Institution
Xiamen University
Education•Amoy, Fujian, China•
About: Xiamen University is a education organization based out in Amoy, Fujian, China. It is known for research contribution in the topics: Catalysis & Population. The organization has 50472 authors who have published 54480 publications receiving 1058239 citations. The organization is also known as: Amoy University & Xiàmén Dàxué.
Topics: Catalysis, Population, Graphene, Raman spectroscopy, Anode
Papers published on a yearly basis
Papers
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TL;DR: It is demonstrated that cationic surfactant plays critical roles in forming the hollow mesoporous structure and can be extended as a general strategy to transform silica-coated composite materials into yolk-shell structures with either wormhole-like or oriented mesoporus shell.
Abstract: Hollow mesoporous silica spheres have recently attracted increasing attention. However, effective synthesis of uniform hollow mesoporous spheres with controllable well-defined pore structures for fundamental research and practical applications has remained a significant challenge. In this work, a straightforward and effective “cationic surfactant assisted selective etching” synthetic strategy was developed for the preparation of high-quality hollow mesoporous silica spheres with either wormhole-like or oriented mesoporous shell. The as-prepared hollow mesoporous silica spheres have large surface area, high pore volume, and controllable structure parameters. Our experiments demonstrated that cationic surfactant plays critical roles in forming the hollow mesoporous structure. A formation mechanism involving the etching of solid SiO2 accelerated by cationic surfactant followed by the redeposition of dissolved silica species directed by cationic surfactant is proposed. Furthermore, the strategy can be extended as a general strategy to transform silica-coated composite materials into yolk-shell structures with either wormhole-like or oriented mesoporous shell.
298 citations
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TL;DR: In this paper, a uniform and TiO2 nanoparticle coating on steels has been prepared using sol-gel method and hydrothermal post-treatments, and the morphology and structure of the coatings were analysed using atomic force microscopy and X-ray diffraction.
297 citations
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TL;DR: These findings identify a clinically actionable, epigenetic cause of cetuximab resistance, and describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby Gata6 represses MIR 100HG, but this repression is relieved by miR-125b targeting of GATA 6.
Abstract: De novo and acquired resistance, which are largely attributed to genetic alterations, are barriers to effective anti-epidermal-growth-factor-receptor (EGFR) therapy. To generate cetuximab-resistant cells, we exposed cetuximab-sensitive colorectal cancer cells to cetuximab in three-dimensional culture. Using whole-exome sequencing and transcriptional profiling, we found that the long non-coding RNA MIR100HG and two embedded microRNAs, miR-100 and miR-125b, were overexpressed in the absence of known genetic events linked to cetuximab resistance. MIR100HG, miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/β-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6. These findings identify a clinically actionable, epigenetic cause of cetuximab resistance.
297 citations
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Royal College of Surgeons in Ireland1, University of Southern California2, University College London3, UCL Institute of Neurology4, Université libre de Bruxelles5, Montreal Neurological Institute and Hospital6, State University of Campinas7, University of Eastern Finland8, University of Florence9, St. George's University10, New York University11, National Research Council12, King's College London13, Ohio State University14, Xiamen University15, Greifswald University Hospital16, Cardiff University17, University of Erlangen-Nuremberg18, University of Liverpool19, University of Tübingen20, Florey Institute of Neuroscience and Mental Health21, University of California, San Diego22, Boston Children's Hospital23, National Autonomous University of Mexico24, University of Bern25, Istituto Giannina Gaslini26, University Hospital of Wales27, University of Modena and Reggio Emilia28, Royal Melbourne Hospital29, University of Melbourne30, University of Marburg31, University Hospital Bonn32, University of Maryland, Baltimore County33, Medical College of Wisconsin34, Beaumont Hospital35, University of Maryland, Baltimore36, University of Cambridge37, University of Genoa38, Mario Negri Institute for Pharmacological Research39
TL;DR: In the largest neuroimaging study to date, Whelan and colleagues report robust structural alterations across and within epilepsy syndromes, including shared volume loss in the thalamus, and widespread cortical thickness differences.
Abstract: Progressive functional decline in the epilepsies is largely unexplained. We formed the ENIGMA-Epilepsy consortium to understand factors that influence brain measures in epilepsy, pooling data from 24 research centres in 14 countries across Europe, North and South America, Asia, and Australia. Structural brain measures were extracted from MRI brain scans across 2149 individuals with epilepsy, divided into four epilepsy subgroups including idiopathic generalized epilepsies (n =367), mesial temporal lobe epilepsies with hippocampal sclerosis (MTLE; left, n = 415; right, n = 339), and all other epilepsies in aggregate (n = 1026), and compared to 1727 matched healthy controls. We ranked brain structures in order of greatest differences between patients and controls, by meta-analysing effect sizes across 16 subcortical and 68 cortical brain regions. We also tested effects of duration of disease, age at onset, and age-by-diagnosis interactions on structural measures. We observed widespread patterns of altered subcortical volume and reduced cortical grey matter thickness. Compared to controls, all epilepsy groups showed lower volume in the right thalamus (Cohen's d = -0.24 to -0.73; P < 1.49 × 10-4), and lower thickness in the precentral gyri bilaterally (d = -0.34 to -0.52; P < 4.31 × 10-6). Both MTLE subgroups showed profound volume reduction in the ipsilateral hippocampus (d = -1.73 to -1.91, P < 1.4 × 10-19), and lower thickness in extrahippocampal cortical regions, including the precentral and paracentral gyri, compared to controls (d = -0.36 to -0.52; P < 1.49 × 10-4). Thickness differences of the ipsilateral temporopolar, parahippocampal, entorhinal, and fusiform gyri, contralateral pars triangularis, and bilateral precuneus, superior frontal and caudal middle frontal gyri were observed in left, but not right, MTLE (d = -0.29 to -0.54; P < 1.49 × 10-4). Contrastingly, thickness differences of the ipsilateral pars opercularis, and contralateral transverse temporal gyrus, were observed in right, but not left, MTLE (d = -0.27 to -0.51; P < 1.49 × 10-4). Lower subcortical volume and cortical thickness associated with a longer duration of epilepsy in the all-epilepsies, all-other-epilepsies, and right MTLE groups (beta, b < -0.0018; P < 1.49 × 10-4). In the largest neuroimaging study of epilepsy to date, we provide information on the common epilepsies that could not be realistically acquired in any other way. Our study provides a robust ranking of brain measures that can be further targeted for study in genetic and neuropathological studies. This worldwide initiative identifies patterns of shared grey matter reduction across epilepsy syndromes, and distinctive abnormalities between epilepsy syndromes, which inform our understanding of epilepsy as a network disorder, and indicate that certain epilepsy syndromes involve more widespread structural compromise than previously assumed.
296 citations
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TL;DR: The idea of the importance of mounting an inflammatory response for effective immunity is supported by a multiplicity of experimental data and it is also well understood that resolution of inflammation is essential for maintaining the balance between health and disease as mentioned in this paper.
Abstract: The idea of the importance of mounting an inflammatory response for effective immunity is supported by a multiplicity of experimental data. It is also well understood that resolution of inflammation is essential for maintaining the balance between health and disease. When the normal regulatory mechanisms are disturbed, the potential for developing chronic inflammatory diseases is increased. Inflammation is a key element in the response of the innate immune system to a variety of challenges, including those provided by bacterial and viral infection as well as by damaged or dying host cells. Here we review elements of innate immunity that lead to inflammation and some of the host mechanisms that allow for the resolution of the inflammatory responses.
296 citations
Authors
Showing all 50945 results
Name | H-index | Papers | Citations |
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Zhong Lin Wang | 245 | 2529 | 259003 |
Lei Jiang | 170 | 2244 | 135205 |
Yang Gao | 168 | 2047 | 146301 |
William A. Goddard | 151 | 1653 | 123322 |
Rui Zhang | 151 | 2625 | 107917 |
Xiaoyuan Chen | 149 | 994 | 89870 |
Fuqiang Wang | 145 | 1518 | 95014 |
Galen D. Stucky | 144 | 958 | 101796 |
Shu-Hong Yu | 144 | 799 | 70853 |
Wei Huang | 139 | 2417 | 93522 |
Bin Liu | 138 | 2181 | 87085 |
Jie Liu | 131 | 1531 | 68891 |
Han Zhang | 130 | 970 | 58863 |
Lei Zhang | 130 | 2312 | 86950 |
Jian Zhou | 128 | 3007 | 91402 |