coding醫學的問題，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資訊懶人包

Buck’s 2023 ICD-10-CM for Hospitals

為了解決coding醫學的問題，作者Elsevier 這樣論述：

Selecting diagnosis codes is faster and easier with Buck’s 2023 ICD-10-CM for Hospitals. Designed by coders for coders, this full-color manual includes all the ICD-10 codes that you need for today’s inpatient coding. As coders need extensive knowledge to code with ICD-10-CM - and to choose from t

he thousands of possible codes - this edition makes it easier with colorful anatomy plates (including Netter’s Anatomy illustrations) to help you understand anatomy and how it can affect your code choices. In addition, it comes with durable spiral binding, and includes a companion website with the l

atest coding updates.At-a-glance Guide to the 2023 ICD-10-CMUpdates in the front of the book lists all new, revised, and deleted codes, providing a quick lookup of the coding changes.Official Guidelines for Coding and Reporting (OGCRs) are listed in full in the Introduction, at the beginning of each

chapter, and integrated within the code set, providing easier reference to coding rules when they are needed most.Unique!Full-color anatomy plates (including Netter’s Anatomy art) are included in a separate section for easy reference and cross-referenced within the Tabular List of Diseases and Inju

ries, to help users understand anatomy and how it may affect choosing codes.Full-color design includesconsistent color-coded symbols and text, providing easier access to codes and coding information.American Hospital Association’s Coding Clinic(R)citations include official ICD-10-CM coding advice re

lating to specific codes and their usage.More than 190 illustrations providevisual orientation and enhance understanding of specific coding situations.Itemsare included throughout the Tabular List to ensure accurate coding, providing additional information on common diseases and conditions.Additiona

l elements within specific codes define terms and add coding instructionsrelating to difficult terminology, diseases and conditions, or coding in a specific category.Symbols and highlights draw attention to codes that may require special consideration before coding, including: New, revised, and dele

tedUnacceptable Principle DiagnosisCodes that call for the use of additional character(s)Includes, Excludes 1 and Excludes 2Use AdditionalUnspecifiedCode First and Code AlsoPlaceholder X symbol reminds users to assign placeholder X for codes less than 6 characters that require a 7th character.CC (Co

mplications & Comorbidities) and MCC (Major CC) symbols identify codes associated with the presence of secondary diagnoses from MS-DRGs, and call attention to CC and MCC exceptions.Hospital Acquired Condition symbol clearly identifies conditions that will always be coded as hospital acquired.Man

ifestation code symbol identifies conditions for which it is important to record both the etiology and the symptom of the disease.HCC symbol indicates diagnoses in the Tabular List associated with Hierarchical Condition Categories.Age and Sex edits from the Definition of Medicare Code Edits help to

ensure accuracy by denoting codes that are used only with patients of a specific age or sex.NEW! Updated2023 Official Code set reflects the latest ICD-10 codes needed for diagnosis coding.

coding醫學進入發燒排行的影片

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coding醫學的問題，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。

2023 ICD-10-PCs Expert

為了解決coding醫學的問題，作者 這樣論述：

DecisionHealth’s 2023 ICD-10-PCS Expert enables coders to familiarize themselves with valid code construction via tables rather than code lists, making this resource very easy to use. Quickly navigate the 16 sections and get up to speed on the PCS coding system with tables arranged by general pro

cedure type, and official guidelines for coding and reporting. Plus, all the knowledge required to assign the correct ICD-10-PCS codes!Stay HIPAA compliant and get easy-to-understand coding information from experts that you can rely on for accurate and efficient procedural coding.Features include: U

PDATED! All ICD-10-PCS codes and full descriptions--all 70,000+ ICD-10-PCS codes and their official code descriptions, listed sequentially for easy lookup. UPDATED! Official ICD-10-PCS Coding Guidelines--for assigning codes in the Medical, Surgical and Obstetrics sections UPDATED! Tables for code se

lection--organized into 16 sections for easy reference, each containing detailed tables that specify valid combinations of code values UPDATED! Instruction regarding ICD-10-PCS conventions--including the unique 7-character structure and its dependencies UPDATED! Coverage icons--identify non-covered

and limited coverage procedures UPDATED! Alphabetical index--listing procedures by keyword UPDATED! ICD-10-PCS coding scenarios--more than 100 procedure descriptions to test your use of the alphabetic index and code tables, with answers provided in the appendix

研究AGTPBP1在男性不孕症中於病理和生殖中所扮演的角色

為了解決coding醫學的問題，作者鄧日隆 這樣論述：

近年已婚夫婦患有不孕症日漸增多，發生率約有9 %，而其中近一半的病例與男方因素相關，目前研究表明基因的遺傳變異與男性不孕症具有相關性。男性不孕的主要原因之一是畸形性精子症 (Teratozoospermia)，其定義為超過 96% 的精子形態異常。研究中又指出異常形態精子經常伴有精子DNA缺陷。我們實驗室利用全外顯子定序 (WES, Whole exome sequence) 以及生物資訊分析(bioinformatic analysis)，從漢族及台灣人族群的12個畸形性精子症患者身上，鑑別尋找新穎的不孕相關基因。於其中兩個個案中，發現3個AGTPBP1變異位點，後續實驗室針對了AGTPB

P1基因變異進行深入的分析。AGTPBP (ATP/GTP Binding Protein ) 家族屬於ATP、GTP的結合蛋白，在小鼠中發現Agtpbp1基因主要表現於小腦、大腦皮質、額葉、睪丸、心臟、神經節及所有神經元中。另Agtpbp1低表現於骨骼肌、腎臟中。Agtpbp1轉譯的蛋白，包含armadillo-type fold和carboxypeptidase A domain。AGTPBP1的carboxypeptidase A domain參與蛋白轉譯後修飾，主要是從α-tubulin蛋白C-terminal去除過長的聚谷氨酸 (polyglutamates) 鏈修飾。聚谷氨酸修飾是

通過Tubulin tyrosine like family memeber 6 (Ttll6) 將這種修飾加於microtubules中。Agtpbp1被鑑定為Purkinje cell degeneration（pcd）小鼠表型中的突變基因。pcd突變在C57BR / cdJ中自發發生，其特徵是在成年初期時，小腦pcd細胞的缺失而導致的共濟失調。在本篇研究中，我們先尋找出和男性不孕症相關的新穎基因AGTPBP1，並對帶有AGTPBP1缺失的患者，使用免疫螢光染色法發現，AGTPBP1於精子的表現下降與表現位置錯誤，接著使用穿透式電子顯微鏡觀察到精子頭尾部結構缺陷。在動物模式上，我們使用免疫

螢光染色法分析野生型小鼠的睪丸切片及分離出來的精細胞 (male germ cell)，發現AGTPBP1會表現於精細胞造精過程後期late stage spermatocyte, elongated spermatids與mature sperm。並委託台大基因中心，產製Agtpbp1基因剃除小鼠。與Wild-type小鼠相比，體重、睪丸、副睪的重量都顯著下降，精液分析發現Agtpbp1del/del小鼠精子數量顯著減少、出現未分化完全的精子與精子活動力顯著下降。使用西方墨點法發現Agtpbp1del/del小鼠α-tubulin的Polyglutamylation異常累積，推測為缺失AGT

PBP1使α-tubulin polyglutamylation無法有效被去除。而穩定形態的α-tubulin (delta2-α-tubulin) 表現也減少。使用免疫螢光染色法證實，在Agtpbp1del/de小鼠的精細胞形態變化過程中，Polyglutamylation表現出錯誤累積在精細胞頸部，delta2-tubulin表現減弱且錯誤的表現在精細胞頸部。我們證實AGTPBP1的變異，影響了α-tubulin的轉譯後修飾作用，導致精細胞形態變化過程出現錯誤，產生出錯誤形態的精子。這些結果能作為提供臨床男性不孕個案中的參考依據。