Institution
Katholieke Universiteit Leuven
Education•Leuven, Belgium•
About: Katholieke Universiteit Leuven is a education organization based out in Leuven, Belgium. It is known for research contribution in the topics: Population & Transplantation. The organization has 61109 authors who have published 176584 publications receiving 6210872 citations.
Topics: Population, Transplantation, CMOS, European union, Stars
Papers published on a yearly basis
Papers
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TL;DR: In this article, the energy distribution of electron states at SiC/SiO 2 interfaces produced by oxidation of various (3C, 4H, 6H) SiC polytypes is studied by electrical analysis techniques and internal photoemission spectroscopy.
Abstract: The energy distribution of electron states at SiC/SiO 2 interfaces produced by oxidation of various (3C, 4H, 6H) SiC polytypes is studied by electrical analysis techniques and internal photoemission spectroscopy. A similar distribution of interface traps over the SiC bandgap is observed for different polytypes indicating a common nature of interfacial defects. Carbon clusters at the SiC/SiO 2 interface and near-interfacial defects in the SiO 2 are proposed to be responsible for the dominant portion of interface traps, while contributions caused by dopant-related defects and dangling bonds at the SiC surface are not observed.
631 citations
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TL;DR: All the fragments are rather resistant to heat‐induced denaturation, and display high conformational stabilities, which has never been reported for any functional conventional antibody fragment, even when engineered antigen binders are considered.
Abstract: A variety of techniques, including high-pressure unfolding monitored by Fourier transform infrared spectroscopy, fluorescence, circular dichroism, and surface plasmon resonance spectroscopy, have been used to investigate the equilibrium folding properties of six single-domain antigen binders derived from camelid heavy-chain antibodies with specificities for lysozymes, β-lactamases, and a dye (RR6). Various denaturing conditions (guanidinium chloride, urea, temperature, and pressure) provided complementary and independent methods for characterizing the stability and unfolding properties of the antibody fragments. With all binders, complete recovery of the biological activity after renaturation demonstrates that chemical-induced unfolding is fully reversible. Furthermore, denaturation experiments followed by optical spectroscopic methods and affinity measurements indicate that the antibody fragments are unfolded cooperatively in a single transition. Thus, unfolding/refolding equilibrium proceeds via a simple two-state mechanism (N⇋U), where only the native and the denatured states are significantly populated. Thermally-induced denaturation, however, is not completely reversible, and the partial loss of binding capacity might be due, at least in part, to incorrect refolding of the long loops (CDRs), which are responsible for antigen recognition. Most interestingly, all the fragments are rather resistant to heat-induced denaturation (apparent Tm = 60–80°C), and display high conformational stabilities (ΔG(H2O) = 30–60 kJ mole−1). Such high thermodynamic stability has never been reported for any functional conventional antibody fragment, even when engineered antigen binders are considered. Hence, the reduced size, improved solubility, and higher stability of the camelid heavy-chain antibody fragments are of special interest for biotechnological and medical applications.
631 citations
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TL;DR: The guidelines described herein may be helpful in the appropriate management of FAP families and, in order to improve the care of these families further, prospective controlled studies should be undertaken.
Abstract: BACKGROUND: Familial adenomatous polyposis (FAP) is a well-described inherited syndrome, which is responsible for <1% of all colorectal cancer (CRC) cases. The syndrome is characterised by the development of hundreds to thousands of adenomas in the colorectum. Almost all patients will develop CRC if they are not identified and treated at an early stage. The syndrome is inherited as an autosomal dominant trait and caused by mutations in the APC gene. Recently, a second gene has been identified that also gives rise to colonic adenomatous polyposis, although the phenotype is less severe than typical FAP. The gene is the MUTYH gene and the inheritance is autosomal recessive. In April 2006 and February 2007, a workshop was organised in Mallorca by European experts on hereditary gastrointestinal cancer aiming to establish guidelines for the clinical management of FAP and to initiate collaborative studies. Thirty-one experts from nine European countries participated in these workshops. Prior to the meeting, various participants examined the most important management issues according to the latest publications. A systematic literature search using Pubmed and reference lists of retrieved articles, and manual searches of relevant articles, was performed. During the workshop, all recommendations were discussed in detail. Because most of the studies that form the basis for the recommendations were descriptive and/or retrospective in nature, many of them were based on expert opinion. The guidelines described herein may be helpful in the appropriate management of FAP families. In order to improve the care of these families further, prospective controlled studies should be undertaken.
631 citations
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Bernhard Nocht Institute for Tropical Medicine1, Public Health England2, World Health Organization3, Icahn School of Medicine at Mount Sinai4, University of North Carolina at Chapel Hill5, European Medicines Agency6, Peking Union Medical College7, Katholieke Universiteit Leuven8, National Institutes of Health9, University of Alabama at Birmingham10, University of Pittsburgh11, University of Saskatchewan12, University of Maryland, Baltimore13, Erasmus University Medical Center14, Center for Biologics Evaluation and Research15, Université Paris-Saclay16, Wageningen University and Research Centre17, Columbia University18, University of California, San Diego19, University of Texas Medical Branch20, Autonomous University of Barcelona21, Friedrich Loeffler Institute22, Li Ka Shing Faculty of Medicine, University of Hong Kong23, University of Iowa24, Kansas State University25, Tulane University26, Geelong Football Club27, University of York28, Beth Israel Deaconess Medical Center29
TL;DR: The findings of a World Health Organization expert working group that is developing animal models to test vaccines and therapeutic agents for the treatment of COVID-19, and their relevance for preclinical testing, are reviewed.
Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the aetiological agent of coronavirus disease 2019 (COVID-19), an emerging respiratory infection caused by the introduction of a novel coronavirus into humans late in 2019 (first detected in Hubei province, China). As of 18 September 2020, SARS-CoV-2 has spread to 215 countries, has infected more than 30 million people and has caused more than 950,000 deaths. As humans do not have pre-existing immunity to SARS-CoV-2, there is an urgent need to develop therapeutic agents and vaccines to mitigate the current pandemic and to prevent the re-emergence of COVID-19. In February 2020, the World Health Organization (WHO) assembled an international panel to develop animal models for COVID-19 to accelerate the testing of vaccines and therapeutic agents. Here we summarize the findings to date and provides relevant information for preclinical testing of vaccine candidates and therapeutic agents for COVID-19.
630 citations
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TL;DR: TRPV4 is a functional temperature-sensing channel in native endothelium, that is likely involved in temperature-dependent Ca2+ signaling, and the failure to activate TRPV 4 channels by heat in inside-out patches, which responded to 4αPDD, may indicate that heat activation depends on the presence of an endogenous ligand, which is missing in inside/out patches.
630 citations
Authors
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Name | H-index | Papers | Citations |
---|---|---|---|
Eugene Braunwald | 230 | 1711 | 264576 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Stefan Schreiber | 178 | 1233 | 138528 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Jun Wang | 166 | 1093 | 141621 |
David R. Jacobs | 165 | 1262 | 113892 |
Klaus Müllen | 164 | 2125 | 140748 |
Peter Carmeliet | 164 | 844 | 122918 |
Hua Zhang | 163 | 1503 | 116769 |
William J. Sandborn | 162 | 1317 | 108564 |
Elliott M. Antman | 161 | 716 | 179462 |
Tobin J. Marks | 159 | 1621 | 111604 |
Ian A. Wilson | 158 | 971 | 98221 |
Johan Auwerx | 158 | 653 | 95779 |