以複合圓形顆粒模式探討不規則單粒落石之運動行為

【摘 要】 落石幾何型態為影響落石運動行為的因子之一，有鑑於前人進行數值模擬落石之運動行為時，落石形狀大多僅考慮二維圓盤及三維圓球，但根據落石事件之調查，落石形狀並無一定規則可循，而不同形狀之落石與邊坡碰撞後其運動行為也將有所差異。故本文主要以複合圓形顆粒模式模擬多種落石形狀，探討落石形狀對落石運動行為之影響。本文之數值分析結果如下： 運動軌跡部份：(1)本研究發現球度對落石運動型態有較為顯著的影響。當邊坡坡角為30°、45°、60°時，球度0.7、0.9的落石有較佳的滾動與彈跳能力。(2)球度0.3的落石由於形狀扁長之故，在邊坡坡角小於或等於45°時，多以滑動型態運動為主，邊坡坡角60°時則是先滾動後，再以滑動型態運動。(3)球度0.5之落石在坡角30°時多以滑動為主，隨著坡角增加至45°、60°時，運動型態轉為滾動後彈跳之型態。(4)邊坡坡角達75度時，落石型態多以自由落體為主，受落石形狀之影響並不大。（5）本研究發現，圓度對落石運動型態並無顯著之影響。 防護牆受撞擊力部份：(1)落石外形將影響落石於邊坡上之運動型態，進而導致防護牆所受的衝擊力會有所差異。(2)隨著球度的增加，落石運動型態會由滑動逐漸轉變為滾動或彈跳型態，且彈跳次數有減少的趨勢，因此造成防護牆所受的衝擊力，有隨著球度增加而增大的趨勢。【論文目次】 摘 要 Ⅰ 目 錄 Ⅱ 表目錄 Ⅴ 圖目錄 Ⅵ 第一章 緒論 1 1.1 背景 1 1.2 研究動機與目的 1 1.3 研究範圍 3 第二章 相關文獻回顧 5 2.1落石運動基本特性 5 2.1.1落石之定義與特性 5 2.1.2落石之發生機制 6 2.2國內外之落石防護工法 7 2.3影響落石運動軌跡之相關因子 10 2.3.1邊坡之幾何型態 10 2.3.2邊坡與岩塊之組合材料特性 11 2.3.3落石之幾何型態與材料特性 12 2.4落石運動軌跡之分析方法 13 第三章 複合圓形顆粒模式之理論基礎 24 3.1複合圓形整合模式概述 24 3.2顆粒形狀 25 3.2.1複合圓形顆25 3.2.2複合圓形顆粒有效圓弧判斷 25 3.2.3顆粒面積(A)與轉動二次矩(I) 26 3.3運動方程式 26 3.4時間積分法27 3.5接觸判斷 29 3.5.1接觸方向定義 29 3.5.2顆粒與邊界之接觸判斷 30 3.5.3顆粒與顆粒之接觸判斷 30 3.6接觸力計算 31 3.6.1顆粒與邊界接觸形式 31 3.6.2顆粒與顆粒接觸形式 33 3.7接觸組成模式 35 3.8其他不規則形狀落石之數值模擬 36 第四章 研究方法及基本參數之決定 49 4.1 研究方法 49 4.1.1落石之運動行為之探討 49 4.1.2 防護牆所受衝擊力之探討 49 4.2 顆粒基本參數之決定 49 4.3 圓形與不規則形狀落石軌跡之比較 52 第五章 數值分析之結果與討論 58 5.1落石運動軌跡之探討 58 5.2防護牆所受衝擊力之探討 59 第六章 結論與建議 88 6.1結論 88 6.2建議 89 參考文獻 90 附錄A落石運動軌跡示意圖 93 附錄B落石衝擊防護牆示意圖 118 表 目 錄 表2-1 Sharpe塊體運動分類 17 表2-2 Varnes山崩分類表 17 表2-3 不同地質材料坡面之回彈係數值 18 表4-1 落石之各項基本參數值 54 圖 目 錄 圖1-1球度與圓度視覺估計圖 4 圖2-1落石之發生型態：(a) 滾石形 ; (b) 浮石形 19 圖2-2 落石運動型態示意圖 19 圖2-3 落石事件之示意圖 19 圖2-4 北橫附近之落石柵工法 20 圖2-5 蘇花公路東澳段之明隧道工法 20 圖2-6 消能環裝置 21 圖2-7 防護網攔截落石後之變形行為 21 圖2-8 落石運動型態與坡度關係示意圖 21 圖2-9 粗糙角與落石半徑及坡面起伏高度關係圖 22 圖2-10粗糙角量測示意圖 22 圖2-11落石回彈係數與速度關係之示意圖 22 圖2-12圓度示意圖 23 圖2-13實驗方法與計算模式之關係流程圖 23 圖3-1（a）複合圓形組成之各元素示意圖 38 圖3-1（b）組合後之顆粒形狀示意圖 38 圖3.2接觸力矩從圓心修正到質心之示意圖 38 圖3-3（a）複合圓形顆粒之各元素示意圖 39 圖3-3（b）複合圓形顆粒組合後之形狀示意圖 39 圖3-4（a）1號圓之有效圓弧判斷示意圖 40 圖3-4（b）2號及3號圓之有效圓弧判斷示意圖 40 圖3-5 複合圓形分割示意圖 41 圖3-6 接觸方向示意圖 41 圖3-7 複合圓形顆粒間之接觸法線及切線方向示意圖 42 圖3-8 顆粒與邊界接觸方向示意圖 42 圖3-9 複合圓形顆粒與邊界接觸法線及切線方向示意圖 43 圖3-10 顆粒與邊界接觸判斷示意圖 43 圖3-11複合圓形顆粒與邊界接觸判斷示意圖 44 圖3-12 顆粒與顆粒接觸判斷示意圖 44 圖3-13 複合圓形顆粒間之接觸判斷示意圖 45 圖3-14 以複合圓形整合模式模擬顆粒圖 45 圖3-15 以複合圓形整合模式模擬顆粒圖 46 圖3-16 以複合圓形整合模式模擬顆粒圖 46 圖3-17 以複合圓形整合模式模擬顆粒圖 47 圖3-18 以複合圓形整合模式模擬顆粒圖 47 圖3-19 以複合圓形整合模式模擬顆粒圖 48 圖4-1 單一斜坡示意圖 54 圖4-2 落石衝擊剛性地板之力學機制 55 圖4.3 坡面粗糙起伏之示意圖 55 圖4.4 圓度1，球度1 (圓形)落石之運動軌跡 56 圖4.5 圓度0.5，球度0.5落石之運動軌跡 56 圖4.6 圓度0.1，球度0.3落石之運動軌跡 57 圖5-1 a，30度邊坡，圓度0.1，球度0.3之運動軌跡 62 圖5-1 b，30度邊坡，圓度0.5，球度0.5之運動軌跡 62 圖5-1 c，30度邊坡，圓度0.7，球度0.7之運動軌跡 62 圖5-1 d，30度邊坡，圓度0.9，球度0.9之運動軌跡 62 圖5-2 a，45度邊坡，圓度0.1，球度0.3之運動軌跡 63 圖5-2 b，45度邊坡，圓度0.5，球度0.5之運動軌跡 63 圖5-2 c，45度邊坡，圓度0.7，球度0.7之運動軌跡 63 圖5-2 d，45度邊坡，圓度0.9，球度0.9之運動軌跡 63 圖5-3 a，60度邊坡，圓度0.1，球度0.3之運動軌跡 64 圖5-3 b，60度邊坡，圓度0.5，球度0.5之運動軌跡 64 圖5-3 c，60度邊坡，圓度0.7，球度0.7之運動軌跡 64 圖5-3 d，60度邊坡，圓度0.9，球度0.9之運動軌跡 64 圖5-4 a，75度邊坡，圓度0.1，球度0.3之運動軌跡 65 圖5-4 b，75度邊坡，圓度0.5，球度0.5之運動軌跡 65 圖5-4 c，75度邊坡，圓度0.7，球度0.7之運動軌跡 65 圖5-4 d，75度邊坡，圓度0.9，球度0.9之運動軌跡 65 圖5-5 a，30度邊坡，圓度0.5，球度0.3之撞擊軌跡 66 圖5-5 b，30度邊坡，圓度0.5，球度0.5之撞擊軌跡 66 圖5-5 c，30度邊坡，圓度0.5，球度0.7之撞擊軌跡 66 圖5-5 d，30度邊坡，圓度0.5，球度0.9之撞擊軌跡 66 圖5-6 a，45度邊坡，圓度0.7，球度0.3之撞擊軌跡 67 圖5-6 b，45度邊坡，圓度0.7，球度0.5之撞擊軌跡 67 圖5-6 c，45度邊坡，圓度0.7，球度0.7之撞擊軌跡 67 圖5-6 d，45度邊坡，圓度0.7，球度0.9之撞擊軌跡 67 圖5-7 a，60度邊坡，圓度0.1，球度0.3之撞擊軌跡 68 圖5-7 b，60度邊坡，圓度0.1，球度0.5之撞擊軌跡 68 圖5-7 c，60度邊坡，圓度0.1，球度0.7之撞擊軌跡 68 圖5-7 d ， 60度邊坡， 圓度0.1，球度0.9之撞擊軌跡 68 圖5-8 a，75度邊坡，圓度0.5，球度0.3之撞擊軌跡 69 圖5-8 b，75度邊坡，圓度0.5，球度0.5之撞擊軌跡 69 圖5-8 c，75度邊坡，圓度0.5，球度0.7之撞擊軌跡 69 圖5-8 d，75度邊坡，圓度0.5，球度0.9之撞擊軌跡 69 圖5-9，坡角30度，落石形狀圓度0.1，球度0.1∼0.9 70 圖5-10，坡角30度，落石形狀圓度0.3，球度0.1∼0.9 70 圖5-11，坡角30度，落石形狀圓度0.5，球度0.1∼0.9 71 圖5-12，坡角30度，落石形狀圓度0.7，球度0.1∼0.9 71 圖5-13，坡角30度，落石形狀圓度0.9，球度0.1∼0.9 72 圖5-14，坡角30度，落石形狀圓度0.1∼0.9，球度0.1∼0.9 72 圖5-15，坡角30度，落石形狀球度0.3，圓度0.1∼0.9 73 圖5-16，坡角30度，落石形狀球度0.5，圓度0.1∼0.9 73 圖5-17，坡角30度，落石形狀球度0.7，圓度0.1∼0.9 74 圖5-18，坡角30度，落石形狀球度0.9，圓度0.1∼0.9 74 圖5-19，坡角30度，落石形狀球度0.3∼0.9，圓度0.1∼0.9 75 圖5-20，坡角45度落石形狀圓度0.1，球度0.3∼0.9 76 圖5-21，坡角45度落石形狀圓度0.3，球度0.3∼0.9 76 圖5-22，坡角45度落石形狀圓度0.5，球度0.3∼0.9 77 圖5-23，坡角45度落石形狀圓度0.7，球度0.3∼0.9 77 圖5-24，坡角45度落石形狀圓度0.9，球度0.3∼0.9 78 圖5-25，坡角45度落石形狀圓度0.1∼0.9，球度0.3∼0.9 78 圖5-26，坡角45度落石形狀球度0.3，圓度0.1∼0.9 79 圖5-27，坡角45度落石形狀球度0.5，圓度0.1∼0.9 79 圖5-28，坡角45度落石形狀球度0.7，圓度0.1∼0.9 80 圖5-29，坡角45度落石形狀球度0.9，圓度0.1∼0.9 80 圖5-30，坡角45度落石形狀球度0.3∼0.9，圓度0.1∼0.9 81 圖5-31，坡角60度落石形狀圓度0.1，球度0.3∼0.9 82 圖5-32，坡角60度落石形狀圓度0.3，球度0.3∼0.9 82 圖5-33，坡角60度落石形狀圓度0.5，球度0.3∼0.9 83 圖5-34，坡角60度落石形狀圓度0.7，球度0.3∼0.9 83 圖5-35，坡角60度落石形狀圓度0.9，球度0.3∼0.9 84 圖5-36，坡角60度落石形狀圓度0.1∼0.9，球度0.3∼0.9 84 圖5-37，坡角60度落石形狀球度0.3，圓度0.1∼0.9 85 圖5-38，坡角60度落石形狀球度0.5，圓度0.1∼0.9 85 圖5-39，坡角60度落石形狀球度0.7，圓度0.1∼0.9 86 圖5-40，坡角60度落石形狀球度0.9，圓度0.1∼0.9 86 圖5-41，坡角60度落石形狀球度0.3∼0.9，圓度0.1∼0.9 8

Emission Tax and Compensation Subsidy with Cross-Industry Pollution

This paper establishes a cross-industry pollution externality model. To explain a benevolent government, it may be possible to tax part of the welfare gains and use the revenue to compensate the affected polluted industry for the damage cost, thereby improving welfare. We show that the social welfare under emission tax with production subsidy is higher than the results of emission tax without production subsidy. The welfare of the polluted sector under emissions trading will be lower than the results of unbalanced budget environmental policy with subsidy. The welfare of the polluted labor union under lobby for compensation will be higher than the results of environmental policy with subsidy if the pollution damage and the weight on political contributions are sufficiently high

Methylation in pericytes after acute injury promotes chronic kidney disease

The origin and fate of renal myofibroblasts is not clear after acute kidney injury (AKI). Here, we demonstrate that myofibroblasts were activated from quiescent pericytes (qPericytes) and the cell numbers increased after ischemia/reperfusion injury-induced AKI (IRI-AKI). Myofibroblasts underwent apoptosis during renal recovery but one-fifth of them survived in the recovered kidneys on day 28 after IRI-AKI and their cell numbers increased again after day 56. Microarray data showed the distinctive gene expression patterns of qPericytes, activated pericytes (aPericytes, myofibroblasts), and inactivated pericytes (iPericytes) isolated from kidneys before, on day 7, and on day 28 after IRI-AKI. Hypermethylation of the Acta2 repressor Ybx2 during IRI-AKI resulted in epigenetic modification of iPericytes to promote the transition to chronic kidney disease (CKD) and aggravated fibrogenesis induced by a second AKI induced by adenine. Mechanistically, transforming growth factor-β1 decreased the binding of YBX2 to the promoter of Acta2 and induced Ybx2 hypermethylation, thereby increasing α-smooth muscle actin expression in aPericytes. Demethylation by 5-azacytidine recovered the microvascular stabilizing function of aPericytes, reversed the profibrotic property of iPericytes, prevented AKI-CKD transition, and attenuated fibrogenesis induced by a second adenine-AKI. In conclusion, intervention to erase hypermethylation of pericytes after AKI provides a strategy to stop the transition to CKD

Double Filtration Plasmapheresis with Polyvinyl Alcohol-Based Membrane Lowers Serum Inflammation and Toxins in Patients with Hyperlipidemia

Hyperlipidemia is increasing in prevalence and is highly correlated with cardiovascular disease (CVD). Lipid-lowering medications prevent CVD but may not be suitable when the side effects are intolerable or hypercholesterolemia is too severe. Double-filtration plasmapheresis (DF) has shown its therapeutic effect on hyperlipidemia, but its side effects are not yet known. We enrolled 45 adults with hyperlipidemia in our study. The sera before and two weeks after DF were evaluated, and we also analyzed perfluorochemicals to see if DF could remove these lipophilic toxins. After DF, all lipid profile components (total cholesterol, triglycerides, high-density lipoprotein [HDL], and low-density lipoprotein [LDL]) had significantly decreased. Leukocyte counts increased while platelet levels decreased, which may have been caused by the puncture wound from DF and consumption of platelets during the process. As for uremic toxins and inflammation, levels of C-reactive protein, uric acid, and alanine transaminase (ALT) all decreased, which may be related to the removal of serum perfluorooctane sulfonate (PFOS) and improvement of renal function. The total cholesterol/HDL ratio and triglycerides were significantly higher in the diabetes mellitus (DM) group at baseline but did not significantly differ after DF. In conclusion, DF showed potential for improving inflammation and removing serum lipids and PFOS in adults with hyperlipidemia

IPSS-R in 555 Taiwanese patients with primary MDS: Integration of monosomal karyotype can better risk-stratify the patients

[[abstract]]The revised International Prognostic Scoring System (IPSS-R) was recently developed to better assess the clinical outcome of adult patients with myelodysplastic syndrome (MDS). In this study, we aimed to investigate the prognostic impact of this new risk model on 555 MDS patients in Taiwan. Generally, the IPSS-R could discriminate MDS patients regarding risk of leukemia evolution and overall survival in our cohort and it further refined prognostic stratification in all IPSS risk categories. However, we could not find the inter-group difference between IPSS-R very low and low risk subgroups in both leukemia-free survival (LFS) and overall survival (OS). IPSS-R couldn't distinguish the prognosis between very good and good and between good and intermediate risk cytogenetic categories in OS, and between very good and good and between intermediate and poor cytogenetic-risk categories in LFS, either. On the other hand, incorporation of monosomal karyotype (MK) into IPSS-R could further stratify MDS patients with higher-risk IPSS-R (intermediate, high and very high risk) into four groups, rather than three groups, with different OS (P < 0.001). Intriguingly, patients receiving allogeneic hematopoietic stem cell transplantation had longer survival than those without in the IPSS-R high and very high, but not other risk groups. Similarly, patients treated with hypomethylating agents had better survival than those not in the IPSS-R very high risk group. In conclusion, IPSS-R can risk-stratify MDS patients in Taiwan but with some limitations, especially in very low risk category, and MK has additional prognostic value in discriminating MDS patients with higher-risk IPSS-R