide polymorphism (SNP) encoding a missense variant in the autophagy gene ATG16L1 (rs2241880, Thr300Ala) is strongly associated with the incidence of Crohn's disease. Numerous studies have demonstrated the effect of ATG16L1 deletion or deficiency; however, the molecular consequences of the Thr300Ala (T300A) variant remains unknown. Here we show that amino acids 296-299 constitute a caspase cleavage motif in ATG16L1 and that the T300A variant (T316A in mice) significantly increases ATG16L1 sensitization to caspase-3-mediated processing. We observed that death-receptor activation or starvation-induced metabolic stress in human and murine macrophages increased degradation of the T300A or T316A variants of ATG16L1, respectively, resulting in diminished autophagy. Knock-in mice harbouring the T316A variant showed defective clearance of the ileal pathogen Yersinia enterocolitica and an elevated inflammatory cytokine response. In turn, deletion of the caspase-3-encoding gene, Casp3, or elimination of the caspase cleavage site by site-directed mutagenesis rescued starvation-induced autophagy and pathogen clearance, respectively. These findings demonstrate that caspase 3 activation in the presence of a common risk allele leads to accelerated degradation of ATG16L1, placing cellular stress, apoptotic stimuli and impaired autophagy in a unified pathway that predisposes to Crohn's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murthy, Aditya -- Li, Yun -- Peng, Ivan -- Reichelt, Mike -- Katakam, Anand Kumar -- Noubade, Rajkumar -- Roose-Girma, Merone -- DeVoss, Jason -- Diehl, Lauri -- Graham, Robert R -- van Lookeren Campagne, Menno -- England -- Nature. 2014 Feb 27;506(7489):456-62. doi: 10.1038/nature13044. Epub 2014 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; ITGR Human Genetics, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553140" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Autophagy/genetics ; Carrier Proteins/chemistry/*genetics/*metabolism ; Caspase 3/deficiency/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Crohn Disease/*genetics/pathology ; Cytokines/immunology ; Enzyme Activation ; Female ; Food Deprivation ; Humans ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutagenesis, Site-Directed ; Polymorphism, Single Nucleotide/*genetics ; *Proteolysis ; Stress, Physiological ; Yersinia enterocolitica/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-09-04
    Description: Japanese quail (Coturnix coturnix) learned a category for syllable-initial [d] followed by a dozen different vowels. After learning to categorize syllables consisting of [d], [b], or [g] followed by four different vowels, quail correctly categorized syllables in which the same consonants preceded eight novel vowels. Acoustic analysis of the categorized syllables revealed no single feature or pattern of features that could support generalization, suggesting that the quail adopted a more complex mapping of stimuli into categories. These results challenge theories of speech sound classification that posit uniquely human capacities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kluender, K R -- Diehl, R L -- Killeen, P R -- HD-18060/HD/NICHD NIH HHS/ -- MH-39940/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1195-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coturnix/*physiology ; Female ; Humans ; *Learning ; *Phonetics ; Quail/*physiology ; Reinforcement (Psychology) ; Speech Perception
    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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  • 8
    Publication Date: 2019
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 9
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 80 (2002), S. 3274-3276 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We present intersubband absorption measurements performed on p-type quasistrain-compensated modulation-doped Si0.2Ge0.8/Si quantum wells grown on Si0.5Ge0.5 pseudosubstrates. Several intersubband absorption peaks are observed up to room temperature. A strong confinement shift of the resonance occuring between the ground and the first excited heavy hole states has been observed, with the absorption peak shifting from λ=5.3 μm to as short as 3.8 μm. Excellent overall agreement with a 6 band k⋅p calculation is obtained, proving the accuracy of recently predicted values of band offsets. © 2002 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of low temperature physics 92 (1993), S. 173-180 
    ISSN: 1573-7357
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Adsorption isotherms of para-hydrogen adsorbed on graphite foam were measured for the temperature interval of 9 to 15 K up to about 25 layers, using the standard volumetric method. From these isotherms straight lines were obtained for ln(P 0/P) as a function ofd −3, d being the coverage. These plots obey an equation of the type ln(P 0/P)=ad−3+b. Considering capillary condensation and using the Frenkel-Halsey-Hill equation together with Kelvin's relation an average pore radius of (315±60) Å was found and the van der Waals potential calculated as (2.36±0.07)×10−12 erg Å3. From the data, there seems to be a transition at about 11 K, but it cannot be concluded definitely if it is a complete wetting transition. Whenever possible the obtained results were compared to existing data.
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