Pulmonary fibrosis t的問題,透過圖書和論文來找解法和答案更準確安心。 我們找到下列地圖、推薦、景點和餐廳等資訊懶人包

Pulmonary fibrosis t的問題,我們搜遍了碩博士論文和台灣出版的書籍,推薦寫的 Oxidative Stress in Lung Diseases: Volume 2 和Alper, Scott (EDT)/ Janssen, William (EDT)的 Lung Innate Immunity and Inflammation: Methods and Protocols都 可以從中找到所需的評價。

這兩本書分別來自 和所出版 。

國立陽明交通大學 分子醫學與生物工程研究所 趙啟宏所指導 王慶弘的 探討CPT1C在類基底型乳癌中調控上皮-間質轉型及腫瘤幹細胞特性所扮演的角色 (2021),提出Pulmonary fibrosis t關鍵因素是什麼,來自於脂肪酸氧化、CPT1C、類基底型乳癌、上皮-間質細胞轉型、腫瘤幹細胞特性。

而第二篇論文國防醫學院 醫學科學研究所 余慕賢、張正昌所指導 蘇國銘的 透過基於基因本體之整合性分析識別卵巢上皮性腫瘤發病機轉的失調基因功能體 (2021),提出因為有 漿液性上皮性卵巢癌、卵巢清亮細胞癌、邊緣性卵巢腫瘤、基因本體、機器學習、整合性分析、補體系統、SRC基因、芳烴受體結合路徑、上皮細胞間質轉化的重點而找出了 Pulmonary fibrosis t的解答。

接下來讓我們看這些論文和書籍都說些什麼吧:

除了Pulmonary fibrosis t,大家也想知道這些:

Oxidative Stress in Lung Diseases: Volume 2

為了解決Pulmonary fibrosis t的問題,作者 這樣論述:

This is the second volume of the comprehensive, two-volume work on oxidative stress in lung diseases. Adopting a multidisciplinary approach, it demonstrates the cellular and molecular mechanisms associated with ROS (reactive oxygen species)-induced initiation and progression of a variety of lung dis

eases, such as COPD, emphysema, asthma, cystic fibrosis, occupational pulmonary diseases and pulmonary hypertension and discusses points for therapeutic intervention. The book also covers translational research and the latest research on prevention and therapeutics. Each chapter includes in-depth in

sights into the mechanisms associated with lung diseases and into identifying targets for drug development. Bridging the gap between fundamental and translational research, and examining applications in the biomedical and pharmaceutical industry, it is a thought- provoking read for basic and applied

scientists engaged in biomedical research. Prof. Sajal Chakraborti is a Professor of Biochemistry at the University of Kalyani, West Bengal, India. His research covers the role of proteases, oxidant and Ca2+ signalling in the pathogenesis of a variety of diseases. Prof. Chakraborti did is PhD fro

m Calcutta University (1982) and DSc from Kalyani University (2014). He did his post- doctoral research at Johns Hopkins University, University of Utah and New York Medical College. He received DBT-Senior overseas research award for his research at the Brain Institute, University of Florida, Gainesv

ille (1998-1999). He has been engaged in teaching and research in biochemistry for the past 40 years. He has published more than hundred original papers, 22 book chapters, 15 review articles and edited seven books published by Springer.Dr. Tapati Chakraborti is a Professor of Biochemistry at the Uni

versity of Kalyani, West Bengal, India. Her research focuses on the determination of the Mechanisms Associated with the Role of Proteases in the Oxidant-mediated Cellular Dysregulation of Pulmonary Vascular Endothelial and Smooth Muscle Cells. She received Ph.D. from the CSIR-Indian Institute of Che

mical Biology (affiliated to Jadavpur University, Kolkata in the year 1992 and did post-doctoral research at the Brain Institute, University of Florida, Gainesville, Florida during 1999-2002. Dr. Tapati Chakraborti has been actively involved in teaching and research for the past 30 years. She has pu

blished more than 80 original research papers, 18 book chapters, and 12 review articles. She also edited a book entitled "Proteases in human diseases" published by Springer in the year 2017.Prof. Rita Ghosh is a Professor of Biophysics in the Department of Biochemistry and Biophysics, University of

Kalyani, Kalyani, West Bengal, India. She did her MSc in Physics from Calcutta University and PhD from Saha Institute of Nuclear Physics, Kolkata. She did her post doctoral research at the Swiss Institute of Experimental Cancer Research, Lausanne, Switzerland (1991-1993). Her research covers mainly

in the area of cell biology.. She has been engaged in teaching and research for more than 30 years. She has published above 40 original research papers, review articles and books chapters. Prof. Nirmal K. Ganguly was the Director General of Indian Council of Medical Research (ICMR), New Delhi and th

e Director of PGIMER (Chandigarh) and National Institute of Biologicals (Noida). Dr. Ganguly is currently a Distinguished Professor, Global Health Strategies at New Delhi, India and the Chief Advisor of the Policy Centre for Biomedical Research, Translational Health Science & Technology Institute, F

aridabad, India and at Ganga Ram Institute for Postgraduate Medical Education & Research (GRIPMER). Dr. Ganguly has published over 780 research papers and has mentored 130 doctoral students leading to the fulfillment of Ph.D. dissertations as the Doctoral Advisor/Joint Advisor. Currently, Dr. Gangul

y also focuses on the Immunological Basis of Cancer as a major area of his research. Dr. Ganguly is a Fellow of the Imperial College Faculty of Medicine, London, the Royal College of Pathologists, London, the International Academy of Cardiovascular Sciences, Canada, the Third World Academy of Scienc

es, Italy, and the International Medical Sciences Academy, New Delhi. Dr. Ganguly is also a Fellow of all the National Academies of Sciences. He has received more than 119 awards, including 8 International and 111 National Awards. He has been honored with the prestigious Indian National Padma Bhusha

n Award presented to him by the President of India, on 26th January, 2008 in the field of Medicine.Dr. Narasimham L Parinandi is currently an Associate Professor in Department of Internal Medicine and Division of Pharmacology, The Ohio State University, Columbus, Ohio. Dr. Parinandi earned his Ph.D.

(1986) at the University of Toledo, Toledo, OH, USA. He did his post doctoral research (1986-90) at the Hormel Institute, University of Minnesota, where he was associated with Prof. Harald Schmid (a celebrity in the area of lipid biochemistry) and Prof. Ralph T. Holman (Member of the National Acade

my of Sciences, USA). He was a research scientist at the Johns Hopkins University School of Medicine (1998-2002). Dr. Parinandi also collaborated with Dr. Louis J. Ignarro, a recipient of the 1998 Nobel Prize in Physiology (for signaling properties of nitric oxide). He has published 120 original res

earch papers, reviews, and book chapters, and edited a book on Free Radicals and Antioxidant Protocols with Prof. William Pryor, the legendary Free Radical and Lipid Peroxidation Scientist. Dr. Parinandi is an Associate Editor of Cell Biophysics & Biochemistry (Springer). Dr. Parinandi has teaching

and mentoring experience of more than 37 years in the US universities and has mentored over 75 students in his laboratory at 4 major US universities.

探討CPT1C在類基底型乳癌中調控上皮-間質轉型及腫瘤幹細胞特性所扮演的角色

為了解決Pulmonary fibrosis t的問題,作者王慶弘 這樣論述:

代謝途徑重整是腫瘤的重要特徵之一,腫瘤細胞可藉由調控自身的代謝偏好而有利其在代謝壓力的情況下存活,並維持高速增生。有研究更進一步指出乳癌細胞傾向於透過調控脂肪酸氧化代謝的效率限制酶CPT1C來增加脂肪酸氧化的活性,進而促進細胞增生,甚至維持腫瘤幹細胞特性及產生抗藥性。因此,本研究旨在釐清類基底型乳癌是否透過調節CPT1C影響細胞脂肪酸氧化代謝的活性,進而誘發上皮-間質細胞轉型及腫瘤幹細胞特性。我們的先導結果指出,透過TCGA數據資料庫分析,CPT1C表現量在類基底型乳癌患者中高於其他乳癌類型,並在具有淋巴結轉移或遠端轉移的患者中具有較高的表現量;而在類基底型乳癌患者中,擁有較高CPT1C表現

量的族群同時存活率也較差。此外,在類基底型乳癌患者中,相較於其他CPT1同功酶(CPT1A、CPT1B), 唯有CPT1C的表現量和存活率呈現負相關。接著,正常類基底型人類乳腺上皮細胞中過度表現CPT1C會增加脂肪酸氧化代謝活性,同時也誘導上皮-間質細胞轉型、細胞遷移、侵襲,並且提升腫瘤幹細胞特性;反之,利用微小干擾RNA抑制類基底型乳癌細胞株的CPT1C表現則可降低腫瘤的發展。以上結果顯示CPT1C確實在類基底型乳癌細胞的高度上皮-間質細胞轉型及癌幹性中扮演不可或缺的角色,未來我將繼續探討調控CPT1C的分子機制及利用動物實驗進行驗證。我們的研究不僅對於新穎療法的開發有很大的幫助,也釐清現行

生酮飲食療法用於類基底型乳癌的謬誤。關鍵詞: 脂肪酸氧化、CPT1C、類基底型乳癌、上皮-間質細胞轉型、腫瘤幹細胞特性

Lung Innate Immunity and Inflammation: Methods and Protocols

為了解決Pulmonary fibrosis t的問題,作者Alper, Scott (EDT)/ Janssen, William (EDT) 這樣論述:

Part I: Lung Innate, Immunity, and Inflammation1. 500 Million Alveoli from 30,000 Feet: A Brief Primer on Lung AnatomyWilliam McKleroyand Kenneth Lyn-Kew2. Overview of Innate Lung Immunity and InflammationDavid W.H. Riches and Thomas R. MartinPart II: Isolation and Characterization of Lung Innate

Immune Cells3. Isolation and Characterization of Mononuclear Phagocytes in the Mouse Lung and Lymph Nodes Sophie L. Gibbingsand Claudia V. Jakubzick4. Isolation and Characterization of Mouse NeutrophilsNiki D.J. Ubags and Benjamin T. Suratt 5. Isolation and Characterization of Mouse Fibroblasts Ben

jamin L. Edelman and Elizabeth F. Redente6. Isolation of Rat and Mouse Alveolar Type II Epithelial CellsNicole L. Jansing, Jazalle McClendon, Hidenori Kage, Mitsuhiro Sunohara, Juan R. Alvarez, Zea Borok, and Rachel L. Zemans 7. Isolation and Characterization of Human Alveolar type II Cells Beata Ko

smider, Robert J. Mason, and Karim Bahmed 8. Air-liquid Interface Culture of Human and Mouse Airway Epithelial CellsDi Jiang, Niccolette Schaefer, and Hong Wei Chu9. Isolation and Characterization of Human Lung Myeloid CellsYen-Rei A. Yu and Robert M. Tighe10. Measurement of Protein Permeability and

Fluid Transport of Human Alveolar Epithelial Type II Cells under Pathological ConditionsXiaohui Fang and Michael A. Matthay 11. Measuring Innate Immune Function in Mouse Mononuclear PhagocytesJohn Matthew Craig and Neil Raj Aggarwal12. Measuring Neutrophil Bactericidal ActivityKenneth C. Malcolm13.

Modulation of Myeloid Cell Function Using Conditional and Inducible Transgenic ApproachesAlexandra L McCubbrey and William J. Janssen14. Modulation of Lung Epithelial Cell Function Using Conditional and Inducible Transgenic Approaches Adrianne L. Stefanski, Dorota S. Raclawska, and Christopher M. E

vans15. Computational Analysis of RNA-seq Data from Airway Epithelial Cells for Studying Lung DiseaseNathan D. Jackson, Lando Ringel, and Max A. Seibold 16. Application of Proteomics in Lung ResearchNichole A. Reisdorph, Cole Michel, Kristofer Fritz, and Richard Reisdorph 17. Application of Metabolo

mics in Lung ResearchNichole A. Reisdorph, Charmion Cruickshank-Quinn, Yasmeen Nkrumah-Elie, and Richard Reisdorph18. Functional Genomics in Murine MacrophagesFrank Fang-Yao Lee and Scott AlperPart III: Analysis of Lung Innate Immunity and Inflammation19. Assessment of Ozone-induced Lung Injury in M

iceVandy P. Stober and Stavros Garantziotis20. Lung Histological MethodsAneta Gandjeva and Rubin M. Tuder21. Intravital Microscopy in the Mouse LungYimu Yang, Joseph A Hippensteel, and Eric P Schmidt 22. Mouse Models of Acute Lung Injury and ARDSFranco R. D’Alessio 23. Mouse Models of AsthmaMagdale

na M. Gorska24. Animal Models of Pulmonary FibrosisDavid N. O’Dwyer and Bethany B. Moore25. Mouse Models of COPDKarina A. Serban and Irina Petrache26. Mouse Models of COPDKarina A. Serban and Irina Petrache27. Delivery of Therapeutics to the L

透過基於基因本體之整合性分析識別卵巢上皮性腫瘤發病機轉的失調基因功能體

為了解決Pulmonary fibrosis t的問題,作者蘇國銘 這樣論述:

上皮性卵巢癌(EOCs)在晚期或復發的婦科惡性腫瘤中常是致命的和頑固的,其中漿液性佔絕大多數而卵巢清亮細胞癌(OCCC)是僅次於漿液性上皮性卵巢癌的第二常見的上皮性卵巢癌。即便經過腫瘤減積手術後加上化學藥物治療後仍有不少的患者有著較差的預後或是復發,故整體而言,對於卵巢癌的治療仍是一個相當大的挑戰。此外,邊緣性卵巢腫瘤(BOT),包括漿液性 BOT與黏液性BOT,是屬於介於良性與惡性之間的卵巢疾病,雖然大部分的預後不差但是也有與卵巢癌不同的組織病理學特性。本研究使用以基因本體(GO)為基礎加上機器學習輔助運算的綜合分析去探討卵巢清亮細胞癌以及漿液性卵巢腫瘤包含漿液性邊緣性卵巢腫瘤與漿液性卵巢

癌的GEO資料庫中失調的基因體、功能途徑,藉以去識別重要的差異表達基因(DEG)。首先在卵巢清亮細胞癌的整合性分析中,發現無論是早期抑或是晚期,與免疫功能相關尤其是活化補體系統的替代途徑的功能失調在腫瘤發生佔有相當重要的關聯性,而補體C3與補體C5也影響了疾病無惡化存活期(Progression-free survival, PFS)和整體存活率(Overall survival, OS)且免疫染色結果是有意義的。而在漿液性卵巢腫瘤的分析中發現,SRC基因和功能失調的芳烴受體(AHR)結合路徑(Binding pathway)確實影響PFS和OS,而且與上皮細胞間質轉化(Epithelial-

mesenchymal transition, EMT)相關的鋅指蛋白SNAI2在腫瘤發生過程中有重要角色,並顯示出從漿液性 BOT 到卵巢癌有著逐漸上升的影響趨勢。未來,標靶治療可以專注於這些有意義的生物標誌並結合精確監測,以提高治療效果和患者存活率。