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
More filters
••
TL;DR: Although no significant difference in progression-free survival was noted between groups, the addition of erlotinib to gemcitabine and oxaliplatin showed antitumour activity and might be a treatment option for patients with cholangiocarcinoma.
Abstract: Summary Background Combination chemotherapy with gemcitabine and a platinum-based agent is regarded as a standard treatment for patients with advanced biliary-tract cancer. Results of phase 2 trials of single-agent erlotinib in biliary-tract cancer and of gemcitabine plus erlotinib in pancreatic cancer have shown modest benefits. Therefore, we aimed to investigate the efficacy of gemcitabine and oxaliplatin plus erlotinib versus chemotherapy alone for advanced biliary-tract cancer. Methods In this open label, randomised, phase 3 trial, we randomly assigned patients (in a 1:1 ratio) with metastatic biliary-tract cancer (cholangiocarcinoma, gallbladder cancer, or ampulla of Vater cancer) to receive either first-line treatment with chemotherapy alone (gemcitabine 1000 mg/m 2 on day 1 and oxaliplatin 100 mg/m 2 on day 2) or chemotherapy plus erlotinib (100 mg daily). Treatment was repeated every 2 weeks until disease progression or unacceptable toxic effects. Randomisation was done centrally (stratified by participating centre and presence of measurable lesion). The primary endpoint was progression-free survival. Analyses were by intention-to-treat. This study is registered with ClinicalTrials.gov, number NCT01149122. Findings 133 patients were randomly assigned to the chemotherapy alone group and 135 to the chemotherapy plus erlotinib group. The groups were balanced except for a higher proportion of patients with cholangiocarcinoma in the group given erlotinib than in the chemotherapy alone group (96 [71%] patients vs 84 [63%]). Median progression-free survival was 4·2 months (95% CI 2·7–5·7) in the chemotherapy alone group and 5·8 months (95% CI 4·6–7·0) in the chemotherapy plus erlotinib group (hazard ratio [HR] 0·80, 95% CI 0·61–1·03; p=0·087). Significantly more patients had an objective response in the chemotherapy plus erlotinib group than in the chemotherapy alone group (40 patients vs 21 patients; p=0·005), but median overall survival was the same in both groups (9·5 months [95% CI 7·5–11·5] in the chemotherapy alone group and 9·5 months [7·6–11·4] in the chemotherapy plus erlotinib group; HR 0·93, 0·69–1·25; p=0·611). All-cause deaths within 30 days of random assignment occurred in one (1%) of the patients in the chemotherapy alone group and in four (3%) of those in the chemotherapy plus erlotinib group. The most common grade 3–4 adverse event was febrile neutropenia (eight [6%] patients in the chemotherapy alone group and six [4%] in the chemotherapy plus erlotinib group). No patient died of treatment-related causes during the study. Subgroup analyses by primary site of disease showed that for patients with cholangiocarcinoma, the addition of erlotinib to chemotherapy significantly prolonged median progression-free survival (5·9 months [95% CI 4·7–7·1] for chemotherapy plus erlotinib vs 3·0 months [1·1–4·9] for chemotherapy alone; HR 0·73, 95% CI 0·53–1·00; p=0·049). Interpretation Although no significant difference in progression-free survival was noted between groups, the addition of erlotinib to gemcitabine and oxaliplatin showed antitumour activity and might be a treatment option for patients with cholangiocarcinoma. Funding None.
401 citations
••
TL;DR: The demonstrated strain-modulation of the phase transition temperature is expected to be compatible with other T MDs enabling the 2D electronics utilizing polymorphism of TMDs along with the established materials.
Abstract: We demonstrate a room temperature semiconductor–metal transition in thin film MoTe2 engineered by strain. Reduction of the 2H-1T′ phase transition temperature of MoTe2 to room temperature was realized by introducing a tensile strain of 0.2%. The observed first-order SM transition improved conductance ∼10 000 times and was made possible by an unusually large temperature-stress coefficient, which results from a large volume change and small latent heat. The demonstrated strain-modulation of the phase transition temperature is expected to be compatible with other TMDs enabling the 2D electronics utilizing polymorphism of TMDs along with the established materials.
400 citations
••
400 citations
••
Cornell University1, Harvard University2, The Chinese University of Hong Kong3, Sarah Cannon Research Institute4, University of California, San Francisco5, University of Bern6, Institut Gustave Roussy7, Yonsei University8, Ben-Gurion University of the Negev9, University of North Carolina at Chapel Hill10, Seoul National University11, Japanese Foundation for Cancer Research12, Sungkyunkwan University13, University of Chicago14, Tottori University15, Ohio State University16, University of California, San Diego17, New York University18, Okayama University19, University of Milan20, City of Hope National Medical Center21, Roswell Park Cancer Institute22, University of Cologne23, Peter MacCallum Cancer Centre24, University of Texas MD Anderson Cancer Center25
TL;DR: Selpercatinib had durable efficacy, including intracranial activity, with mainly low-grade toxic effects in patients with RET fusion-positive NSCLC who had previously received platinum-based chemotherapy and those who were previously untreated.
Abstract: Background RET fusions are oncogenic drivers in 1 to 2% of non–small-cell lung cancers (NSCLCs). In patients with RET fusion–positive NSCLC, the efficacy and safety of selective RET inhibi...
400 citations
••
TL;DR: Evidence is provided that the NLRP1 and NLRP3 inflammasomes have a major role in neuronal cell death and behavioral deficits in stroke, and that IVIg treatment can protect brain cells against ischemic damage, suggesting a potential clinical benefit of therapeutic interventions that targetinflammasome assembly and activity.
Abstract: Multi-protein complexes called inflammasomes have recently been identified and shown to contribute to cell death in tissue injury. Intravenous immunoglobulin (IVIg) is an FDA-approved therapeutic modality used for various inflammatory diseases. The objective of this study is to investigate dynamic responses of the NLRP1 and NLRP3 inflammasomes in stroke and to determine whether the NLRP1 and NLRP3 inflammasomes can be targeted with IVIg for therapeutic intervention. Primary cortical neurons were subjected to glucose deprivation (GD), oxygen–glucose deprivation (OGD) or simulated ischemia-reperfusion (I/R). Ischemic stroke was induced in C57BL/6J mice by middle cerebral artery occlusion, followed by reperfusion. Neurological assessment was performed, brain tissue damage was quantified, and NLRP1 and NLRP3 inflammasome protein levels were evaluated. NLRP1 and NLRP3 inflammasome components were also analyzed in postmortem brain tissue samples from stroke patients. Ischemia-like conditions increased the levels of NLRP1 and NLRP3 inflammasome proteins, and IL-1β and IL-18, in primary cortical neurons. Similarly, levels of NLRP1 and NLRP3 inflammasome proteins, IL-1β and IL-18 were elevated in ipsilateral brain tissues of cerebral I/R mice and stroke patients. Caspase-1 inhibitor treatment protected cultured cortical neurons and brain cells in vivo in experimental stroke models. IVIg treatment protected neurons in experimental stroke models by a mechanism involving suppression of NLRP1 and NLRP3 inflammasome activity. Our findings provide evidence that the NLRP1 and NLRP3 inflammasomes have a major role in neuronal cell death and behavioral deficits in stroke. We also identified NLRP1 and NLRP3 inflammasome inhibition as a novel mechanism by which IVIg can protect brain cells against ischemic damage, suggesting a potential clinical benefit of therapeutic interventions that target inflammasome assembly and activity.
399 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 |