Fibrosis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

Exercise and Respiratory Diseases in Paediatrics

為了解決Fibrosis的問題，作者 這樣論述：

Craig Williams is Director of the Children’s Health and Exercise Research Centre (CHERC). As a Fellow of the American College of Sports Medicine and the British Association of Sport and Exercise Sciences, he is a passionate advocate for the health and well-being of young people. He has lectured in H

igher Education for the last 30 years and is currently based at University of Exeter, UK.　Patrick J Oades, PhD has been a Consultant Paediatrician at the Royal Devon and Exeter Foundation NHS Trust for over 25 years, providing care in neonatal, acute and community settings. He has a specialist inter

est in paediatric pulmonology and was Clinical Director of the Exeter Cystic Fibrosis Center and the SW Peninsula Cystic Fibrosis Services in the UK for more than a decade. As an advocate for the role of exercise in medicine, he has collaborated with the University of Exeter CHERC, to promote joint

working and innovation.

Fibrosis進入發燒排行的影片

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Fibrosis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

Guide to Pulmonary Fibrosis & Interstitial Lung Diseases: For Patients, Caregivers & Clinicians by Patients, Caregivers, & Clini

為了解決Fibrosis的問題，作者Emt-B, Noah Greenspan Pt Dpt Ccs 這樣論述：

Dr. Noah Greenspan, DPT, CCS, EMT-B is a Board-Certified Clinical Specialist in Cardiovascular and Pulmonary Physical Therapy with almost thirty years of cardiopulmonary physical therapy and rehabilitation experience. Dr. Greenspan began his professional career at the New York University (now Langon

e) Medical Center’s Rusk Institute of Rehabilitation Medicine, with clinical rotations in medical, surgical, orthopedic and neurologic rehabilitation, chest physical therapy and ultimately cardiovascular and pulmonary rehabilitation. From 1995-1999, he served as the chief physical therapist of the C

ardiac Prevention and Rehabilitation Center under the direction of Physiatrist, Horacio Pineda, MD and Cardiologist, Mariano Rey, MD. In 1998, he founded the Pulmonary Wellness & Rehabilitation Center, a Manhattan-based physical therapy practice specializing in the care of patients with cardiovascul

ar and pulmonary diseases and New York Wellness, a comprehensive outpatient physical therapy practice with orthopedic, cardiovascular and pulmonary, complex medical and airway clearance units. Under his direction, the Center has conducted over 100,000 exercise sessions and been named Best of the Uni

ted States in the area of cardiovascular and pulmonary physical therapy. In 2014, he founded the Pulmonary Wellness Research and Education Society (renamed the Pulmonary Wellness Foundation) with the objective of coupling excellence in respiratory care with educational material of the highest calibe

r, delivered free of charge to patients, their family members, caregivers and clinicians, and to support new research projects aimed at better understanding the impact of cardiopulmonary rehabilitation and lifestyle change on safety, efficacy, lung function and quality of life in people living with

pulmonary diseases. In 2017, Dr. Greenspan’s Ultimate Pulmonary Wellness was published and is also available to read online free of charge and his Ultimate Pulmonary Wellness Lecture & Webinar Series is also available to attend online. He is the principal investigator in three ongoing research proje

cts: The Impact of High Intensity Exercise on Pulmonary Function in Patients with Chronic Obstructive Pulmonary Disease (COPD); The Impact of High Intensity Exercise on Pulmonary Function in Patients with Idiopathic Pulmonary Fibrosis (IPF); and Safety and Efficacy of Cardiopulmonary Rehabilitation

in Patients with Pulmonary Hypertension (PH). A consummate educator, Dr. Greenspan has trained thousands of patients and hundreds of students and clinicians. From 1995-2003, he was on the faculty of New York University, during which time he was awarded the title of Master Clinician in the area of ca

rdiovascular and pulmonary physical therapy. He has since taught at Dominican College, New York Medical College, and Long Island University in the areas of Cardiovascular and Pulmonary Pathology, Diagnosis and Management. He has previously served as the Pulmonary Rehabilitation Fellowship Coordinato

r for St. Vincent’s Medical Center and the Weill Cornell Medical College. In response to the COVID Pandemic of 2019, Dr. Greenspan started a daily Coronavirus prevention program and later, the COVID Rehabilitation & Recovery Lecture Series, a COVID-Specific Online Bootcamp for COVID Survivors and Lo

ng Haulers and in October of 2020, he and Marion Mackles, PT, opened the PWF’s COVID Rehabilitation & Recovery Clinic at H&D Physical Therapy in NYC. Dr. Greenspan has served as the Federal Affairs Liaison representing the Cardiovascular and Pulmonary Section of the American Physical Therapy Associa

tion and on the Leadership Board of the American Lung Association of the Northeast. In addition to his role at the Center, Dr. Noah Greenspan is a New York State Emergency Medical Technician (EMT) and Advanced Cardiac Life Support Provider; a professional SCUBA Diving International Open Water Instru

ctor, and underwater naturalist, with a passion for shark photography; a musician, artist and clothing designer under the moniker, Noah G Pop!

潛藏危機：Musashi-1固有無序區域介導與神經退行性疾病相關蛋白之異常聚集

為了解決Fibrosis的問題，作者杜岱芸 這樣論述：

蛋白質病變(proteopathy)是退行性疾病的常見原因，通過錯誤折疊的蛋白質異常聚集形成類澱粉沉積症(amyloidogenesis)，從而導致破壞組織內的穩態。尤其是，近期研究表明細胞內具有固有無序區域 (intrinsically disordered regions)的蛋白容易進行液-液相分離(liquid-liquid phase separation)，從而在細胞中組裝蛋白質凝聚層(coacervates)。在本研究中，我們假設具有固有無序區域的蛋白質受環境壓力影響，促進異常折疊甚至形成聚集體，這將進一步形成澱粉樣斑塊(amyloid plaques)並在組織內堆積，導致蛋白質

病變。我們主要探討不僅是RNA結合蛋白、也是幹性基因的Musashi-1，是否與具有豐富IDR的Musashi-1 C-末端區域相互作用以進行液-液相分離，最終形成澱粉樣原纖維(amyloid fibrils)。為了確認哪些序列更易於形成澱粉樣蛋白，因此對Musashi-1的C-末端進行了序列連續刪除來取得不同長度的片段。我們的研究結果表明Musashi-1 C-末端面對不同pH值和鹽濃度會影響液-液相分離狀態，包含改變蛋白質相分離的出現時間、形狀和大小，隨著時間的推移，Musashi-1 C-末端也可以形成澱粉樣蛋白原纖維。而當在氧化壓力下，它會在細胞內誘導組裝應激顆粒與不可逆的聚集體的形成

，另一方面，當細胞同時表達Musashi-1 C-末端和內源性TDP-43，Musashi-1 C-末端誘導TDP-43從細胞核錯誤定位到細胞質。此外，Musashi-1 C-末端促進磷酸化和泛素化TDP-43。總結來說，我們提出了關於Musashi-1與神經退行性疾病相關蛋白相互作用導致異常聚集的新見解，這些發現有助於提供解決退行性疾病的新思路。