mt15 r15比較的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列各種有用的問答集和懶人包

探討 ADAM9 下游調控 UBN2 及 AKR1C3 在前列腺癌症惡化過程中的生物機轉

為了解決mt15 r15比較的問題，作者LE THI HUYNH TRANG 這樣論述：

A progressively diagnosed resistance mechanism to androgen deprivation in prostate cancer (PCa) is still lacking in understanding. Many genes involved in the androgen and androgen receptor (AR) pathway contribute to this aggressive subset. The essential role of the disintegrin and metalloproteinase

domain-containing protein 9 (ADAM9) in driving the solid tumor aggressiveness and metastasis has been well-defined. In PCa, ADAM9 is promoted the metastasis state through an activation by androgen. A secreted isoform of ADAM9 (sADAM9) is released by stromal cells and upregulated the cancer cell inv

asion. In our study, by stimulating PCa cells with sADAM9, we noticed an increased ubinuclein 2 (UBN2) expression and a positive association between ADAM9 with UBN2 expression was also observed in the PCa cell lines and clinical tissues. Latterly, by analysis of the genetic modification approach we

revealed UBN2 as a downstream target gene of ADAM9 in androgen-dependent PCa cell lines. Here, we showed that UBN2 expression was up-regulated in PCa with those normal samples by Oncomine database and immunohistochemistry. Moreover, PCa tissues and clinical relevance confirmed the certainly correlat

ion between AR with ADAM9 and UBN2 expression for which ADAM9 and UBN2 expression were induced in PCa cells by AR genetic modification or treatment with synthetic androgen (R1881). Remarkably, this study provides a novel mechanism of progression in PCa by which the regulatory role of UBN2 and its up

stream ADAM9 on the aldo-keto reductase family 1 member C3 (AKR1C3) expression regulated PCa cell growth against androgen-targeted therapy . We also supported the causal relationship of ADAM9-UBN2-AKR1C3 in promoting the progression to castration-resistant PCa (CRPC) of androgen-dependent PCa. Coll

ectively, our finding of the ADAM9/UBN2/AKR1C3 axis might be considered as a new driver in resistance to androgen-deprivation therapy of PCa progression .

建立代謝症候群動物模式及探索與氧化壓力和抗氧化防禦相關基因之表現圖譜

為了解決mt15 r15比較的問題，作者王旖云 這樣論述：

代謝症候群是包含了中樞型肥胖、系統性高血壓、胰島素阻抗及動脈粥狀硬化血脂異常 （特別是高三酸甘油酯血症和高密度脂蛋白膽固醇水平降低） 等所有疾病在內的狀態。其對腎臟的影響與許多併發症有關，主要表現為慢性腎衰竭和由此導致的終末期腎臟疾病。研究指出，與代謝症候群相關的胰島素阻抗和高胰島素血症被認為是引起腎臟發炎和纖維化的原因。氧化壓力在腎臟損傷中很重要，且已有文獻指出活性氧物質的活性升高可能以多種方式引起腎損傷。因此，在本研究中，我們試圖建立具有代謝症候群的大鼠模式，然後評估在具有代謝症候群的大鼠其氧化壓力基因的表現。在雄性 Wistar 大鼠餵食高脂飲食和腹膜內注射鏈脲佐菌素 （strepto

zotocin; STZ） 後，實驗動物的空腹血糖、三酸甘油酯、血清總膽固醇及血壓與血流量顯著升高，同時飲水量和尿液排出量也明顯上升，另外腎臟之鈉、鈣、鉀離子、尿蛋白及 urine LDH 等生化值也出現異常情形，顯示我們成功建立了代謝症候群的動物模式。我們將犧牲後老鼠的腎臟組織以氧化壓力 PCR 微陣列 （oxidative stress PCR microarray） 分析顯示腎臟組織中 heme oxygenase (decycling) 1 (Hmox1) 的表現水平顯著上升，而chemokine (C-C motif) ligand 5 (Ccl5)、glutathione S-tr

ansferase π 1 (Gstp1)、lactoperoxidase (Lpo)、myeloperoxidase (Mpo)、glutamate-cysteine ligase, catalytic subunit (Gclc)、glutathione peroxidase 6 (Gpx6)、recombination activating gene 2 (Rg2)、NAD(P)H dehydrogenase, quinone 1 (Nqo1) 和 selenoprotein P plasma 1 (Sepp1) 的表現水平顯著下降。利用 Real-time PCR、RT-PCR、IHC

以及 ELISA 的結果也證實了 CCL5 有下調節之情形。平行發現代謝症候群的大鼠其血液血清中之 CCL5 亦呈現下降。但有趣的是，測量控制組及代謝症候群組全血中之氧化壓力未上升反而略微下降，至於全血當中之抗氧化防禦能力則是未受影響。綜合以上，我們成功地建立大鼠代謝症候群動物模式並且發現在代謝症候群的大鼠腎臟中 Hmox1 gene 表現上升及有數個基因包括 Ccl5, Gstp1, Gclc, Gpx6, Rg2, Nqo1, and Sepp1表現下降。其中，我們發現 CCL5 在腎臟及血液血清中的下降或許可以當作一個指示代謝症候群情況的一個生物標記。