Independent agent的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列股價、配息、目標價等股票新聞資訊

Let Me Take You by the Hand: True Tales from London’’s Streets

為了解決Independent agent的問題，作者Kavanagh, Jennifer 這樣論述：

Jennifer Kavanagh worked in publishing for nearly thirty years, the last fourteen as an independent literary agent. Books she represented included world rights for Chinese Lives, an oral history of China just before the Tiananmen Square atrocity, and the British rights for classic American oral hist

orian Studs Terkel. Since leaving publishing, she has started and run a community centre in one of the poorest wards in London’s East End, started a mobile library for homeless people, volunteered at an asylum seeker centre in central London, and set up a microcredit programme for women in poverty i

n London, as well as in Africa. She has also been a prison visitor at Pentonville and Dorchester, and for six years was a research associate for the Prison Reform Trust, working with inmates and staff in many prisons round the country. In one of her previous books, Journey Home, she interviewed a nu

mber of homeless people, refugees and women in a refuge. She lives in central London, and talks to people on the streets on a daily basis. Jennifer is a Churchill Fellow and a Fellow of the Royal Society of Arts. She has published nine books of non-fiction and two novels., ,

Independent agent進入發燒排行的影片

Asiatic Acid和Rigosertib對T315I Bcr-Abl CML細胞凋亡 和有氧糖酵解的影響

為了解決Independent agent的問題，作者黃加 這樣論述：

Chronic myeloid leukemia （CML）是一種由 Bcr-Abl 融合基因引起的骨髓增殖性疾病 ，其中 T315I 突變使 CML 細胞對 imatinib 產生耐藥性 。第三代酪氨酸激酶抑製劑 ponatinib 雖然可以抑制 Bcr-Abl 激 酶 ，但也存在嚴重的副作用 。Warburg effect ，即有氧糖酵解，是腫瘤細胞獲取能量的重要來源 。先 前的研究證明 ，抑制 Warburg effect 可能是一種有前途的癌症治療策略 。本研究旨在探討 rigosertib 和 Asiatic Acid(AA)對 T315I 突變 CML 細胞 的影響及機制 。 R

igosertib 是一種非 ATP 競爭性多靶向 抑製劑 ，可抑制 CML 細胞增殖 。AA 是一種天然小分子藥物 ， 可誘導實體瘤細胞凋亡 。我們首先發現 AA 在 48 小時處理後抑制 K562、BaF3/p210 和 BaF3/T315I 細胞的增殖並誘導細胞凋亡 。 Rigosertib 和 AA 具有誘導 K562、BaF3/p210 和 BaF3/T315I 細胞凋亡的能力 。AA 在處理 48 後能 夠增加 c-caspase3/PARP 蛋白量表達 。Rigosertib 和 AA 在處理 48 小時後能夠下調 K562、 BaF3/p210 和 BaF3/T315I 細胞

HK1、HK2、HIF1α、PDK1 和 Glut1 Warburg effect 相關基因 mRNA 的表達 。Rigosertib 能夠誘導 K562、BaF3/p210 和 BaF3/T315I 細胞凋亡，並下調 HK2，PDK1 蛋白 表達與增加細胞週期的 G2/M 期停滯 。這些結果表明 ，rigosertib 和 AA 可通過抑制具有 T315I 突變 的 CML 細胞的 Warburg 效應來誘導生長抑制和細胞凋亡 。

Land of the Dead: A Stoker’’s Wilde Novel

為了解決Independent agent的問題，作者Hopstaken, Steven,Prusi, Melissa 這樣論述：

Bram Stoker and Oscar Wilde unite once more to battle spirits and demons invading our world. Third book in the series. Grimdark Magazine called the first book an addictive, clever and extremely fun horror adventure. Book 3 in the Stoker’s Wilde series!Booklist on the first book in this series, St

oker’s Wilde: Pass this volume on to readers who are hungry for more historical stories with a supernatural frame. Science and the supernatural collide in this terrifying tale of witches, reanimated corpses and spirits invading our world from beyond the grave. Bram Stoker and Oscar Wilde have return

ed to their lives in London after their adventures in the American West. Bram is managing a theatre and Oscar is rising to fame and planning his upcoming wedding when they are once again called upon to battle supernatural evil. Grief-crazed scientist Victor Mueller needs Bram’s unusual blood for his

mad quest to bring his dead wife back to life, and he’ll resort to kidnapping to get it. Meanwhile, a young medium named Lorna Bow runs fake séances in London under the thumb of an abusive uncle. When her mother Endora returns, Lorna learns the truth: they come from a long line of witches, and soon

Endora has awakened Lorna’s dormant powers. When the scientist and the witches combine forces, all Hell breaks loose. Long-dead souls find themselves back in the land of the living, and some of them have scores to settle with our heroes. But as Mueller’s ambition and her mother’s desire for vengean

ce against the men who imprisoned her become clear, Lorna soon finds herself questioning the morality of their work. Bram and Oscar must team up with American secret agent Cora Chase to protect all they hold dear. Only a mission into the Land of the Dead can stop Mueller and Endora from bringing bac

k more souls. Bram’s wife Florence must call on the monster-fighting skills she honed in America, and even Oscar’s bride Constance has to face new challenges as she learns how the supernatural has shaped her own history. In an adventure that spans continents - and even other worlds - they confront o

ld enemies and unknown dangers. Teaming up with old friends Teddy Roosevelt and Richard Burton and new allies like Arthur Conan Doyle and Nicola Tesla, they too must harness both science and magic to protect our world from intruders from the Land of the Dead. FLAME TREE PRESS is the imprint of long-

standing independent Flame Tree Publishing, dedicated to full-length original fiction in the horror and suspense, science fiction & fantasy, and crime / mystery / thriller categories. The list brings together fantastic new authors and the more established; the award winners, and exciting, origin

al voices. Learn more about Flame Tree Press at www.flametreepress.com and connect on social media @FlameTreePress

Melatonin inhibits chondrosarcoma cell metastasis by suppressing MMP7 expression

為了解決Independent agent的問題，作者NGUYEN BAO TRAN 這樣論述：

Chondrosarcoma is rare but has intense metastasis and limited response to chemotherapy and radiation treatment. Enzymatic activity of matrix metalloproteinase (MMP) family members has an important role in chondrosarcoma metastasis. Melatonin exhibits anticarcinogenic activity in many types of cance

rs by suppressing the expression of certain MMP family members, but this has not been clearly determined as yet in chondrosarcoma. Using a human protease array kit, this study analyzed the protein expression of two chondrosarcoma cell lines (JJ012 and SW1353) with and without melatonin treatment, re

vealing that matrix metalloproteinase-7 (MMP7) was among the top three proteins suppressed by melatonin. Further cell experiments showed that melatonin effectively suppresses proliferative and metastatic activities in chondrosarcoma cells. Moreover, melatonin suppressed anoikis resistance, as determ

ined by anchorage-independent growth under suspension conditions in an anoikis assay and by low quantities of chondrosarcoma cells in the circulation of an in vivo study. In nude BALB/c mice, melatonin significantly inhibited tumor growth and lung metastases. Cell culture revealed that overexpressio

n of MMP7 significantly promoted chondrosarcoma cell proliferation and migration, which was significantly inhibited by melatonin. A subsequent tissue array demonstrated significantly higher levels of MMP7 expression in chondrosarcoma tissue compared with normal cartilage tissue specimens; chondrosar

coma disease stage/grade was correlated with MMP7 expression. Next, a comparison of micro-RNA (miRNA) expression profiles of melatonin-treated and melatonin-untreated chondrosarcoma cells identified that several miRNAs were up-regulated in the melatonin-treated cells. A computational prediction was

performed using four publicly available miRNA databases (TargetScan, miRanda, miRMap and miRWalk) to predict miRNA targeting MMP7. The intersection of 11 candidate miRNAs identified miR-520f-3p as the most up-regulated miRNA in response to melatonin. Thus, our study suggests that melatonin reduces M

MP7 synthesis, chondrosarcoma cell motility and metastasis via the miR-520f-3p/MMP7 axis.Keywords: Chondrosarcoma, proliferation, metastasis, melatonin, MMP7, miR-520f-3p