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  • Articles  (36)
  • American Institute of Physics (AIP)  (20)
  • Nature Publishing Group (NPG)  (9)
  • Institute of Physics (IOP)  (7)
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  • Articles  (36)
  • 1
    Publication Date: 2016-09-21
    Description: This work reports on InP-based metamorphic quantum well structures with bismuth incorporation for mid-infrared applications. InAs 1-x Bi x quantum well structures have been grown on InP-based metamorphic In 0.83 Al 0.17 As buffers and photoluminescence beyond 3.1  μ m has been achieved at 300 K, which is longer than the referenced InAs quantum well. X-ray diffraction, cross-sectional transmission electron microscopy, and energy dispersive X-ray spectroscopy measurements reveal clear interfaces of InAsBi quantum well with low bismuth, while more defects and bismuth inhomogeneity were observed as more bismuth was incorporated.
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  • 2
    Publication Date: 2016-01-21
    Description: This work reports on the demonstration of a short-wave infrared detector nearly lattice matched to InP substrate using quaternary InGaAsBi as the absorption layer. The bismuth content of about 3.2% has red-shifted the 50% cut-off wavelength from about 1.6  μ m to 2.1  μ m at room temperature, indicating a bandgap reduction of about 180 meV due to bismuth incorporation. The detector shows an encouraging dark current density of 2.4 × 10 −4 A/cm 2 at bias voltage of −10 mV at 300 K. This work shows the promising potential of InP-based lattice-matched InGaAsBi detectors for short-wave infrared detection.
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  • 3
    Publication Date: 2015-11-25
    Description: We report the effect of Bi surfactant on the properties of highly strained InAs/InGaAs triangular quantum wells grown on InP substrates. Reduced surface roughness, improved heterostructure interfaces and enhanced photoluminescence intensity at 2.2  μ m are observed by moderate Bi-mediated growth. The nonradiative processes are analysed based on temperature-dependent photoluminescence. It is confirmed that Bi incorporation is insignificant in the samples, whereas excessive Bi flux during the growth results in deteriorated performance. The surfactant effect of Bi is promising to improve InP-based highly strained structures while the excess of Bi flux needs to be avoided.
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  • 4
    Publication Date: 2015-03-24
    Description: This work reports on up to 2.9  μ m lasing at 230 K of InP-based type-I quantum well lasers. This record long wavelength lasing is achieved by applying InP-based Sb-free structures with eight periods of strain-compensated InAs quantum wells grown on metamorphic In 0.8 Al 0.2 As template layers. The continuous-wave threshold current density is 797 A/cm 2 and the idealized extrapolated threshold current density for infinite cavity length is as low as 58 A/cm 2 per quantum well at 120 K. This scheme is a promising pathway for extending the wavelength range of type-I quantum well lasers on InP substrates.
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  • 5
    Publication Date: 2014-12-03
    Description: Contactless electroreflectance is applied to study the band gap (E 0 ) and spin-orbit splitting (Δ SO ) in InP 1−x Bi x alloys with 0 
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  • 6
    Publication Date: 2009-02-27
    Description: Lung disease is the major cause of morbidity and mortality in cystic fibrosis, an autosomal recessive disease caused by mutations in CFTR. In cystic fibrosis, chronic infection and dysregulated neutrophilic inflammation lead to progressive airway destruction. The severity of cystic fibrosis lung disease has considerable heritability, independent of CFTR genotype. To identify genetic modifiers, here we performed a genome-wide single nucleotide polymorphism scan in one cohort of cystic fibrosis patients, replicating top candidates in an independent cohort. This approach identified IFRD1 as a modifier of cystic fibrosis lung disease severity. IFRD1 is a histone-deacetylase-dependent transcriptional co-regulator expressed during terminal neutrophil differentiation. Neutrophils, but not macrophages, from Ifrd1-deficient mice showed blunted effector function, associated with decreased NF-kappaB p65 transactivation. In vivo, IFRD1 deficiency caused delayed bacterial clearance from the airway, but also less inflammation and disease-a phenotype primarily dependent on haematopoietic cell expression, or lack of expression, of IFRD1. In humans, IFRD1 polymorphisms were significantly associated with variation in neutrophil effector function. These data indicate that IFRD1 modulates the pathogenesis of cystic fibrosis lung disease through the regulation of neutrophil effector function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841516/" 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/PMC2841516/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, YuanYuan -- Harley, Isaac T W -- Henderson, Lindsay B -- Aronow, Bruce J -- Vietor, Ilja -- Huber, Lukas A -- Harley, John B -- Kilpatrick, Jeffrey R -- Langefeld, Carl D -- Williams, Adrienne H -- Jegga, Anil G -- Chen, Jing -- Wills-Karp, Marsha -- Arshad, S Hasan -- Ewart, Susan L -- Thio, Chloe L -- Flick, Leah M -- Filippi, Marie-Dominique -- Grimes, H Leighton -- Drumm, Mitchell L -- Cutting, Garry R -- Knowles, Michael R -- Karp, Christopher L -- R01 AI024717/AI/NIAID NIH HHS/ -- R01 HL068890/HL/NHLBI NIH HHS/ -- R01 HL068890-01/HL/NHLBI NIH HHS/ -- R01 HL068927/HL/NHLBI NIH HHS/ -- R01 HL068927-01/HL/NHLBI NIH HHS/ -- R01 HL079312/HL/NHLBI NIH HHS/ -- R01 HL079312-01A1/HL/NHLBI NIH HHS/ -- R37 AI024717/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Apr 23;458(7241):1039-42. doi: 10.1038/nature07811. Epub 2009 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation and the University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19242412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cohort Studies ; Cystic Fibrosis/*genetics/*pathology ; Disease Models, Animal ; Genotype ; Humans ; Immediate-Early Proteins/deficiency/*genetics ; Inflammation/genetics/pathology ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology/metabolism ; Polymorphism, Single Nucleotide/genetics ; Pseudomonas aeruginosa/immunology/pathogenicity ; Transcription Factor RelA/metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2009-07-17
    Description: Schistosoma mansoni is responsible for the neglected tropical disease schistosomiasis that affects 210 million people in 76 countries. Here we present analysis of the 363 megabase nuclear genome of the blood fluke. It encodes at least 11,809 genes, with an unusual intron size distribution, and new families of micro-exon genes that undergo frequent alternative splicing. As the first sequenced flatworm, and a representative of the Lophotrochozoa, it offers insights into early events in the evolution of the animals, including the development of a body pattern with bilateral symmetry, and the development of tissues into organs. Our analysis has been informed by the need to find new drug targets. The deficits in lipid metabolism that make schistosomes dependent on the host are revealed, and the identification of membrane receptors, ion channels and more than 300 proteases provide new insights into the biology of the life cycle and new targets. Bioinformatics approaches have identified metabolic chokepoints, and a chemogenomic screen has pinpointed schistosome proteins for which existing drugs may be active. The information generated provides an invaluable resource for the research community to develop much needed new control tools for the treatment and eradication of this important and neglected disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756445/" 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/PMC2756445/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berriman, Matthew -- Haas, Brian J -- LoVerde, Philip T -- Wilson, R Alan -- Dillon, Gary P -- Cerqueira, Gustavo C -- Mashiyama, Susan T -- Al-Lazikani, Bissan -- Andrade, Luiza F -- Ashton, Peter D -- Aslett, Martin A -- Bartholomeu, Daniella C -- Blandin, Gaelle -- Caffrey, Conor R -- Coghlan, Avril -- Coulson, Richard -- Day, Tim A -- Delcher, Art -- DeMarco, Ricardo -- Djikeng, Appolinaire -- Eyre, Tina -- Gamble, John A -- Ghedin, Elodie -- Gu, Yong -- Hertz-Fowler, Christiane -- Hirai, Hirohisha -- Hirai, Yuriko -- Houston, Robin -- Ivens, Alasdair -- Johnston, David A -- Lacerda, Daniela -- Macedo, Camila D -- McVeigh, Paul -- Ning, Zemin -- Oliveira, Guilherme -- Overington, John P -- Parkhill, Julian -- Pertea, Mihaela -- Pierce, Raymond J -- Protasio, Anna V -- Quail, Michael A -- Rajandream, Marie-Adele -- Rogers, Jane -- Sajid, Mohammed -- Salzberg, Steven L -- Stanke, Mario -- Tivey, Adrian R -- White, Owen -- Williams, David L -- Wortman, Jennifer -- Wu, Wenjie -- Zamanian, Mostafa -- Zerlotini, Adhemar -- Fraser-Liggett, Claire M -- Barrell, Barclay G -- El-Sayed, Najib M -- 086151/Wellcome Trust/United Kingdom -- 5D43TW006580/TW/FIC NIH HHS/ -- 5D43TW007012-03/TW/FIC NIH HHS/ -- AI054711-01A2/AI/NIAID NIH HHS/ -- AI48828/AI/NIAID NIH HHS/ -- R01 GM083873/GM/NIGMS NIH HHS/ -- R01 GM083873-07/GM/NIGMS NIH HHS/ -- R01 GM083873-08/GM/NIGMS NIH HHS/ -- R01 LM006845/LM/NLM NIH HHS/ -- R01 LM006845-08/LM/NLM NIH HHS/ -- R01 LM006845-09/LM/NLM NIH HHS/ -- U01 AI048828/AI/NIAID NIH HHS/ -- U01 AI048828-01/AI/NIAID NIH HHS/ -- U01 AI048828-02/AI/NIAID NIH HHS/ -- WT085775/Z/08/Z/Wellcome Trust/United Kingdom -- England -- Nature. 2009 Jul 16;460(7253):352-8. doi: 10.1038/nature08160.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Cambridge CB10 1SD, UK. mb4@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19606141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Exons/genetics ; Genes, Helminth/genetics ; Genome, Helminth/*genetics ; Host-Parasite Interactions/genetics ; Introns/genetics ; Molecular Sequence Data ; Physical Chromosome Mapping ; Schistosoma mansoni/drug effects/embryology/*genetics/physiology ; Schistosomiasis mansoni/drug therapy/parasitology
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  • 8
    Publication Date: 2015-08-20
    Description: Epigenetic modifiers have fundamental roles in defining unique cellular identity through the establishment and maintenance of lineage-specific chromatin and methylation status. Several DNA modifications such as 5-hydroxymethylcytosine (5hmC) are catalysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles of Tet proteins in regulating chromatin architecture and gene transcription independently of DNA methylation have been gradually uncovered. However, the regulation of immunity and inflammation by Tet proteins independent of their role in modulating DNA methylation remains largely unknown. Here we show that Tet2 selectively mediates active repression of interleukin-6 (IL-6) transcription during inflammation resolution in innate myeloid cells, including dendritic cells and macrophages. Loss of Tet2 resulted in the upregulation of several inflammatory mediators, including IL-6, at late phase during the response to lipopolysaccharide challenge. Tet2-deficient mice were more susceptible to endotoxin shock and dextran-sulfate-sodium-induced colitis, displaying a more severe inflammatory phenotype and increased IL-6 production compared to wild-type mice. IkappaBzeta, an IL-6-specific transcription factor, mediated specific targeting of Tet2 to the Il6 promoter, further indicating opposite regulatory roles of IkappaBzeta at initial and resolution phases of inflammation. For the repression mechanism, independent of DNA methylation and hydroxymethylation, Tet2 recruited Hdac2 and repressed transcription of Il6 via histone deacetylation. We provide mechanistic evidence for the gene-specific transcription repression activity of Tet2 via histone deacetylation and for the prevention of constant transcription activation at the chromatin level for resolving inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697747/" 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/PMC4697747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qian -- Zhao, Kai -- Shen, Qicong -- Han, Yanmei -- Gu, Yan -- Li, Xia -- Zhao, Dezhi -- Liu, Yiqi -- Wang, Chunmei -- Zhang, Xiang -- Su, Xiaoping -- Liu, Juan -- Ge, Wei -- Levine, Ross L -- Li, Nan -- Cao, Xuetao -- P30 CA008748/CA/NCI NIH HHS/ -- R01 CA173636/CA/NCI NIH HHS/ -- England -- Nature. 2015 Sep 17;525(7569):389-93. doi: 10.1038/nature15252. Epub 2015 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Key Laboratory of Medical Molecular Biology &Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China. ; National Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China. ; Human Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan-Kettering Cancer, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26287468" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Chromatin/chemistry/genetics/metabolism ; Colitis/enzymology/immunology/metabolism ; DNA Methylation ; DNA-Binding Proteins/deficiency/*metabolism ; Dendritic Cells/cytology/metabolism ; Down-Regulation/genetics ; Epigenesis, Genetic ; Female ; HEK293 Cells ; Histone Deacetylase 2/*metabolism ; Histones/chemistry/metabolism ; Humans ; I-kappa B Proteins/metabolism ; Inflammation/enzymology/immunology/*metabolism ; Interleukin-6/*antagonists & inhibitors/*biosynthesis/genetics/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins/deficiency/*metabolism ; Transcription, Genetic
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  • 9
    Publication Date: 2016-03-12
    Description: By combining electrical measurements, scanning Kelvin probe microscopy, and numerical electrical simulations, we find significant current crowding in two-dimensional (2D) black phosphorus field-effect transistors. This current crowding can lead to localized Joule heating close to the metal contacts, and it is consistent with the features of the device failure observed in this study. Importantly, by considering both Schottky and resistive Ohmic contact models, we find that the commonly used transmission-line model, in general, significantly underestimates the extent of the current crowding. These findings, which are likely to be relevant in other 2D materials, suggest the need to take into account the current crowding effect in designing 2D devices.
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  • 10
    Publication Date: 2018-11-08
    Description: To obtain the intuitive data of magic field changes with nonwoven metal shielding material, the Al / PET / Rayon needle punched webs was processed with varied parameters, which were position of Al film, mass proportion of Al, needle punched density, and needle punched depth. Magnetic flux density values of Al / PET / Rayon needle punched webs were measured to calculate their magnetic flux density attenuation (MFDA) values under the exposure to mobile phone field. It was found that position of Al film, Al proportion, and needle punched density have a great effect on magnetic flux density attenuation. When Al proportion in needle punched web increases from 10% to 18%, MFDA values increase accordingly, and tend to converge around Al mass ratio 18%. Besides, the promotion range of MFDA values is particularly obvious in the case of needle punched density 50 g m −2 . When needle punched density increases from 50 g m −2 to 150 g m −2 , MFDA values decrease o...
    Print ISSN: 1757-8981
    Electronic ISSN: 1757-899X
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
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