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Cell Surface Sialylation Mediates the Binding of Enterovirus 71 to Host Cells
Pei-Yi Su,Yueh-Tung Liu,Chuan-Fa Chang 한국당과학회 2012 한국당과학회 학술대회 Vol.2012 No.1
Enterovirus 71 (EV71) is a major causative agent of hand-foot-and-mouth disease (HFMD). The clinical severity of EV71central nerve system (CNS) infection is mostly in children less than 5 years-old. Recently, the twoglycosylated membrane proteins SCARB2 and PSGL-1 have been identifiedas the cellular and functional receptors of EV71.But the role of glycosylation in EV71 infection remainsunclear. In this study, we demonstrated thatthe attachment of EV71 to two susceptible cell lines werediminished after the removal of cell surface sialic acids. Pre-incubatecells with sialic acid specific lectins, MAA and SNA,reducedthe binding of EV71. Additionally, we found that SCARB2 was a sialylated glycoprotein,andthe interaction of SCARB2and EV71was decreased after desialylation. Based on these results, we concluded that the attachment of EV71 to cell surface was assisted bysialic acids.Cell surface sialylation should be a key regulator that facilitates the binding and infection of EV71.
Yi-Chuan Hsieh,Su-Fen Cheng,Pei-Kwei Tsay,Wen-Jen Su,Yen-Hua Cho,Chi-Wen Chen 한국간호과학회 2017 Asian Nursing Research Vol.11 No.4
Purpose: This study aimed to evaluate the effects of cognitive-behavioral program on pain and medical fear in hospitalized school-aged children receiving intravenous (IV) placement. Methods: This study used an quasi-experimental design. Thirty-five participants were assigned to the experimental group and 33 to the control group in the acute internal medicine ward of a children's hospital. The cognitive-behavioral program entailed having the patients read an educational photo book about IV placement before the procedure and having them watch their favorite music video during the procedure. The outcome measures were numeric rating scales for pain intensity and fear during the procedure. Results: After applying the cognitive-behavioral program, the mean scores on pain and fear decreased in the experimental group. However, the difference in pain intensity between these two groups was nonsignificant. The intensity of fear in the experimental group was significantly lower than that in the control group. Conclusion: In this study, the cognitive-behavioral program used with school-aged hospitalized children promoted less fear during IV placement. The results of this study can serve as a reference for empirical nursing care and as care guidance for clinical IV injections involving children.
Yi-Chu Nie,Hao Wu,Pei-Bo Li,Yu-Long Luo,Kang Long,Li-Ming Xie,Jian-Gang Shen,Wei-Wei Su 한국식품영양과학회 2012 Journal of medicinal food Vol.15 No.10
Naringin, a well-known flavanone glycoside of grapefruit and citrus fruits, was found to be as an effective anti-inflammatory compound in our previous lipopolysaccharide-induced acute lung injury mouse model via blockading activity of nuclear factor κB. The current study sought to explore the anti-inflammatory effects of naringin on chronic pulmonary neutrophilic inflammation in cigarette smoke (CS)-induced rats. Seventy Sprague-Dawley rats were randomly divided into seven groups to study the effects of CS with or without various concentrations of naringin or saline for 8 weeks. The results revealed that naringin supplementation at 20, 40, and 80 mg/kg significantly increased body weight of CS-induced rats as compared to that in the CS group. Moreover, naringin of 20, 40, and 80 mg/kg prevented CS-induced infiltration of neutrophils and activation of myeloperoxidase and matrix metalloproteinase-9, in parallel with suppression of the release of cytokines, such as tumor necrosis factor-α and interleukin-8 (IL-8). IL-10 in bronchoalveolar lavage fluid was significantly suppressed after CS exposure, but dose dependently elevated by naringin. The results from hematoxylin and eosin staining revealed that naringin dose dependently reduced CS-induced infiltration of inflammatory cells, thickening of the bronchial wall, and expansion of average alveolar airspace. In conclusion, our data suggest that naringin is an effective anti-inflammatory compound for attenuating chronic pulmonary neutrophilic inflammation in CS-induced rats.
Hong Yi Kenneth Tan,Jong Dae Baek,Chen-Nan Sun,JUN WEI,이성혁,Pei-Chen Su 한국정밀공학회 2019 International Journal of Precision Engineering and Vol.6 No.2
A simple and effective technique to reduce the overall fuel cell polarization resistance was introduced on a conventionally sintered YSZ electrolyte by creating a hybrid microstructure using low-intensity CO2 laser scanning methods. After laser modification of the YSZ electrolyte surface on the cathode side, the overall polarization resistance was reduced from 513 to 124 Ω cm2, and the maximum power density was increased by 28% from 1.86 to 2.38 mW/cm2 at 450 °C. This improvement was due to the enhanced surface kinetics by higher grain boundary density on the YSZ surface from recrystallization after laser scanning.
Hsiao, Wen-Ting,Su, Hui-Min,Su, Kuan-Pin,Chen, Szu-Han,Wu, Hai-Ping,You, Yi-Ling,Fu, Ru-Huei,Chao, Pei-Min The Korean Nutrition Society 2019 Nutrition Research and Practice Vol.13 No.4
BACKGROUND/OBJECTIVES: Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the in vivo conversion of ${\alpha}$-linolenic acid. Many enzymes participating in LCPUFA synthesis are regulated by peroxisome proliferator-activated receptor alpha ($PPAR{\alpha}$). Therefore, it was hypothesized that the tissue accretion of endogenously synthesized DHA could be modified by $PPAR{\alpha}$. MATERIALS/METHODS: The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among $PPAR{\alpha}$ homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate ($PPAR{\alpha}$ agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. RESULTS: $PPAR{\alpha}$ ablation reduced the hepatic Acox, Fads1, and Fads2 mRNA levels, as well as the DHA concentration in the liver, but not in the brain cortex. In contrast, $PPAR{\alpha}$ activation increased hepatic Acox, Fads1, Fads2, and Elovl5 mRNA levels, but reduced the DHA concentrations in the liver, retina, and phospholipid of brain cortex, and decreased mRNA and protein levels of the brain-derived neurotrophic factor in brain cortex. CONCLUSIONS: LCPUFA enzyme expression was altered by $PPAR{\alpha}$. Either $PPAR{\alpha}$ deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance.
Wen-Ting Hsiao,Hui-Min Su,Kuan-Pin Su,Szu-Han Chen,Hai-Ping Wu,Yi-Ling You,Ru-Huei Fu,Pei-Min Chao 한국영양학회 2019 Nutrition Research and Practice Vol.13 No.4
BACKGROUND/OBJECTIVES: Docosahexaenoic acid (DHA), an n-3 long chain polyunsaturated fatty acid (LCPUFA), is acquired by dietary intake or the in vivo conversion of α-linolenic acid. Many enzymes participating in LCPUFA synthesis are regulated by peroxisome proliferator-activated receptor alpha (PPARα). Therefore, it was hypothesized that the tissue accretion of endogenously synthesized DHA could be modified by PPARα. MATERIALS/METHODS: The tissue DHA concentrations and mRNA levels of genes participating in DHA biosynthesis were compared among PPARα homozygous (KO), heterozygous (HZ), and wild type (WT) mice (Exp I), and between WT mice treated with clofibrate (PPARα agonist) or those not treated (Exp II). In ExpII, the expression levels of the proteins associated with DHA function in the brain cortex and retina were also measured. An n3-PUFA depleted/replenished regimen was applied to mitigate the confounding effects of maternal DHA. RESULTS: PPARα ablation reduced the hepatic Acox, Fads1, and Fads2 mRNA levels, as well as the DHA concentration in the liver, but not in the brain cortex. In contrast, PPARα activation increased hepatic Acox, Fads1, Fads2, and Elovl5 mRNA levels, but reduced the DHA concentrations in the liver, retina, and phospholipid of brain cortex, and decreased mRNA and protein levels of the brain-derived neurotrophic factor in brain cortex. CONCLUSIONS: LCPUFA enzyme expression was altered by PPARα. Either PPARα deficiency or activation-decreased tissue DHA concentration is a stimulus for further studies to determine the functional significance.
Chun-Yu Liu,Tzu-Ting Huang,Pei-Yi Chu,Chun-Teng Huang,Chia-Han Lee,Wan-Lun Wang,Ka-Yi Lau,Wen-Chun Tsai,Tzu-I Chao,Jung-Chen Su,Ming-Huang Chen,Chung-Wai Shiau,Ling-Ming Tseng,Kuen-Feng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.
Lee, Sang-Kyu,Song, Min-Young,Seo, Young-Su,Kim, Hye-Kyung,Ko, Seho,Cao, Pei-Jian,Suh, Jung-Pil,Yi, Gihwan,Roh, Jae-Hwan,Lee, Sichul,An, Gynheung,Hahn, Tae-Ryong,Wang, Guo-Liang,Ronald, Pamela,Jeon, J Genetics Society of America [etc.] 2009 Genetics Vol.181 No.4
<P>Rice blast, caused by the fungus Magnaporthe oryzae, is one of the most devastating diseases of rice. To understand the molecular basis of Pi5-mediated resistance to M. oryzae, we cloned the resistance (R) gene at this locus using a map-based cloning strategy. Genetic and phenotypic analyses of 2014 F2 progeny from a mapping population derived from a cross between IR50, a susceptible rice cultivar, and the RIL260 line carrying Pi5 enabled us to narrow down the Pi5 locus to a 130-kb interval. Sequence analysis of this genomic region identified two candidate genes, Pi5-1 and Pi5-2, which encode proteins carrying three motifs characteristic of R genes: an N-terminal coiled-coil (CC) motif, a nucleotide-binding (NB) domain, and a leucine-rich repeat (LRR) motif. In genetic transformation experiments of a susceptible rice cultivar, neither the Pi5-1 nor the Pi5-2 gene was found to confer resistance to M. oryzae. In contrast, transgenic rice plants expressing both of these genes, generated by crossing transgenic lines carrying each gene individually, conferred Pi5-mediated resistance to M. oryzae. Gene expression analysis revealed that Pi5-1 transcripts accumulate after pathogen challenge, whereas the Pi5-2 gene is constitutively expressed. These results indicate that the presence of these two genes is required for rice Pi5-mediated resistance to M. oryzae.</P>