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  • Linguistics  (780)
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  • 1
    Online Resource
    Online Resource
    Experimental Observation of the Quantum Anomalous Hall Effect in a Magnetic Topological Insulator
    American Association for the Advancement of Science (AAAS) ; 2013
    In:  Science Vol. 340, No. 6129 ( 2013-04-12), p. 167-170
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 340, No. 6129 ( 2013-04-12), p. 167-170
    Abstract: The quantized version of the anomalous Hall effect has been predicted to occur in magnetic topological insulators, but the experimental realization has been challenging. Here, we report the observation of the quantum anomalous Hall (QAH) effect in thin films of chromium-doped (Bi,Sb) 2 Te 3 , a magnetic topological insulator. At zero magnetic field, the gate-tuned anomalous Hall resistance reaches the predicted quantized value of h/e 2 , accompanied by a considerable drop in the longitudinal resistance. Under a strong magnetic field, the longitudinal resistance vanishes, whereas the Hall resistance remains at the quantized value. The realization of the QAH effect may lead to the development of low-power-consumption electronics.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1234414
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2013
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 2
    Online Resource
    Online Resource
    Satellite testing of a gravitationally induced quantum decoherence model
    American Association for the Advancement of Science (AAAS) ; 2019
    In:  Science Vol. 366, No. 6461 ( 2019-10-04), p. 132-135
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 366, No. 6461 ( 2019-10-04), p. 132-135
    Abstract: Quantum mechanics and the general theory of relativity are two pillars of modern physics. However, a coherent unified framework of the two theories remains an open problem. Attempts to quantize general relativity have led to many rival models of quantum gravity, which, however, generally lack experimental foundations. We report a quantum optical experimental test of event formalism of quantum fields, a theory that attempts to present a coherent description of quantum fields in exotic spacetimes containing closed timelike curves and ordinary spacetime. We experimentally test a prediction of the theory with the quantum satellite Micius that a pair of time-energy–entangled particles probabilistically decorrelate passing through different regions of the gravitational potential of Earth. Our measurement results are consistent with the standard quantum theory and hence do not support the prediction of event formalism.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aay5820
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2019
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 3
    Online Resource
    Online Resource
    Attention Modulates the Role of Speakers' Voice Identity and Linguistic Information in Spoken Word Processing: Evidence From Event-Related Potentials
    American Speech Language Hearing Association ; 2023
    In:  Journal of Speech, Language, and Hearing Research Vol. 66, No. 5 ( 2023-05-09), p. 1678-1693
    Details
    In: Journal of Speech, Language, and Hearing Research, American Speech Language Hearing Association, Vol. 66, No. 5 ( 2023-05-09), p. 1678-1693
    Abstract: The human voice usually contains two types of information: linguistic and identity information. However, whether and how linguistic information interacts with identity information remains controversial. This study aimed to explore the processing of identity and linguistic information during spoken word processing by considering the modulation of attention. Method: We conducted two event-related potentials (ERPs) experiments in the study. Different speakers (self, friend, and unfamiliar speakers) and emotional words (positive, negative, and neutral words) were used to manipulate the identity and linguistic information. With the manipulation, Experiment 1 explored the identity and linguistic information processing with a word decision task that requires participants' explicit attention to linguistic information. Experiment 2 further investigated the issue with a passive oddball paradigm that requires rare attention to either the identity or linguistic information. Results: Experiment 1 revealed an interaction among speaker, word type, and hemisphere in N400 amplitudes but not in N100 and P200, which suggests that identity information interacted with linguistic information at the later stage of spoken word processing. The mismatch negativity results of Experiment 2 showed no significant interaction between speaker and word pair, which indicates that identity and linguistic information were processed independently. Conclusions: The identity information would interact with linguistic information during spoken word processing. However, the interaction was modulated by the task demands on attention involvement. We propose an attention-modulated explanation to explain the mechanism underlying identity and linguistic information processing. Implications of our findings are discussed in light of the integration and independence theories.
    Type of Medium: Online Resource
    ISSN: 1092-4388 , 1558-9102
    URL: Article
    DOI: 10.1044/2023_JSLHR-22-00420
    Language: English
    Publisher: American Speech Language Hearing Association
    Publication Date: 2023
    detail.hit.zdb_id: 2070420-3
    SSG: 5,2
    SSG: 7,11
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  • 4
    Online Resource
    Online Resource
    Single-crystal x-ray diffraction structures of covalent organic frameworks
    American Association for the Advancement of Science (AAAS) ; 2018
    In:  Science Vol. 361, No. 6397 ( 2018-07-06), p. 48-52
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 361, No. 6397 ( 2018-07-06), p. 48-52
    Abstract: The crystallization problem is an outstanding challenge in the chemistry of porous covalent organic frameworks (COFs). Their structural characterization has been limited to modeling and solutions based on powder x-ray or electron diffraction data. Single crystals of COFs amenable to x-ray diffraction characterization have not been reported. Here, we developed a general procedure to grow large single crystals of three-dimensional imine-based COFs (COF-300, hydrated form of COF-300, COF-303, LZU-79, and LZU-111). The high quality of the crystals allowed collection of single-crystal x-ray diffraction data of up to 0.83-angstrom resolution, leading to unambiguous solution and precise anisotropic refinement. Characteristics such as degree of interpenetration, arrangement of water guests, the reversed imine connectivity, linker disorder, and uncommon topology were deciphered with atomic precision—aspects impossible to determine without single crystals.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aat7679
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2018
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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    Online Resource
  • 5
    Online Resource
    Online Resource
    A small molecule protects mitochondrial integrity by inhibiting mTOR activity
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 46 ( 2019-11-12), p. 23332-23338
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 46 ( 2019-11-12), p. 23332-23338
    Abstract: Apoptosis activation by cytochrome c release from mitochondria to cytosol is a normal cellular response to mitochondrial damage. Using cellular apoptosis assay, we have found small-molecule apoptosis inhibitors that protect cells from mitochondrial damage. Previously, we reported the discovery of a small molecule, Compound A, which blocks dopaminergic neuron death in a rat model of Parkinson’s disease through targeting succinate dehydrogenase subunit B (SDHB) of complex II to protect the integrity of the mitochondrial respiratory chain. Here, we report a small molecule, Compound R6, which saves cells from apoptosis via mammalian target of rapamycin (mTOR)-mediated induction of autophagy. Additionally, we show that Compound R6 protects mitochondrial integrity and respiration after induction of the intrinsic apoptosis pathway. Encouragingly, and supporting the potential further application of Compound R6 as a tool for basic and medicinal research, a pharmacokinetics (PK) profiling study showed that Compound R6 is metabolically stable and can pass the blood−brain barrier. Moreover, Compound R6 accumulates in the brain of test animals via intravenous and intraperitoneal administration. Finally, we found that Compound R6 confers significant neuroprotective effects on a rat cerebral ischemia/reperfusion model, demonstrating its potential as a promising drug candidate for neurodegenerative diseases.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1911246116
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Structural and functional studies of TBC1D23 C-terminal domain provide a link between endosomal trafficking and PCH
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 45 ( 2019-11-05), p. 22598-22608
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 45 ( 2019-11-05), p. 22598-22608
    Abstract: Pontocerebellar hypoplasia (PCH) is a group of neurological disorders that affect the development of the brain, in particular, the pons and cerebellum. Homozygous mutations of TBC1D23 have been found recently to lead to PCH; however, the underlying molecular mechanisms remain unclear. Here, we show that the crystal structure of the TBC1D23 C-terminal domain adopts a Pleckstrin homology domain fold and selectively binds to phosphoinositides, in particular, PtdIns(4)P, through one surface while binding FAM21 via the opposite surface. Mutation of key residues of TBC1D23 or FAM21 selectively disrupts the endosomal vesicular trafficking toward the Trans-Golgi Network. Finally, using the zebrafish model, we show that PCH patient-derived mutants, impacting either phosphoinositide binding or FAM21 binding, lead to abnormal neuronal growth and brain development. Taken together, our data provide a molecular basis for the interaction between TBC1D23 and FAM21, and suggest a plausible role for PtdIns(4)P in the TBC1D23-mediating endosome-to-TGN trafficking pathway. Defects in this trafficking pathway are, at least partially, responsible for the pathogenesis of certain types of PCH.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1909316116
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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    Online Resource
  • 7
    Online Resource
    Online Resource
    Autophagy protects C. elegans against necrosis during Pseudomonas aeruginosa infection
    Proceedings of the National Academy of Sciences ; 2014
    In:  Proceedings of the National Academy of Sciences Vol. 111, No. 34 ( 2014-08-26), p. 12480-12485
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 111, No. 34 ( 2014-08-26), p. 12480-12485
    Abstract: Autophagy, a conserved pathway that delivers intracellular materials into lysosomes for degradation, is involved in development, aging, and a variety of diseases. Accumulating evidence demonstrates that autophagy plays a protective role against infectious diseases by diminishing intracellular pathogens, including bacteria, viruses, and parasites. However, the mechanism by which autophagy regulates innate immunity remains largely unknown. Here, we show that autophagy is involved in host defense against a pathogenic bacterium Pseudomonas aeruginosa in the metazoan Caenorhabditis elegans . P. aeruginosa infection induces autophagy via a conserved extracellular signal-regulated kinase (ERK). Intriguingly, impairment of autophagy does not influence the intestinal accumulation of P. aeruginosa , but instead induces intestinal necrosis. Inhibition of necrosis results in the survival of autophagy-deficient worms after P. aeruginosa infection. These findings reveal a previously unidentified role for autophagy in protection against necrosis triggered by pathogenic bacteria in C. elegans and implicate that such a function of autophagy may be conserved through the inflammatory response in diverse organisms.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1405032111
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2014
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Request sequence in Chinese public service calls
    SAGE Publications ; 2016
    In:  Discourse Studies Vol. 18, No. 3 ( 2016-06), p. 269-285
    Details
    In: Discourse Studies, SAGE Publications, Vol. 18, No. 3 ( 2016-06), p. 269-285
    Abstract: This study examines the characteristics of request sequences in Chinese public service calls. The data analysis indicates that a prominent characteristic of Chinese public service calls is the frequent appearance of insert expansions and non-minimal post-expansions, with the latter occurring after both preferred response and dispreferred response. This is closely related to participants’ institutional identities and epistemic asymmetry; operators handling such service calls should pay due attention to this asymmetry to ensure mutual understanding in conversation.
    Type of Medium: Online Resource
    ISSN: 1461-4456 , 1461-7080
    URL: Article
    DOI: 10.1177/1461445616634552
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2016
    detail.hit.zdb_id: 1482715-3
    SSG: 25
    SSG: 7,11
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  • 9
    Online Resource
    Online Resource
    FLT3/D835Y mutation knock-in mice display less aggressive disease compared with FLT3/internal tandem duplication (ITD) mice
    Proceedings of the National Academy of Sciences ; 2013
    In:  Proceedings of the National Academy of Sciences Vol. 110, No. 52 ( 2013-12-24), p. 21113-21118
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 110, No. 52 ( 2013-12-24), p. 21113-21118
    Abstract: FMS-like tyrosine kinase 3 (FLT3) is mutated in approximately one third of acute myeloid leukemia cases. The most common FLT3 mutations in acute myeloid leukemia are internal tandem duplication (ITD) mutations in the juxtamembrane domain (23%) and point mutations in the tyrosine kinase domain (10%). The mutation substituting the aspartic acid at position 838 (equivalent to the human aspartic acid residue at position 835) with a tyrosine (referred to as FLT3/D835Y hereafter) is the most frequent kinase domain mutation, converting aspartic acid to tyrosine. Although both of these mutations constitutively activate FLT3, patients with an ITD mutation have a significantly poorer prognosis. To elucidate the mechanisms behind this prognostic difference, we have generated a knock-in mouse model with a D838Y point mutation in FLT3 that corresponds to the FLT3/D835Y mutation described in humans. Compared with FLT3/ITD knock-in mice, the FLT3/D835Y knock-in mice survive significantly longer. The majority of these mice develop myeloproliferative neoplasms with a less-aggressive phenotype. In addition, FLT3/D835Y mice have distinct hematopoietic development patterns. Unlike the tremendous depletion of the hematopoietic stem cell compartment we have observed in FLT3/ITD mice, FLT3/D835Y mutant mice are not depleted in hematopoietic stem cells. Further comparisons of these FLT3/D835Y knock-in mice with FLT3/ITD mice should provide an ideal platform for dissecting the molecular mechanisms that underlie the prognostic differences between the two different types of FLT3 mutations.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1310559110
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2013
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    LKB1 inhibits lung cancer progression through lysyl oxidase and extracellular matrix remodeling
    Proceedings of the National Academy of Sciences ; 2010
    In:  Proceedings of the National Academy of Sciences Vol. 107, No. 44 ( 2010-11-02), p. 18892-18897
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 107, No. 44 ( 2010-11-02), p. 18892-18897
    Abstract: LKB1 loss-of-function mutations, observed in ∼30% of human lung adenocarcinomas, contribute significantly to lung cancer malignancy progression. We show that lysyl oxidase (LOX), negatively regulated by LKB1 through mTOR-HIF-1α signaling axis, mediates lung cancer progression. Inhibition of LOX activity dramatically alleviates lung cancer malignancy progression. Up-regulated LOX expression triggers excess collagen deposition in Lkb1 -deficient lung tumors, and thereafter results in enhanced cancer cell proliferation and invasiveness through activation of β1 integrin signaling. High LOX level and activity correlate with poor prognosis and metastasis. Our findings provide evidence of how LKB1 loss of function promotes lung cancer malignancy through remodeling of extracellular matrix microenvironment, and identify LOX as a potential target for disease treatment in lung cancer patients.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1004952107
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2010
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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