Institution
Sungkyunkwan University
Education•Seoul, South Korea•
About: Sungkyunkwan University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Graphene & Thin film. The organization has 28229 authors who have published 56428 publications receiving 1352733 citations. The organization is also known as: 성균관대학교.
Topics: Graphene, Thin film, Population, Carbon nanotube, Layer (electronics)
Papers published on a yearly basis
Papers
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University of Maryland, College Park1, Queen's University2, Cornell University3, University of Minnesota4, Nanyang Technological University5, McKinsey & Company6, Koç University7, Jacobs University Bremen8, University of Minho9, The Chinese University of Hong Kong10, Indian Institute of Management Ahmedabad11, Pontifical Catholic University of Peru12, University of Valencia13, Johannes Kepler University of Linz14, Victoria University of Wellington15, Hungarian Academy of Sciences16, National and Kapodistrian University of Athens17, La Trobe University18, University of Melbourne19, Sungkyunkwan University20, ESSEC Business School21, University of San Diego22, Katholieke Universiteit Leuven23, University of Patras24, Human Sciences Research Council25, ODESSA26, University of Tartu27, Norwegian School of Economics28, University of Koblenz and Landau29, University of Sussex30, University of Sindh31, Gakushuin University32, University of Groningen33, University of Tokyo34
TL;DR: The differences across cultures in the enforcement of conformity may reflect their specific histories and advances knowledge that can foster cross-cultural understanding in a world of increasing global interdependence and has implications for modeling cultural change.
Abstract: With data from 33 nations, we illustrate the differences between cultures that are tight (have many strong norms and a low tolerance of deviant behavior) versus loose (have weak social norms and a high tolerance of deviant behavior). Tightness-looseness is part of a complex, loosely integrated multilevel system that comprises distal ecological and historical threats (e.g., high population density, resource scarcity, a history of territorial conflict, and disease and environmental threats), broad versus narrow socialization in societal institutions (e.g., autocracy, media regulations), the strength of everyday recurring situations, and micro-level psychological affordances (e.g., prevention self-guides, high regulatory strength, need for structure). This research advances knowledge that can foster cross-cultural understanding in a world of increasing global interdependence and has implications for modeling cultural change.
1,895 citations
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TL;DR: It is shown that metformin, one of the most widely prescribed type 2 diabetes therapeutics, requires LKB1 in the liver to lower blood glucose levels, and TORC2 is a critical target of L KB1/AMPK signals in the regulation of gluconeogenesis.
Abstract: The Peutz-Jegher syndrome tumor-suppressor gene encodes a protein-threonine kinase, LKB1, which phosphorylates and activates AMPK [adenosine monophosphate (AMP)–activated protein kinase]. The deletion of LKB1 in the liver of adult mice resulted in a nearly complete loss of AMPK activity. Loss of LKB1 function resulted in hyperglycemia with increased gluconeogenic and lipogenic gene expression. In LKB1-deficient livers, TORC2, a transcriptional coactivator of CREB (cAMP response element–binding protein), was dephosphorylated and entered the nucleus, driving the expression of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which in turn drives gluconeogenesis. Adenoviral small hairpin RNA (shRNA) for TORC2 reduced PGC-1α expression and normalized blood glucose levels in mice with deleted liver LKB1, indicating that TORC2 is a critical target of LKB1/AMPK signals in the regulation of gluconeogenesis. Finally, we show that metformin, one of the most widely prescribed type 2 diabetes therapeutics, requires LKB1 in the liver to lower blood glucose levels.
1,850 citations
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TL;DR: Jeon et al. as discussed by the authors synthesize a fluorene-terminated hole-transporting material with a fine-tuned energy level and a high glass transition temperature to ensure highly efficient and thermally stable perovskite solar cells.
Abstract: Perovskite solar cells (PSCs) require both high efficiency and good long-term stability if they are to be commercialized. It is crucial to finely optimize the energy level matching between the perovskites and hole-transporting materials to achieve better performance. Here, we synthesize a fluorene-terminated hole-transporting material with a fine-tuned energy level and a high glass transition temperature to ensure highly efficient and thermally stable PSCs. We use this material to fabricate photovoltaic devices with 23.2% efficiency (under reverse scanning) with a steady-state efficiency of 22.85% for small-area (~0.094 cm2) cells and 21.7% efficiency (under reverse scanning) for large-area (~1 cm2) cells. We also achieve certified efficiencies of 22.6% (small-area cells, ~0.094 cm2) and 20.9% (large-area, ~1 cm2). The resultant device shows better thermal stability than the device with spiro-OMeTAD, maintaining almost 95% of its initial performance for more than 500 h after thermal annealing at 60 °C. Interfacial losses between device layers play a key role in determining characteristics of solar cells. Jeon et al. address this in perovskite solar cells by synthesizing a hole-transporting layer that is better matched to the surrounding layers, and show high-efficiency and high-stability devices.
1,771 citations
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TL;DR: In this paper, the recent progress in 2D materials beyond graphene and includes mainly transition metal dichalcogenides (TMDs) (e.g., MoS2, WS2, MoSe2, and WSe2).
1,728 citations
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Harvard University1, National Taiwan University2, Seoul National University3, Institut Gustave Roussy4, Emory University5, Sungkyunkwan University6, University of Ulsan7, Hebron University8, Vanderbilt University9, Carolinas Healthcare System10, Yonsei University11, AstraZeneca12, University of Manchester13
TL;DR: AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors.
Abstract: Background The EGFR T790M mutation is the most common mechanism of drug resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in patients who have lung cancer with an EGFR mutation (EGFR-mutated lung cancer). In preclinical models, the EGFR inhibitor AZD9291 has been shown to be effective against both EGFR tyrosine kinase inhibitor-sensitizing and T790M resistance mutations. Methods We administered AZD9291 at doses of 20 to 240 mg once daily in patients with advanced lung cancer who had radiologically documented disease progression after previous treatment with EGFR tyrosine kinase inhibitors. The study included dose-escalation cohorts and dose-expansion cohorts. In the expansion cohorts, prestudy tumor biopsies were required for central determination of EGFR T790M status. Patients were assessed for safety, pharmacokinetics, and efficacy. Results A total of 253 patients were treated. Among 31 patients enrolled in the dose-escalation cohorts, no dose-limiting toxic effects occurred at the doses evaluated. An additional 222 patients were treated in five expansion cohorts. The most common all-cause adverse events were diarrhea, rash, nausea, and decreased appetite. The overall objective tumor response rate was 51% (95% confidence interval [CI], 45 to 58). Among 127 patients with centrally confirmed EGFR T790M who could be evaluated for response, the response rate was 61% (95% CI, 52 to 70). In contrast, among 61 patients without centrally detectable EGFR T790M who could be evaluated for response, the response rate was 21% (95% CI, 12 to 34). The median progression-free survival was 9.6 months (95% CI, 8.3 to not reached) in EGFR T790M-positive patients and 2.8 months (95% CI, 2.1 to 4.3) in EGFR T790M-negative patients. Conclusions AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors. (Funded by AstraZeneca; ClinicalTrials.gov number, NCT01802632.).
1,722 citations
Authors
Showing all 28506 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Grätzel | 248 | 1423 | 303599 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Yongsun Kim | 156 | 2588 | 145619 |
David J. Mooney | 156 | 695 | 94172 |
Jongmin Lee | 150 | 2257 | 134772 |
Byung-Sik Hong | 146 | 1557 | 105696 |
Inkyu Park | 144 | 1767 | 109433 |
Y. Choi | 141 | 1631 | 98709 |
Kazunori Kataoka | 138 | 908 | 70412 |
E. J. Corey | 136 | 1377 | 84110 |
Pasi A. Jänne | 136 | 685 | 89488 |
Suyong Choi | 135 | 1495 | 97053 |
Intae Yu | 134 | 1372 | 89870 |
Tae Jeong Kim | 132 | 1420 | 93959 |
Anders Hagfeldt | 129 | 600 | 79912 |