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Yi-Hsin Lien,Jhaol-Huei Wu,Jiunn-Wang Liao,Tzong-Ming Wu 한국고분자학회 2013 Macromolecular Research Vol.21 No.5
Thermosensitive and magnetic nanoparticles as “smart” drug carriers have shown great potential in the field of controlled drug delivery owing to their unique properties. Previously, poly(N-isopropylacrylamide)-coated silica/magnetic nanoparticles (PNIPAM/SiO2/Fe3O4 nanoparticles) were synthesized using SiO2-coated Fe3O4 nanoparticles as a template. The properties of these nanoparticles such as the transition of the lower critical solution temperature (LCST), biocompatibility, drug loading efficiency, and drug release kinetics were investigated in vitro for both targeted and controlled drug delivery. The release profile and the in vitro cancer cell inhibition activity of vitamin D3 loading for PNIPAM/SiO2/Fe3O4 nanoparticles were systemically studied. The loading and release behavior of vitamin D3 were found to be dependent on the LCST of PNIPAM/SiO2/Fe3O4 nanoparticles. HepG2 liver cancer cells were incubated with PNIPAM/SiO2/Fe3O4 nanoparticles loaded with vitamin D3 for 5 days, and cell viability significantly decreased, as observed by 3-(4,5-cimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays, which was further confirmed by transmission electron microscopy (TEM)images. In conclusion, the current study demonstrated that PNIPAM/SiO2/Fe3O4 nanoparticles can be used as potential drug delivery systems for controlled release.
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Nai-Yun Chang,Zeng-Weng Chen,Ter-Hsin Chen,Jiunn-Wang Liao,Cheng-Chung Lin,Maw-Sheng Chien,Wei-Cheng Lee,Jiunn-Horng Lin,Shih-Ling Hsuan 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.1
Exotoxins produced by Actinobacillus (A.) pleuropneumoniae(Apx) play major roles in the pathogenesis of pleuropneumoniain swine. This study investigated the role of ApxI in hemolysisand cellular damage using a novel apxIA mutant, ApxIA336,which was developed from the parental strain A. pleuropneumoniae serotype 10 that produces only ApxI in vitro. The genotype of ApxIA336 was confirmed by PCR, Southernblotting, and gene sequencing. Exotoxin preparation derivedfrom ApxIA336 was analyzed for its bioactivity towardsporcine erythrocytes and alveolar macrophages. Analysisresults indicated that ApxIA336 contained a kanamycinresistantcassette inserted immediately after 1005 bp of theapxIA gene. Phenotype analysis of ApxIA336 revealed nodifference in the growth rate as compared to the parentalstrain. Meanwhile, ApxI production was abolished in thebacterial culture supernatant, i.e. exotoxin preparation. Theinability of ApxIA336 to produce ApxI corresponded to the lossof hemolytic and cytotoxic bioactivity in exotoxin preparation,as demonstrated by hemolysis, lactate dehydrogenase release,mitochondrial activity, and apoptosis assays. Additionally, thevirulence of ApxIA336 appeared to be attenuated by 15-fold inBALB/c mice. Collectively, ApxI, but not other components inthe exotoxin preparation of A. pleuropneumoniae serotype 10,was responsible for the hemolytic and cytotoxic effects onporcine erythrocytes and alveolar macrophages.
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Yi-Chih Chang,Hao-Ping Liu,Hsiao-Li Chuang,Jiunn-Wang Liao,Pei-Ling Kao,Hsun-Lung Chan,Ter-Hsin Chen,Yu-Chih Wang 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.4
Background: Feline mammary carcinoma (FMC) is one of the most prevalent malignancies of female cats. FMC is highly metastatic and thus leads to poor disease outcomes. Among all metastases, liver metastasis occurs in about 25% of FMC patients. However, the mechanism underlying hepatic metastasis of FMC remains largely uncharacterized. Results: Herein, we demonstrate that FMC-derived extracellular vesicles (FMC-EVs) promotes the liver metastasis of FMC by activating hepatic stellate cells (HSCs) to prime a hepatic premetastatic niche (PMN). Moreover, we provide evidence that sphingosine kinase 1 (SK1) delivered by FMC-EV was pivotal for the activation of HSC and the formation of hepatic PMN. Depletion of SK1 impaired cargo sorting in FMC-EV and the EV-potentiated HSC activation, and abolished hepatic colonization of FMC cells. Conclusions: Taken together, our findings uncover a previously uncharacterized mechanism underlying liver-metastasis of FMC and provide new insights into prognosis and treatment of this feline malignancy.
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