Institution
Shanghai University
Education•Shanghai, Shanghai, China•
About: Shanghai University is a education organization based out in Shanghai, Shanghai, China. It is known for research contribution in the topics: Microstructure & Graphene. The organization has 59583 authors who have published 56840 publications receiving 753549 citations. The organization is also known as: Shànghǎi Dàxué.
Topics: Microstructure, Graphene, Nonlinear system, Catalysis, Thin film
Papers published on a yearly basis
Papers
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TL;DR: The GO-PseAA predictor is very promising for predicting protein-protein interactions from protein sequences, and might become a useful vehicle for studying the network biology in the postgenomic era.
Abstract: To understand the networks in living cells, it is indispensably important to identify protein−protein interactions on a genomic scale Unfortunately, it is both time-consuming and expensive to do so solely based on experiments due to the nature of the problem whose complexity is obviously overwhelming, just like the fact that “life is complicated” Therefore, developing computational techniques for predicting protein−protein interactions would be of significant value in this regard By fusing the approach based on the gene ontology and the approach of pseudo-amino acid composition, a predictor called “GO-PseAA” predictor was established to deal with this problem As a showcase, prediction was performed on 6323 protein pairs from yeast To avoid redundancy and homology bias, none of the protein pairs investigated has ≥40% sequence identity with any other The overall success rate obtained by jackknife cross-validation was 816%, indicating the GO-PseAA predictor is very promising for predicting protein−pro
151 citations
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TL;DR: Findings indicate that lymphangiogenesis and lymphatic drainage are reciprocally related to the severity of joint lesions during the development of chronic arthritis.
Abstract: Lymphatic vessels are present in almost all tissues of the body. They are composed of an extensive network of thin-walled capillaries that drain protein-rich lymph from extracellular spaces (1). Under normal conditions, the major functions of the lymphatic system include maintenance of tissue fluid homeostasis, absorption of fatty acids, and mediation of the afferent immune response (2, 3). Recent studies show increasing evidence that the lymphatic system also plays key roles in disease processes such as cancer metastasis, lymphedema, obesity, and inflammation (4, 5).
Lymphatic endothelial cell proliferation and lymphatic hyperplasia are reported in psoriatic skin lesions in humans and in chronic skin inflammation in mice (6). Kidney transplant rejection is frequently accompanied by enhanced lymphangiogenesis and production of lymphatic endothelial cell-derived chemokines in grafted tissues (7). Synovial specimens from patients with rheumatoid arthritis (RA) and osteoarthritis have an increased number of lymphatic vessels and increased expression of the lymphatic growth factor, vascular endothelial growth factor-C (VEGF-C) (8, 9). Furthermore, clinical reports have described larger lymph nodes (10) and increased lymphatic flow rates in lymphatic vessels draining arthritic joints in RA patients (11). Similarly, recent studies in animal models of RA demonstrated increased lymphatic vessel formation in inflamed joints and in draining popliteal lymph nodes (PLN) (12–14). These clinical and preclinical studies have demonstrated that inflammation stimulates proximal lymphangiogenesis in the joints and distal lymphangiogenesis in the draining lymph nodes. Thus, inflammation is the primary cause of lymphangiogenesis in arthritis. However, the effects of inflammation-induced lymphangiogenesis on joint inflammation in RA have yet to be determined.
VEGF-A- and VEGF-C-mediated signaling pathways are centrally involved in inflammatory lymphangiogenesis. VEGF-A signals through VEGF receptors (VEGFR)-1 and VEGFR-2. The effect of VEGF-A on lymphatics is mediated by VEGFR-2. Blockade of VEGF-A/VEGFR-2 interaction, using VEGFR-2 neutralizing antibody, reduces adjuvant-induced (15) and delayed-type hypersensitivity reaction-induced (16) lymphangiogenesis in lymph nodes. VEGF-C signals primarily through VEGFR-3 on lymphatic endothelial cells. VEGFR-3 blockade specifically inhibits the effects of VEGF-C, but not VEGF-A, on lymphatics. VEGFR-3 neutralizing antibody reduces bacterial infection associated-airway inflammation (17) and surgical blockade-induced lymphangiogenesis (18, 19). These studies have established a direct role for VEGF-C:VEGFR3 signaling in inflammation-induced lymphangiogenesis. However, most published studies have used acute inflammation models in which inflammation is triggered within hours to days. The effects of lymphangiogenesis on the natural course of chronic inflammation, such as that occurring in RA, have not been addressed. Specifically, it is not known how newly-generated lymphatic vessels affect drainage from inflamed joints, or if reduced lymphatics exacerbates inflammation. These questions are even more important in chronic inflammation where monocytes/macrophages are the major infiltrating cell type, given the fact that macrophages are the main source of VEGF-C in response to pro-inflammatory cytokines TNF and IL-1 (12, 20, 21)
In the current study, we used TNF transgenic (Tg) mice as a model of chronic inflammatory arthritis (22), and examined the effect of lymphatic inhibition by VEGFR-2 and VEGFR-3 neutralizing antibodies on lymphatic drainage and the severity of joint inflammation. Contrast enhancement (CE) MRI (13, 23) and indocyanine green-near infrared (ICG-NIR) in vivo imaging technologies were used to monitor the changes of synovial and PLN volumes during the 8-week treatment period. We found that VEGFR-3 neutralizing antibody significantly decreased joint and PLN lymphangiogenesis, lymphatic drainage from inflamed paws to PLNs, and the number of VEGF-C expressing CD11b+ myeloid cells in the PLNs. However, it significantly exacerbated joint inflammation. In contrast, VEGFR-2 neutralization inhibited both joint inflammation and lymphangiogenesis. These data indicate that inflammation-induced lymphangiogenesis is an important compensatory mechanism to limit joint inflammation during the course of chronic arthritis, and that improving lymphatic drainage represents a new potential therapeutic strategy for chronic inflammatory disorders.
151 citations
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TL;DR: In this paper, the authors investigated the role of export diversification, environment-related technological innovation, and fiscal decentralization in effectively achieving carbon neutrality target for 37 OECD economies from 1970 to 2019.
151 citations
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TL;DR: The lower the tampering rate, the more levels of content data are recovered, and the better the quality of restored results.
Abstract: This paper proposes two novel self-embedding watermarking schemes based upon a reference sharing mechanism, in which the watermark to be embedded is a reference derived from the original principal content in different regions and shared by these regions for content restoration. After identifying tampered blocks, both the reference data and the original content in the reserved area are used to recover the principal content in the tampered area. By using the first scheme, the original data in five most significant bit layers of a cover image can be recovered and the original watermarked image can also be retrieved when the content replacement is not too extensive. In the second scheme, the host content is decomposed into three levels, and the reference sharing methods with different restoration capabilities are employed to protect the data at different levels. Therefore, the lower the tampering rate, the more levels of content data are recovered, and the better the quality of restored results.
151 citations
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TL;DR: The powder and extracts of Psoralea corylifolia L. were tested in lard at 100 °C by using the oxidative stability instrument (OSI) and were found to have strong antioxidant effects as discussed by the authors.
151 citations
Authors
Showing all 59993 results
Name | H-index | Papers | Citations |
---|---|---|---|
Zhong Lin Wang | 245 | 2529 | 259003 |
Yang Yang | 171 | 2644 | 153049 |
Yang Liu | 129 | 2506 | 122380 |
Zhen Li | 127 | 1712 | 71351 |
Xin Wang | 121 | 1503 | 64930 |
Jian Liu | 117 | 2090 | 73156 |
Xin Li | 114 | 2778 | 71389 |
Wei Zhang | 112 | 1189 | 93641 |
Jianjun Liu | 112 | 1040 | 71032 |
Liquan Chen | 111 | 689 | 44229 |
Jin-Quan Yu | 111 | 438 | 43324 |
Jonathan L. Sessler | 111 | 997 | 48758 |
Peng Wang | 108 | 1672 | 54529 |
Qian Wang | 108 | 2148 | 65557 |
Wei Zhang | 104 | 2911 | 64923 |