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24S LV進入發燒排行的影片

Pentraxins 3 在肺動脈高壓中的角色

為了解決24S LV的問題，作者王惠玄 這樣論述：

Abstract I中文摘要 II致謝 IIITable of contents IVAbbreviations VIIChapter 1. Introduction 11.1 Pulmonary arterial hypertension (PAH) 11.2 Inflammation in PAH 21.3 Treatment of PAH 21.4 Pentraxins and pentraxin 3 (PTX3) 31.5 The correlation of PAH with PTX3 41.6 Monocrotaline (MCT)-induced PAH model 41.7

Research motivation 51.8 Hypothesis 51.9 Specific aims 5Chapter 2. Materials and Methods 62.1 MCT induced PAH animal model and treatment 62.2 Echo and hemodynamic 62.3 Tissue harvest 72.4 Protein extraction and quantitative analyze 72.5 Western blotting 82.6 RNA extraction and reverse transcriptio

n 92.7 Real-time quantitative PCR 92.8 Hematoxylin and Eosin staining 92.9 Masson’s trichrome staining 102.10 Quantified vascular collagen and thickness 102.11 Immunohistochemistry (IHC) staining 112.12 Double immunofluorescence (IF) staining 112.13 Statistical analysis 12Chapter 3. Results 133.1 Es

tablishing MCT-induced PAH model in rats 133.2 The association between PTX3 and rats with PAH 143.3 The effect of PTX3 Ab in PAH rat model 153.3.1 The expression of PTX3 after PTX3 Ab treatment 153.3.2 The influence of biological parameters after PTX3Ab treatment in PAH 163.3.3 The change of vascul

ar in lungs 173.4 Anti-PTX3 Ab attenuated inflammation in rats with PAH 183.5 Anti-PTX3 Ab improved fibrosis in rats with PAH 193.6 The producers of PTX3 21Chapter 4. Discussion 224.1 Sildenafil decreases PTX3 expression in PAH 224.2 The other reasons of PTX3 may influence the survival rate in the

MCT-inducedPAH animal model 224.3 Mechanisms of PTX3 in PAH based on in vitro study 234.4 The potential pathway for PTX3 in PAH 234.5 The feasibility and the alternative program of PTX3 Ab 24Future perspective 25Knock out PTX3 is necessary 25Chapter 5. Conclusions 26References 27List of figures an

d tables 36Figure. 1. Establishing MCT-induced PAH rat model in different time points 36Figure. 2. PTX3 expression increases in the vehicle group 36Figure. 3. PTX3 expression after treatment in rats with PAH 38Figure. 4. PTX3 Ab decreases RV hypertrophy and heart enlargement 41Figure. 5. PTX3 Ab imp

roves RV function by echocardiographic evaluation 42Figure. 6. PA wall thickness was improved in PTX3 Ab group 43Figure. 7. The difference between PTX3 Ab and sildenafil treatment 46Figure. 8. PTX3 Ab decreases inflammation in lung of rats with PAH 47Figure. 9. PTX3 Ab decreases inflammation in RV o

f rats with PAH 48Figure. 10. PTX3 Ab decreases collagen deposition around PAs of rats with PAH 49Figure. 11. PTX3 Ab decreases the relative gene of fibrosis in lung 51Figure. 12. PTX3 Ab decreases fibrosis in RV in rats with PAH 52Figure. 13. PAAFs was one of major producers to PTX3 in rats with PA

H 53Figure. 14. Macrophages/monocytes did not the major producer to PTX3 in ratswith PAH 54Figure. 15. The schematic diagram about the role of PTX3 in the MCT-inducedPAH rat model 55Supplementary figure. 1. PTX3 expression of the lung in an MCT-induced PAHanimal model 56Table 1. Primer sequence for

qPCR 57Table 2. The physiological and hemodynamic parameters in rats with PAH 58Table 3. The target gene in lung and RV tissue of rats with PAH 59Table 4. The echocardiographic evaluation in rats with PAH 60Table 5. The change of vascular in rats with PAH 61