HS2000MX PTT的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列懶人包和總整理

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HS2000MX PTT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.

神經調節治療在憂鬱症動物模式中之機轉

為了解決HS2000MX PTT的問題，作者李旂緯 這樣論述：

頑固型憂鬱症(treatment-resistant depression，TRD)是一群對於足夠劑量和療程的抗憂鬱劑治療後仍無法改善的憂鬱症病患。而先前研究指出，創傷後壓力症候群(post-traumatic stress disorder，PTSD)所伴隨的憂鬱徵狀，會展現更強的藥物阻抗性。然而針對TRD的動物模式目前仍須建立。因此，在此研究將利用不同程度的壓力探討在大鼠模式中創傷壓力所誘導的憂鬱症之效果，並嘗試建立一具有抗憂鬱藥物阻抗性的動物模式。為探討創傷壓力在大鼠模式中之效果，我們利用足部電刺激之壓力做為創傷事件。大鼠分別接受3次、6次、10次的聲音與足部電刺激的搭配，以模擬輕度

、中度、重度的壓力創傷事件。此外，近期研究指出，新形的重覆透顱磁刺激(repetitive transcranial magnetic stimulation，rTMS)，theta波經顱磁刺激(theta burst stimulation，TBS)，例如間歇性theta波經顱磁刺激(intermittent theta burst stimulation，iTBS)以及持續性theta波經顱磁刺激(continuous theta burst stimulation，cTBS)，相較於傳統的rTMS施打形式，具有更快速和強力的效應。然而，目前對於iTBS與cTBS在治療TRD的機轉仍不清楚

。因此，我們以足部電刺激壓力作為壓力創傷所建立之抗憂鬱劑藥物阻抗動物模式，嘗試更進一步探討iTBS與cTBS在治療TRD上機轉的異同。