冰冷的城市需要更多的綠手指論文書籍站
Pleural的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列問答集和整理懶人包
Pleural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 Pleural Disease, an Issue of Clinics in Chest Medicine, 42 和Popper, Helmut的 Pathology of Lung Disease: Morphology - Pathogenesis - Etiology都 可以從中找到所需的評價。
另外網站Pleural Definition & Meaning | Dictionary.com也說明：Save This Word! ... Anatomy. of or relating to the pleura. Entomology. of or relating to a pleuron. ... ARE YOU A TRUE BLUE CHAMPION OF THESE "BLUE" SYNONYMS?
這兩本書分別來自 和所出版 。
國立臺北科技大學 電資學院外國學生專班(iEECS) 白敦文所指導 VAIBHAV KUMAR SUNKARIA的 An Integrated Approach For Uncovering Novel DNA Methylation Biomarkers For Non-small Cell Lung Carcinoma （2022），提出Pleural關鍵因素是什麼，來自於Lung Cancer、LUAD、LUSC、NSCLC、DNA methylation、Comorbidity Disease、Biomarkers、SCT、FOXD3、TRIM58、TAC1。
而第二篇論文國立陽明交通大學 臨床醫學研究所 邱士華、王錦鈿所指導 羅永鴻的 環狀核糖核酸hsa_circ_0000190會促進非小細胞肺癌的發生並透過調升分泌之PD-L1而影響腫瘤逃脫免疫系統 （2021），提出因為有 肺癌、環狀核糖核酸、計畫性細胞死亡蛋白-1、免疫療法、免疫檢查點的重點而找出了 Pleural的解答。
最後網站Pleural Diseases - 第 81 頁 - Google 圖書結果則補充：A few basophils are usually present in pleural effusions with eosinophils . Basophil counts greater than 10 % are most common with leukemic pleural ...
Pleural Disease, an Issue of Clinics in Chest Medicine, 42
為了解決Pleural 的問題，作者 這樣論述：
Pleural進入發燒排行的影片
An Integrated Approach For Uncovering Novel DNA Methylation Biomarkers For Non-small Cell Lung Carcinoma
為了解決Pleural 的問題，作者VAIBHAV KUMAR SUNKARIA 這樣論述：
Introduction - Lung cancer is one of primal and ubiquitous cause of cancer related fatalities in the world. Leading cause of these fatalities is non-small cell lung cancer (NSCLC) with a proportion of 85%. The major subtypes of NSCLC are Lung Adenocarcinoma (LUAD) and Lung Small Cell Carcinoma (LUS
C). Early-stage surgical detection and removal of tumor offers a favorable prognosis and better survival rates. However, a major portion of 75% subjects have stage III/IV at the time of diagnosis and despite advanced major developments in oncology survival rates remain poor. Carcinogens produce wide
spread DNA methylation changes within cells. These changes are characterized by globally hyper or hypo methylated regions around CpG islands, many of these changes occur early in tumorigenesis and are highly prevalent across a tumor type.Structure - This research work took advantage of publicly avai
lable methylation profiling resources and relevant comorbidities for lung cancer patients extracted from meta-analysis of scientific review and journal available at PubMed and CNKI search which were combined systematically to explore effective DNA methylation markers for NSCLC. We also tried to iden
tify common CpG loci between Caucasian, Black and Asian racial groups for identifying ubiquitous candidate genes thoroughly. Statistical analysis and GO ontology were also conducted to explore associated novel biomarkers. These novel findings could facilitate design of accurate diagnostic panel for
practical clinical relevance.Methodology - DNA methylation profiles were extracted from TCGA for 418 LUAD and 370 LUSC tissue samples from patients compared with 32 and 42 non-malignant ones respectively. Standard pipeline was conducted to discover significant differentially methylated sites as prim
ary biomarkers. Secondary biomarkers were extracted by incorporating genes associated with comorbidities from meta-analysis of research articles. Concordant candidates were utilized for NSCLC relevant biomarker candidates. Gene ontology annotations were used to calculate gene-pair distance matrix fo
r all candidate biomarkers. Clustering algorithms were utilized to categorize candidate genes into different functional groups using the gene distance matrix. There were 35 CpG loci identified by comparing TCGA training cohort with GEO testing cohort from these functional groups, and 4 gene-based pa
nel was devised after finding highly discriminatory diagnostic panel through combinatorial validation of each functional cluster.Results – To evaluate the gene panel for NSCLC, the methylation levels of SCT(Secritin), FOXD3(Forkhead Box D3), TRIM58(Tripartite Motif Containing 58) and TAC1(Tachikinin
1) were tested. Individually each gene showed significant methylation difference between LUAD and LUSC training cohort. Combined 4-gene panel AUC, sensitivity/specificity were evaluated with 0.9596, 90.43%/100% in LUAD; 0.949, 86.95%/98.21% in LUSC TCGA training cohort; 0.94, 85.92%/97.37 in GEO 66
836; 0.91,89.17%/100% in GEO 83842 smokers; 0.948, 91.67%/100% in GEO83842 non-smokers independent testing cohort. Our study validates SCT, FOXD3, TRIM58 and TAC1 based gene panel has great potential in early recognition of NSCLC undetermined lung nodules. The findings can yield universally accurate
and robust markers facilitating early diagnosis and rapid severity examination.
Pathology of Lung Disease: Morphology - Pathogenesis - Etiology
為了解決Pleural 的問題，作者Popper, Helmut 這樣論述：
Helmut H. Popper gained his medical degree from the University of Graz, Austria, and subsequently undertook residency and fellowship training at the Institute of Pathology at the university. In 1985 he became Associate Professor of Pathology at the Institute and a year later, Head of the Laboratory
of Experimental Pathology. In 1993 Dr. Popper was appointed Professor of Pathology. Subsequent appointments in 2000 and 2008 were, respectively, as Head of Laboratories of Molecular Cytogenetics and Environmental and Respiratory Tract Pathology and Head of the Research Unit for Molecular Lung and Pl
eural Pathology. Dr. Popper has held a number of prestigious positions during his career, including as Chairman of the Pulmonary Pathology Group of the European Society of Pathology and President of the Austrian Society of Pathology. He is an associate editor of the journal Translational Lung Cancer
Research and a member of the editorial board of the Journal of Thoracic Oncology. He has received awards or medals for Continuous Medical Education from the Swedish Medical Society, the Russian and Turkish Thoracic Societies, and the Italian Pathologic Society.
環狀核糖核酸hsa_circ_0000190會促進非小細胞肺癌的發生並透過調升分泌之PD-L1而影響腫瘤逃脫免疫系統
為了解決Pleural 的問題，作者羅永鴻 這樣論述：
中文摘要................................................i英文摘要................................................ii目錄....................................................iv圖目錄..................................................vii表目錄..................................................viii第一章 緒論.................
............................1第二章 研究目的.........................................4第三章 研究方法.........................................53.1 Patient Population.................................53.2 Cell Culture.......................................63.3 RNA Isolation and qRT-PCR..........................63.4
qRT-PCT and RT-ddPCR for Detecting Plasma circRNA..73.5 RNA-Seq............................................83.6 Cell and Plasmid Preparation for Overexpressing Circular RNA....................................................83.7 Transfection with Small-Interfering RNA (siRNA)....93.8 Cell Prolifera
tion Assay...........................93.9 Migration and Invasion.............................93.10 Wound-Healing Assay...............................103.11 Animal Experiments................................103.12 Western Blotting Analysis.........................113.13 RNA Extraction and RT-qPCR....
....................123.14 Enzyme-Linked Immunosorbent Assay.................133.15 Evaluation of LC Treatment Efficacy...............133.16 Statistical Analysis..............................13第四章 結果.............................................144.1 Identification of Potential Secretory circRNA Biom
arker Candidates Using RNA-Seq...............................144.2. Validation of Expression of hsa_circ_0000190 and hsa_circ_0001649 in LC Cell Lines......................174.3 RT-ddPCR Detection of hsa_circ_0000190 and hsa_circ_0001649 Secreted by LC Cell Lines and in Human Blood Plasma...........
......................................194.4 Expression of hsa_circ_0000190 and hsa_circ_0001649 in LC Patients with Different Stages and Tumor Sizes.........214.5 Plasma Levels of Hsa_circ_0000190 Negatively Correlate with the Response to Immunotherapy.....................254.6 Monitoring the Treatm
ent Response by Plasma Levels of circRNAs in LC Patients Receiving Immunotherapy........284.7 Bioinformatics Analysis of Potential Downstream Network for Hsa_circ_0000190 and Hsa_circ_0001649 in LC........314.8 Overexpression of hsa_circ_0000190 Promoted Tumorigenesis of NSCLC In Vitro..............
........................324.9 Knockdown of hsa_circ_0000190 Hindered Tumorigenesis of NSCLC In Vitro.........................................354.10 Overexpression of C190 Enhanced Tumor Growth In Vivo...................................................374.11 Nanoparticle-Wrapped, siRNA-Mediated C190
Knockdown Inhibited Tumor Growth In Vivo.........................394.12 Interaction among hsa_circ_0000190, microRNA, and Various Immune Checkpoints.............................414.13 PD-L1, CD155, CD80, FGL1, and CD70 Were Expressed in A549 Cells.............................................434.14 O
verexpression of hsa_circ_0000190 Regulated Expression of Immune Checkpoints In Vitro.........................434.15 The Overexpression of hsa_circ_0000190 Promoted Expression of Specific Immune Checkpoint mRNAs in NSCLC Cells..................................................434.16 The Knockdown of
hsa_circ_0000190 by siRNA Impeded Expression of Specific Immune Checkpoint mRNAs in NSCLC Cells..................................................454.17 Overexpression of hsa_circ_0000190 Increased the Expression and Secretion of Soluble PD-L1 in NSCLC Cell Lines and May Be Associated with Decreased
Efficacy of Anti-PD-1 Antibody...............................................47第五章 討論.............................................49第六章 結論.............................................52參考文獻................................................53附錄....................................................63