碩士
中山醫學院
生物化學研究所
88
Nitric oxide (NO) is a common indoor and outdoor environmental toxic pollutant arising from gas and wood-burning stoves, and emissions from auto-motive and other combustion ...engines. There is considerable evidence to suggest that NO-induced injury in mammalian lung cells. NO may cause DNA or tissue damage, contributing to the multistage carcinogenesis. We demonstrated that 8-nitroquanine was formed time- and dose- dependently in human lung fibroblast cells (MRC-5) exposed to gaseous NO. These results suggest that 8-nitroquanine could act as a specific marker for DNA damage induced by pollutant NO. In addition, exposure of isolated DNA in MRC-5 cells to gaseous NO led to 8-nitroquanine produce. NO induced DNA damage also led to p53 protein accumulation and phosphorylation. These results also indicated that gaseous NO directly attack DNA and partly induced endogenous NO by activating inducible nitric oxide synthase (iNOS).
Many studies have identified NO as having a critical role in cellular
碩士
高雄醫學大學
生理及分子醫學研究所
99
英文摘要
Objectives
Osteoarthritis (OA) is a degenerative joint disease and easily to decrease glycosaminoglycan (GAG) and collagen levels, but the mechanism remains unclear. ...During OA progession, articular chondrocytes undergo terminal differentiation and decrease level of GAG and COL. II, but increase level of COL. X, which are similar as those during endochondral ossification. Previous studies showed that parathyroid hormone-related peptide (PTHrP) can suppress hypertrophy and terminal differentiation of chondrocytes. Previous studies also indicated that PTHrP and parathyroid hormone (PTH) share the same receptor, PTHR1, and stimulate activities of adenylate cyclase (PKA pathway) and phospholipase-C (PKC pathway). Our previous finding emphasized that PTH(1-34) can suppress the progress of terminal differentiation in cultured human articular chondrocytes (HACs) and the papain-induced OA in rats. The previous results showed that intra-articular injection of PTH(1-34) once every 3 days sup
碩士
國立臺北大學
法律學系一般生組
107
In 1997, to deal with the commitment of “Machine Cheating”, Taiwan enacted amendments of §339-1 to §339-3 in the Criminal Code of Republic of China (the Criminal Code). By ...comparing the new amendment of §339-3 with the §263a of the German Criminal Law, this thesis mainly focused on the interpretation of “Unlawful Method”, ”Input”, ”False Information”, “Unlawful Instruction Code” , and other statutory elements. Furthermore, this thesis pointed out the lack of certain type of enactments, which would correspondingly govern crimes of computer cheating.
The element “Automatic Payment Machine” of §339-2 also belongs the concept of “Computer”. This leads to the induction that a perpetrator could violate §339-2 and §339-3 at the same time. Since the Legislator has already enacted §339-2, imposing §339-2 on perpetrator would suffice. However, the interpretation of “Unlawful Method” is quite controversial. Some asserted “The Similar Character of Fraud”, some argued “Subjective Intent”, and ot
博士
國立成功大學
生物醫學工程學系
107
Articular cartilage has a limited capacity for self-repair. Injury to cartilage often progresses to development of osteoarthritis (OA). The available medical interventions can ...help to relieve symptoms, but fail to produce functional cartilage. Recently the cell-based therapies for cartilage repair are mainly focused on chondrocytes, mesenchymal stem cells (MSCs) or tissue specific progenitor cells. Tissue-specific progenitor cells not only possess stem cell-like proliferative potential, but also display tissue-specific phenotypes. In the present study, we investigated the osteochondral regeneration potential of two different kinds of progenitor cells. The first are endothelial progenitor cells (EPCs) have proven to have a high capacity for regeneration and vasculogenesis in different tissues. The second are cartilage stem/progenitor cells (CSPCs), which are resident, cartilage-specific, multipotent progenitor cells that have opened new avenues for cartilage repair. The objectives of the current study included Part I (in vivo study): The investigation of the effects of an EPC loaded poly lactic-co-glycolic acid (PLGA) scaffold combined with continuous passive motion (CPM) on osteochondral defect repair in rabbits. Part II-1 (in vitro study): To characterize CSPCs and compare them with osteoarthritis chondrocytes (OACs) and infrapatellar fat pad-derived stem cells (IFPs) through colony formation assay, multilineage differentiation analysis, gene expression analysis, and biochemical analysis. Part II-2 (in vivo study): To evaluate the osteochondral regeneration of the CSPC loaded PLGA scaffold during osteochondral defect repair in rabbits. We found that the combination of CPM with EPC loaded PLGA scaffolds during the regenerative process could enhance the synthesis of cartilage specific matrix, down-regulate subchondral bone formation and promote the synthesis of lubricin. The EPCs offered a microenvironment for angiogenesis; whereas, physical stimulation from CPM promoted tissue regeneration and host integration. The characteristics of CSPCs are similar to those of MSCs and they have chondrogenic and osteogenic phenotypes without chemical induction. Additionally, CSPCs displayed a significantly higher synthesis of GAGs than OACs. However, there was no significantly different in gene expression of chondrogenesis with IFPs. For in vivo study, CSPC loaded PLGA scaffolds produced a hyaline-like cartilaginous tissue, which showed good integration with host tissue and subchondral bone. More importantly, CSPCs involved the mechanism of the endochondral ossification of chondrocytes in the mineralization of the cartilage for promoting subchondral bone regeneration. Overall, this study demonstrated both CSPC and EPC progenitors had the potential to promote osteochondral regeneration. The combination of these cell-based therapies might be beneficial for the repair of complex tissues, such as osteochondral tissue.
