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探討信號轉導及轉錄激活蛋白3於貓注射部位肉瘤之角色

為了解決pleomorphic中文醫學的問題，作者施正心 這樣論述：

貓注射部位肉瘤（Feline injection site sarcomas; FISSs）為組織型態多樣的間質來源惡性腫瘤，最早在1990年代因與含鋁佐劑之狂犬病和貓白血病疫苗之使用有高度相關性而被注意到。目前普遍認為FISS的致病機轉與注射或異物引起之慢性炎症有關。慢性炎症會促進細胞激素及生長因子的分泌與轉錄因子的活化，進而促使纖維母細胞與肌纖維母細胞的增生與腫瘤化。在眾多與慢性炎症相關的轉錄因子中，信號轉導及轉錄激活蛋白3（STAT3）在致腫瘤上扮演了舉足輕重的角色。人類醫學的研究中顯示，有近百分之七十的實質固態腫瘤與血液腫瘤其JAK-STAT3信號傳送路徑呈顯著活化，而STAT3信號

傳送路徑可調控腫瘤細胞的增殖、存活及轉移與血管新生。本研究首先以免疫組織化學染色（immunohistochemitry; IHC）探討福馬林固定和石蠟包埋的FISS組織中，STAT3與磷酸化型STAT3之表現情形，結果證實有88.9％（40/45）的樣本呈現腫瘤細胞細胞質內STAT3陽性反應，53.3%（24/45）的樣本呈現磷酸化型STAT3腫瘤細胞細胞核內陽性反應。為了進一步探討STAT3之表現在貓疫苗注射部位肉瘤之角色，本研究使用兩個來自不同貓隻之FISS初代細胞株，並以STAT3抑制劑5-hydroxy-9,10-dioxo-9,10-dihydroanthracene-1-sulf

onamide （LLL12）證實在STAT3磷酸化路徑受抑制下，FISS初代細胞之增殖與移行能力具劑量依賴性之顯著下降。由此可知STAT3在FISS之致腫瘤機制中扮演重要角色，在腫瘤的治療策略上，STAT3抑制劑可能具有臨床應用潛力。

在帕金森氏症的細胞與生物模式中探討PLA2G6及PLA2G6點突變

為了解決pleomorphic中文醫學的問題，作者劉涵芳 這樣論述：

Table of Contents中文摘要 iAbstract iiTable of Contents iiiList of Figures vList of tables viAbbreviation viiChapter 1. Introduction - 1 -1.1 Phospholipase A2, group VI - 1 -1.2 Parkinson’s disease - 2 -1.3 PLA2G6 and young-onset dystonia-parkinsonism (Parkinson disease-14, P

ARK14) - 3 -1.4 PLA2G6 activity and lipid metabolites - 4 -1.5 Zebrafish as a Model for Neurodegenerative Disorders - 5 -Chapter 2. Materials and Methods - 7 -2.1 Animal Maintenance - 7 -2.2 mRNA preparation and microinjection - 7 -2.3 Zebrafish behavior - 8 -2.4 Histological an

alysis - 8 -2.5 Phospholipase activity assay - 11 -2.6 High performance liquid chromatography (HPLC) - 12 -2.7 Lipophilic metabolites extraction and data processing - 12 -2.8 Mouse behavior - 13 -2.9 Cell culture and Immunocytochemistry - 14 -2.10 Western blot - 15 -2.11 Quantit

ative reverse transcription PCR (qRT-PCR) - 16 -2.12 Statistical analysis - 17 -Chapter 3. Results - 18 -3.1 Characterization of PLA2G6 mutations in zebrafish - 18 -3.1.1 Overexpression of PLA2G6 mutations in zebrafish - 18 -3.1.2 PLA2G6 mutation D331Y and T572I overexpression induced

motility defects in zebrafish - 18 -3.1.3 PLA2G6 mutation D331Y and T572I overexpression caused dopamine neuron loss in zebrafish - 20 -3.2 PLA2G6 phospholipase activity and lipid metabolites - 21 -3.2.1 Zebrafish Pla2g6 is homologous to human PLA2G6 - 21 -3.2.2 PLA2G6 mutation D331Y or

T572I results in decreased phospholipase activity and disturbed lipidome - 22 -3.2.3 Dietary DHA supplementation relieved the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset - 23 -3.3 PLA2G6 in dopaminergic neuron development - 25 -3.3.1 Zebrafish pla2g6 expre

ssed mainly in the central nervous system - 25 -3.3.2 PLA2G6 mutation D331Y or T572I reduced neuronal precursor cells through increased apoptosis - 26 -3.4 The role of PLA2G6 in regulating cellular processes - 27 -3.4.1 Transduction of human wild type PLA2G6 improved proliferation in dopami

nergic neuron cell line - 27 -3.4.2 PLA2G6 play a protective role in dopaminergic neuron cell line under ROS stress - 28 -Chapter 4. Discussion - 29 -4.1 PLA2G6 mutations in PARK14 - 29 -4.2 PLA2G6 mutation and phospholipase activity in PARK14 - 30 -4.3 The role of DHA in PLA2G6 mutat

ion-induced PD - 31 -4.4 PLA2G6-mediated apoptosis in the dopaminergic neuron. - 33 -4.5 PLA2G6 and its metabolites in neurodevelopment. - 34 -4.6 The potential signaling regulation role of PLA2G6 - 36 -Chapter 5. Conclusion - 37 -References - 38 -Figures and Legends - 48 -Table

s - 68 -Publications - 73 -List of FiguresFigure 1. Alignment of PLA2G6 human and zebrafish homologue. - 49 -Figure 2. Schematic illustration of PLA2G6 domains and six point mutations of PARK14. - 50 -Figure 3. Injection of PLA2G6D331Y or PLA2G6T572I causes motility defects in zebrafish.

- 51 -Figure 4. Injection of PLA2G6D331Y or PLA2G6T572I decreases dopaminergic neurons and dopamine levels. - 52 -Figure 5. Injection of PLA2G6D331Y, PLA2G6T572I, or pla2g6 deletion constructs alters phospholipase activity in zebrafish. - 53 -Figure 6. Co-expression of zebrafish pla2g6 res

cues the behavioral defects induced by PLA2G6D331Y or PLA2G6T572I. - 54 -Figure 7. Lipid metabolites are disturbed in PLA2G6D331Y or PLA2G6T572I injected embryos. - 55 -Figure 8. Dietary DHA supplementation does not affect the body weight and diet consumption of PLA2G6 knock-in mice. - 56 -

Figure 9. Dietary DHA supplementation relieves the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset. - 58 -Figure 10. Dietary DHA supplementation does not relieve the motility defects of PLA2G6D331Y/D331Y mice at a late stage of disease onset. - 59 -Figure 11. Zebr

afish pla2g6 is expressed in the developing nervous system. - 60 -Figure 12. Injection of PLA2G6D331Y or PLA2G6T572I reduces the expression of the neuronal precursor marker and induces cell apoptosis. __ - 61 -Figure 13. Injection of PLA2G6D331Y or PLA2G6T572I does not affect the expression of

the neural progenitor marker. - 62 -Figure 14. Expression of human PLA2G6 enhances the proliferation of MN9D cells. - 63 -Figure 15. Expression of hPLA2G6 reduces cell apoptosis upon 6-OHDA treatment in MN9D cells. - 64 -Figure 16. 3D structure predictions of PLA2G6 and the effect of D331Y

or T572I mutation analyzed by PyMOL software. - 65 -Figure 17. Injection of PLA2G6 mutation PLA2G6D331Y or PLA2G6T572I, or pla2g6 deletion constructs pla2g6∆ANK or pla2g6∆Ptt affect the expression of Notch signaling downstream genes. - 66 -Figure 18. The summary of this study. - 67 -List o

f tablesTable 1. List of lipid metabolites identified in PLA2G6D331Y or PLA2G6T572I injected embryos. - 69 -Table 2. Lipid metabolites identified conditions in LC-MS and METLIN database. - 70 -Table 3. Primers used for gene cloning in this thesis. - 71 -Table 4. Primers used for qRT-PCR ana

lysis in this thesis - 72 -