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Institution

Fu Jen Catholic University

EducationTaipei, Taiwan
About: Fu Jen Catholic University is a education organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Medicine. The organization has 6842 authors who have published 9512 publications receiving 171005 citations. The organization is also known as: FJU & Fu Jen.
Topics: Population, Medicine, Cancer, Hazard ratio, Apoptosis


Papers
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Journal ArticleDOI
TL;DR: A simple and efficient authentication scheme for mobile satellite communication systems that is only based on hash functions and exclusive‐OR operations and has a lower computation cost.
Abstract: SUMMARY In this article, the authors shall propose a simple and efficient authentication scheme for mobile satellite communication systems. The proposed scheme can achieve the following security requirements: (S1) withstand impersonation attacks; (S2) withstand denial server attacks; (S3) withstand smart card loss attacks; (S4) withstand replay attacks; and (S5) withstand stolen-verifier attacks, and achieve the following functionality requirements: (F1) freely choose identity; (F2) provide mutual authentication; (F3) provide session key agreement; (F4) provide user anonymity; and (F5) provide perfect forward secrecy. In additional, the proposed scheme does not use the high complex computation, such as public key cryptosystem or secret key cryptosystem, for the mobile users' side. The proposed scheme is only based on hash functions and exclusive-OR operations. Compared with other schemes, the proposed scheme has a lower computation cost. It is more simple and efficient scheme. Copyright © 2011 John Wiley & Sons, Ltd.

52 citations

Journal ArticleDOI
TL;DR: There were differences between AF and AFL in comorbidities and prognosis with regard to ischemic stroke, heart failure hospitalization, and all‐cause mortality.
Abstract: BackgroundAtrial flutter (AFL) has been identified to be equivalent to atrial fibrillation (AF) in terms of preventing ischemic stroke, although differences exist in atrial rate, substrate, and ele...

52 citations

Journal ArticleDOI
TL;DR: It is suggested that increased levels of IL-6 and IL-33 in the serum of mice with BLM-induced lung injury may cause lung fibrosis with thickened interstitial lung tissue accompanied by reduced lung function and muscle mass through the activation of STAT3 and AMPK signals.
Abstract: Weight loss due to skeletal muscle atrophy in patients with chronic pulmonary disease is negatively correlated with clinical outcome. Pulmonary fibrosis is a chronic and progressive interstitial lung disease characterized by the dysregulated deposition of the extracellular matrix (ECM) with the destruction of normal tissue, resulting in end-stage organ failure. BLM-induced fibrosis is one of several different experimental models of pulmonary fibrosis, characterized by inflammation and excessive ECM deposition. We directly induced mouse lung injury by the intratracheal administration of bleomycin and monitored the physiological and biochemical changes in lung and skeletal muscle tissues by using lung function testing, ELISA, Western blotting, and immunohistochemistry. Here, we found that BLM-induced lung fibrosis with thickened interstitial lung tissue, including fibronectin and collagen, was correlated with the increased serum concentrations of IL-6 and IL-33 and accompanied by reduced lung function, including FRC (functional residual capacity), C chord (lung compliance), IC (inspiratory capacity), VC (vital capacity), TLC (total lung capacity), and FVC (forced vital capacity) (p < 0.05). The activity of AKT in lung tissue was suppressed, but conversely, the activity of STAT3 was enhanced during lung fibrosis in mice. In addition, we found that the amount of sST2, the soluble form of the IL-33 receptor, was dramatically decreased in lung fibrosis tissues. The skeletal muscle tissue isolated from lung injury mice increased the activation of STAT3 and AMPK, accompanied by an increased amount of Atrogin-1 protein in BLM-induced lung fibrosis mice. The mouse myoblast cell-based model showed that IL-6 and IL-33 specifically activated STAT3 and AMPK signaling, respectively, to induce the expression of the muscle-specific proteolysis markers MuRF1 and Atrogin-1. These data suggested that increased levels of IL-6 and IL-33 in the serum of mice with BLM-induced lung injury may cause lung fibrosis with thickened interstitial lung tissue accompanied by reduced lung function and muscle mass through the activation of STAT3 and AMPK signals.

52 citations

Journal ArticleDOI
TL;DR: The data suggest that the transcriptional dysregulation in FOXO1 is possibly linked to the pathogenesis of SLE and RA.
Abstract: FOXO forkhead transcription factors play an important role in controlling lymphocyte activation and proliferation. To evaluate the possibility that FOXO transcriptional expression is dysregulated in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients, we determined the quantities of FOXO1, FOXO3a, and FOXO4 transcripts in peripheral blood mononuclear cells (PBMCs) from normal controls as well as from SLE and RA patients. Results showed that FOXO1 and FOXO3a are dominant FOXO factors at the transcript level in PBMCs. Statistical analysis showed that the FOXO1 transcript levels in RA patients and in SLE patients with active disease activity were significantly lower than those in normal controls, and the FOXO1 transcript levels were inversely correlated with lupus disease activity. In contrast, the differences in FOXO3a and FOXO4 transcript levels between normal controls and patients were not significant. These data suggest that the transcriptional dysregulation in FOXO1 is possibly linked to the pathogenesis of SLE and RA.

52 citations

Journal ArticleDOI
10 Aug 2010-Planta
TL;DR: It is shown that SlERF3ΔRD protein retains the character of a transcription factor and becomes a GCC-mediated transcriptional activator and may find important use in crop improvement or genetic engineering to increase stress tolerance in plants.
Abstract: Ethylene-responsive transcription factors (ERFs) bind specifically to cis-acting DNA regulatory elements such as GCC boxes and play an important role in the regulation of defense- and stress-related genes in plants. In contrast to other ERFs, class II ERFs contain an ERF-associated amphiphilic repression (EAR) domain and act as GCC-mediated transcriptional repressors. In this study, SlERF3, a class II ERF was isolated from tomato and characterized. To examine whether the EAR motif of class II ERF proteins participates in ERF-mediated functions in plants, the EAR domain was deleted to generate SlERF3ΔRD. We show that SlERF3ΔRD protein retains the character of a transcription factor and becomes a GCC-mediated transcriptional activator. Constitutive expression of full-length SlERF3 in tomato severely suppressed growth and, as a result, no transgenic plants were obtained. However, no apparent effects on growth and development of SlERF3ΔRD transgenic plants were observed. Overexpression of SlERF3ΔRD in transgenic tomato induced expression of pathogenesis-related protein genes such as PR1, PR2 and PR5, and enhanced tolerance to Ralstonia solanacearum. Furthermore, transgenic Arabidopsis and tomatoes constitutively expressing SlERF3ΔRD exhibited reduced levels of membrane lipid peroxidation and enhanced tolerance to salt stress. In comparison with wild-type plants grown under stress conditions, transgenic SlERF3ΔRD tomatoes produced more flowers, fruits, and seeds. This study illustrates a gene-enhancing tolerance to both biotic and abiotic stresses in transgenic plants with the deletion of a repressor domain. Our findings suggest that class II ERF proteins may find important use in crop improvement or genetic engineering to increase stress tolerance in plants.

52 citations


Authors

Showing all 6861 results

NameH-indexPapersCitations
P. Chang1702154151783
Christian Guilleminault13389768844
Pan-Chyr Yang10278646731
Po-Ren Hsueh92103038811
Shyi-Ming Chen9042522172
Peter J. Rossky7428021183
Chong-Jen Yu7257722940
Shuu Jiun Wang7150224800
Jaw-Town Lin6743415482
Lung Chi Chen6326713929
Ronald E. Taam5929012383
Jiann T. Lin5819010801
Yueh-Hsiung Kuo5761812204
San Lin You5517816572
Liang-Gee Chen5458212073
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202313
202233
2021726
2020666
2019571
2018528