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大數據分析健檢資料庫探討老年人慢性腎臟病的影響相關因素

為了解決x s min nam - minh n的問題，作者林冠礽 這樣論述：

慢性腎臟病已被公認為是全球主要的公共衛生議題，也是台灣健保支出最多的疾病。早期慢性腎臟病常常不易被發現，當出現明顯症狀時通常已到末期，因此透過早期診斷，早期治療，進而防止惡化為末期腎臟病更顯重要。本研究採用橫斷面分析研究設計，使用「台北市老人健檢資料庫」以及美國國家健康與營養檢查調查（NHANES）中提取的老年人（65歲及65歲以上）的數據資料，選取相關變項共分成三個部分進行分析，分別為(1)首先評估生活方式因素（運動習慣、飲酒、吸煙史和嚼檳榔）可能影響65歲與65歲以上老人腎功能下降之間的關聯。(2) 比較台灣台北市老人有或沒有血脂異常和/或心血管疾病（CVD）與老年人慢性腎臟病（CKD）

的危險因素。(3) 再運用美國國家健康與營養檢查調查（NHANES）中提取美國老年人（65歲及65歲以上） 資料庫，橫斷面研究評估生活方式因素與eGFR是否降低之間的關聯性。 主要研究發現: (1) 在65歲以上的社區老年人中，有經常性運動的良好生活習慣老人與 eGFR 延緩下降有關聯，吸煙與 eGFR 降低的風險升高有顯著關聯，此外，運動習慣對降低 eGFR 的保護作用不受高血壓、糖尿病、肥胖和心血管疾病等合併症的影響。(2) 性別、年齡、收入、血脂、尿蛋白和有高尿酸血症、痛風病史是為患有或不患有高脂血症的老年人發展CKD 有效篩選與預防策略的潛在影響因子，而吸煙、飲酒和咀嚼檳榔則不受

影響。高尿酸或 BUN 數值也可考慮用於老年高脂血症和 CVD 患者的 CKD 篩檢策略中。 (3)在美國65 歲及以上老年人中，尿蛋白、心血管疾病、糖尿病、高尿酸血症和高血壓與腎功能降低的機率顯著相關，充足的運動與腎功能降低機率有顯著關聯。

Snail上調FN, LEF, COX2 及 COL1A1基因的分子機轉: Snail轉錄活化間質蛋白的共同模式之建立

為了解決x s min nam - minh n的問題，作者Ly Minh Tam 這樣論述：

Hepatocellular carcinoma (HCC) progression involves a mechanism known as epithelial mesenchymal transition (EMT). Snail (SNA) is one of the most important transcription factors in EMT because it has the ability to decrease epithelial genes while upregulating mesenchymal genes. Nevertheless, the pro

cesses by which SNA transactivates mesenchymal markers remain unknown. Previously, we established that SNA works in collaboration with SP1 and EGR1 to directly induce ZEB1 and MMP9 transcription. Surprisingly, upstream of the EGR/SP1 overlapping area on promoters, a SNA-binding motif (TCACA) was dis

covered. Hence, the point of this research was to identify whether SNA similarly upregulates four other mesenchymal genes: fibronectin (FN), lymphoid enhancer-binding factor (LEF), collagen type alpha I (COL1A1), and cyclooxygenase 2 (COX2). SNA, as expected, is required for the activity of these me

senchymal markers. By using deletion mapping and site directed mutagenesis in combination with a dual luciferase promoter assay, it was found that the SNA-binding motif and the EGR1/SP1 overlapping area are necessary for transcription of FN, LEF, COL1A1, and COX2 genes elicited by the phorbol ester

tumor promoter 12-O-tetradecanoyl-phorbol 13-acetate (TPA) in HCC340 and HepG2 HCC cells. Furthermore, using ChIP and EMSA, TPA consistently promoted SNA and EGR1/SP1 binding to these mesenchymal genes' key promoter regions. So far, we've determined that six mesenchymal markers are activated by SNA

in the same transcriptional manner. Likewise, a systematic screening exhibited similar sequence structures in the promoter areas of other SNA-induced mesenchymal genes, implying the possibility of developing a universal model for SNA-induced mesenchymal genes. In conclusion, we hypothesized a novel

mechanism by which Snail acts as a positive transcriptional regulatory factor essential for EMT and metastasis of HCC.Keywords: snail, lymphoid enhancer-binding factor, fibronectin, collagen type alpha I, cyclooxygenase 2, HCC, transcription.