The Study of Radical Cyclization of Propargyl Silanes And Acylsilane

本篇論文中，我們的研究內容可以分為兩個部份。第一個部分目的在於合成具有末端及propargyl位具有矽基取代的1,3-矽基-6-溴(或碘)己炔化合物，並研究其自由基環化反應。我們發現在propargyl位上的三甲基矽基如預期的提高了炔基的HOMO軌域而因此加快了環合反應。另外我們意外的發現當propargyl位放上二苯基甲基矽基進行自由基環化反應時可以得到環化產物，推測是經由一個分子內1,3氫轉移或分子間的氫轉移的機制而得。 第二個部份的研究為。一磯基一 6 一烯基一。一碘基矽基峒的自由基環化反應，經由改變不同的反應條件，我們發現當使用兩當量丙烯基三正丁基錫炕而只用催化量的正三丁基錫炕來進行反應時，反應可如我們預期的得到環己雙烯矽瞇的產物。目 錄 I. 簡語對照表 II. 摘要 III. 緒論 IV. 結果與討論 一、丙炔基矽化合物之自由基環化反應研究 9 二、矽基酮的自由基環合反應研究 25 V. 結論 35 VI. 實驗部份 36 VII. 參考文獻 44 附錄：1H與13C核磁共振光譜 4

Detection of Osteogenic Differentiation by Differential Mineralized Matrix Production in Mesenchymal Stromal Cells by Raman Spectroscopy

<div><p>Mesenchymal stromal cells (MSCs) hold great potential in skeletal tissue engineering and regenerative medicine. However, conventional methods that are used in molecular biology to evaluate osteogenic differentiation of MSCs require a relatively large amount of cells. Cell lysis and cell fixation are also required and all these steps are time-consuming. Therefore, it is imperative to develop a facile technique which can provide real-time information with high sensitivity and selectivity to detect the osteogenic maturation of MSCs. In this study, we use Raman spectroscopy as a biosensor to monitor the production of mineralized matrices during osteogenic induction of MSCs. In summary, Raman spectroscopy is an excellent biosensor to detect the extent of maturation level during MSCs-osteoblast differentiation with a non-disruptive, real-time and label free manner. We expect that this study will promote further investigation of stem cell research and clinical applications.</p></div

Figure 3

<p>(A) Raman spectra of MSCs during osteogenic differentiation from 900 to 1800 cm⁻¹. (B) Magnified detail region for species from 900 to 1020 cm⁻¹ in stack diagram. OCP at 957 cm⁻¹ decreased upon osteogenic differentiation; β-TCP at 970 cm⁻¹ transiently appeared at Day 9 and HAP at 960 cm⁻¹ significantly increased after day9.</p

Figure 5

<p>(A) Micrographs of MSCs treated with osteogenic media for 0, 3, 9, 15 and 24 days. (Scale bar: 100 µm) (B) Gene expression profiles of RUNX2, periostin, and type I collagen were detected in MSCs after Raman measurements by qPCR and normalized by internal and undifferentiated controls. Data are shown as mean ± SE (n = 3). (C) Alkaline phosphatase and Von Kossa staining of MSC-osteoblast differentiation. (D) Gene expression profiles of RUNX2, periostin, and type I collagen in staining samples were detected by qPCR and normalized by internal and undifferentiated controls. Data are shown as mean ± SE (n = 3).</p

Schematic diagram of the Raman platform set-up.

<p>Schematic diagram of the Raman platform set-up.</p

Figure 2

<p>(A) Background signal of Raman spectra. Magnified details of the region for control and cell species from 900 to 1020 cm⁻¹ in stack diagram.</p

Up-Regulation of Hepatoma-Derived Growth Factor Facilities Tumor Progression in Malignant Melanoma

<div><p>Cutaneous malignant melanoma is the fastest increasing malignancy in humans. Hepatoma-derived growth factor (HDGF) is a novel growth factor identified from human hepatoma cell line. HDGF overexpression is correlated with poor prognosis in various types of cancer including melanoma. However, the underlying mechanism of HDGF overexpression in developing melanoma remains unclear. In this study, human melanoma cell lines (A375, A2058, MEL-RM and MM200) showed higher levels of HDGF gene expression, whereas human epidermal melanocytes (HEMn) expressed less. Exogenous application of HDGF stimulated colony formation and invasion of human melanoma cells. Moreover, HDGF overexpression stimulated the degree of invasion and colony formation of B16–F10 melanoma cells whereas HDGF knockdown exerted opposite effects <i>in vitro</i>. To evaluate the effects of HDGF on tumour growth and metastasis <i>in vivo,</i> syngeneic mouse melanoma and metastatic melanoma models were performed by manipulating the gene expression of HDGF in melanoma cells. It was found that mice injected with HDGF-overexpressing melanoma cells had greater tumour growth and higher metastatic capability. In contrast, mice implanted with HDGF-depleted melanoma cells exhibited reduced tumor burden and lung metastasis. Histological analysis of excised tumors revealed higher degree of cell proliferation and neovascularization in HDGF-overexpressing melanoma. The present study provides evidence that HDGF promotes tumor progression of melanoma and targeting HDGF may constitute a novel strategy for the treatment of melanoma.</p> </div