http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Chang, Shih-Yi,Tso, Tai-Ly,Lo, Jiunn-Gung,Huang, Jer-Luen,Lin, Cheng Ming 한국분석과학회 1995 분석과학 Vol.8 No.4
Toxic air pollutants are investigated in a petrochemical industrial park in Taiwan by using a movable open path FTIR. The results show the qualitative and quantitative analysis of emission gases from plants, and also provide the emission rate of different compounds. More than twenty compounds under usual operation are found from this industrial park. The concentration variation with time can be correlated exactly with wind direction. It means that by changing the measuring points, the source of emission can be unambiguously identified. An EPA proved PAL model is applied to estimate the emission rate of either a point or an area source. Local atmospheric stability is determined by releasing the $SF_6$ tracer. The origins of errors come mainly from the uncertainty of source's configuration and the variation of meteorological condition. Through the continuous measurement (half an hour base in this study) of OP-FTIR sensor, the maximum value of emission rate and the annual amount of emission can be derived. The emission rate of the measured toxic gases are derived by the model technique and the results show that the emission amount are in the order of ten to hundred tons per year.
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.
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.
Chien-Liang Liu,Ming-Jen Chen,Jiunn-Chang Lin,Chi-Hsin Lin,Wen-Chien Huang,Shih-Ping Cheng,Shan-Na Chen,Yuan-Ching Chang 한국유방암학회 2019 Journal of breast cancer Vol.22 No.2
Purpose: Cancer cells develop acquired resistance induced by chemotherapeutic drugs. In this study, we investigated the effects of brief treatment with cytotoxic drugs on the phenotype of breast cancer cells. Methods: Breast cancer cells MCF7 and BT-474 were briefly treated with paclitaxel or doxorubicin. Clonogenic, migration, and invasion assays were performed on the treated cells. Western blot analysis and RhoA activity assay were also performed. Results: Breast cancer cells when briefly treated with paclitaxel or doxorubicin showed reduced clonogenic ability. Doxorubicin, but not paclitaxel, augmented cell migration and invasion. The invasion-promoting effects of doxorubicin were lost when the two drugs were sequentially used in combination. Myosin light chain (MLC) 2 phosphorylation and RhoA activity were upregulated by doxorubicin and downregulated by paclitaxel. Pretreatment with RhoA inhibitors abolished the migration- and invasion-promoting effects of doxorubicin. Conclusion: Doxorubicin activates the RhoA/MLC pathway and enhances breast cancer cell migration and invasion. Therefore, this pathway might be explored as a therapeutic target to suppress anthracycline-enhanced tumor progression.