走在汽車革命的路上論文書籍站
Herman Miller的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列包括價格和評價等資訊懶人包
Herman Miller的問題，我們搜遍了碩博士論文和台灣出版的書籍，推薦海明威寫的 世界文學藏1：老人與海 和Ball, Joan P.的 Flux: Learning to Navigate Change in Times of Uncertainty都 可以從中找到所需的評價。
另外網站Herman Miller | 北歐櫥窗NORDIC也說明：早於1905 年，Herman Miller 的前身Star Furniture Company 即開始於美國密西根州的Zeeland 市，專門從事於高級歐洲複製居家家具生產。1923 年，由於D.J. DePree 和他 ...
這兩本書分別來自韋伯 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Herman Miller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 生物資訊及系統生物研究所 朱智瑋所指導 洪欣筠的 甲基化CpG 序列結構與機械性質之分子動態模擬研究 （2021），提出因為有 雙螺旋去氧核醣核酸、CpG島、DNA甲基化、五碳糖褶皺構型、分子動態模擬的重點而找出了 Herman Miller的解答。
最後網站它可能是個人電腦史上最重要的一張椅子：Herman Miller 和 ...則補充：而說到辦公椅，就很難不提Herman Miller 和其代表作Aeron——它不只是矽谷辦公室常駐成員，還乘載了上個世紀的科技史及人機互動之重。
世界文學藏1：老人與海
為了解決Herman Miller 的問題，作者海明威 這樣論述：
一名老漁夫在海上捕魚八十四天皆一無所獲，而第八十五天出現一條巨大馬林魚與之展開生死搏鬥。歷經兩天兩夜的對決後，老人終於刺死馬林魚，然而鯊魚卻接踵而至，老人因此陷入另一波混戰。 得獎紀錄 ★本書榮獲美國藝術文學院小說金質獎章 ★本書榮獲普立茲小說獎及諾貝爾文學獎 ★本書為美國文豪海明威的巔峰之作
Herman Miller進入發燒排行的影片
購物迴戰之 回饋展開
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Herman Miller SAYL 開箱＋乘坐心得
最近的腰都很新 感覺沒什麼使用 讚讚推
建議大家買椅子前都先坐坐看比較準唷
Aeron神椅ㄅ適合我的屁股嗚嗚
An Integrated Approach For Uncovering Novel DNA Methylation Biomarkers For Non-small Cell Lung Carcinoma
為了解決Herman Miller 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.
Flux: Learning to Navigate Change in Times of Uncertainty
為了解決Herman Miller 的問題，作者Ball, Joan P. 這樣論述：
Joan P. Ball is an associate professor of Marketing at St. John’s University, a researcher and a leadership coach. Joan works with emerging and established leaders to help them navigate flux, build resilience and develop an experimental mindset when faced with tricky transitions. The founder of WOMB
Lab, she works with individuals, teams and organizations to develop new tools to help leader navigate uncertain transitions and teach others to do the same. She has worked with leaders from companies like Verizon Media, Capital One and Herman Miller. She is based in New York City, New York.
甲基化CpG 序列結構與機械性質之分子動態模擬研究
為了解決Herman Miller 的問題，作者洪欣筠 這樣論述：
甲基化DNA為表觀遺傳修飾的一種，在DNA序列不改變的前提下，胞嘧啶中C5的氫原子被催化為甲基團，以微小的差異調控基因表達︒在人類啟動子中的CpG island(CGI)若被甲基化，基因表達量會隨著在CGI中的甲基化濃度越高而下降︒目前對甲基化DNA的理解是甲基化胞嘧啶不會改變雙螺旋DNA的二級結構，反而使局部CGI的磷酸根與五碳糖骨架活動能力下降，且也讓鹼基對間的堆疊結構改變。在這篇研究中，我們為了要暸解被甲基化的胞嘧啶在細節上如何改變CGI局部的DNA結構，設計七種序列為CpG的DNA，利用GROMACS 軟體進行全原子的分子動態模擬，藉著分析分子模擬軌跡檔並應用重原子彈性網路模型理解原
子間剛性的關係，我們瞭解到甲基化後的CpG DNA仍維持B型型態，也發現甲基化鹼基對與相鄰兩個鹼基對的堆疊結構改變︒甲基化胞嘧啶先影響與之相連的氮苷鍵穩定度與旋轉角度，再促使五碳糖轉變為O4’endo構型，改變的五碳糖褶皺構型延伸影響到骨架扭轉角，進而改變相鄰鹼基對的結構與分子穩定度︒藉著我們分子模擬得到的分析結果，我們為甲基化改變CGI局部DNA 結構的機制提供分子層級的看法︒