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Wonder Woman: Her Greatest Victories《神力女超人1984》電影書封漫畫

為了解決神力女超人1984 續集的問題，作者Various 這樣論述：

改編自DC漫畫，全球票房超過8億美元《神力女超人》續集! 《神力女超人1984》終極漫畫導覽書!   　　《神力女超人1984》改編自DC漫畫，是繼2017年全球票房超過8億美元，賣座的《神力女超人》DC超級英雄首部的續集。   　　美如阿芙蘿黛蒂，智慧如雅典娜女神。卻行動敏如荷米斯，肌力強過海克力斯。這是DC漫畫給神力女超人的註解。美艷卻又強壯，長居在無男人的亞馬遜女人國(Themyscira)，俗稱天堂島。公主黛安娜，因為一個男人的闖入，離開了自己的家鄉。來到現代化的城市，在彼岸化名黛安娜普林斯(Diana Prince)。   　　自從1941年第一

次出場，風靡超過一甲子。DC宇宙元老級超級英雄，經典不墜。2017年，為擴展自身的DC宇宙觀，神力女超人再次搬上大螢幕，主演的蓋兒加朵(Gal Gadot)，創造一股新旋風。再續神力女超人傳奇。   　　《神力女超人1984》故事設定於1980年代的冷戰時期，「神力女超人」黛安娜普林斯在此對上了兩個全新的敵人：麥斯威爾洛德和豹女。看來自亞馬遜族的女戰士，如何力挽狂瀾；面對勁敵的陰謀，與誰結盟合力對抗。整部作品風格與首集不同，將是一部全然不同的故事。   　　電影由首集導演派蒂珍金斯(Patty Jenkins)回歸執導，根據DC漫畫的角色而來。導演在幕後的團隊來自《神力

女超人》，包括攝影指導馬修詹森，奧斯卡提名的製作設計《艾蜜莉的異想世界》艾琳班尼托，以及奧斯卡服裝設計《酣歌暢戲》琳蒂漢明。   　　《神力女超人1984》漫畫主要講述亞馬遜族公主的故事，以及神力女超人最大的盟友與敵人，由業界最頂尖的作者與藝術家撰寫，更多故事搶先曝光，讓影迷不用再痴痴等待電影上映，絕對是電影《神力女超人1984》的終極漫畫導覽書!    　　Prepare for the highly anticipated movie Wonder Woman 1984, the sequel to the 2017 blockbuster hit Wonder

Woman starring Gal Gadot, with this trade paperback featuring stories about the Princess of the Amazons from some of the best writers and artists in the industry!   　　This is the ultimate graphic novel companion collection to the Wonder Woman 1984 movie, premiering in 2020. This graphic novel co

ntains stories from legendary writers and artists, and features Wonder Woman's greatest allies and enemies.  

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An Integrated Approach For Uncovering Novel DNA Methylation Biomarkers For Non-small Cell Lung Carcinoma

為了解決神力女超人1984 續集的問題，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.