clot醫學的問題,透過圖書和論文來找解法和答案更準確安心。 我們找到下列股價、配息、目標價等股票新聞資訊

clot醫學的問題,我們搜遍了碩博士論文和台灣出版的書籍,推薦Kartha, C. C. (EDT)/ Ramachandran, Surya (EDT)/ Pillai, Radhakri寫的 Mechanisms of Vascular Defects in Diabetes Mellitus 和Smithson, J. P./ Wetzel, Brian, M.d.的 Von Willebrand Disease: Causes, Tests, and Treatment Options都 可以從中找到所需的評價。

另外網站血塊- A+醫學百科也說明:血塊(blood—clot,blood—cake). 血液因為各種原因(外傷、炎症、腫瘤等)流出血管或循環停止時,便凝固成為暗紅色的團塊,一般稱為血塊,也稱為血餅.

這兩本書分別來自 和所出版 。

國防醫學院 藥理學研究所 李燕媚所指導 謝銘城的 水飛薊素對熱中暑導致大鼠多重器官功能不良及發炎反應的保護作用 (2021),提出clot醫學關鍵因素是什麼,來自於水飛薊素。

而第二篇論文臺北醫學大學 牙醫學系博士班 吳慶榕、李宜達所指導 VO THI THUY TIEN的 Mechanisms of Anticancer Activities of Surfactin from Bacillus subtilis in Oral Squamous Cell Carcinoma (2021),提出因為有 表面活性素、口腔鱗狀細胞癌、細胞凋亡、自噬、細胞週期停滯、活性氧類的重點而找出了 clot醫學的解答。

最後網站Health Help: Veins and blood clots - 首頁| Living with VTE則補充:Veins and blood clots ... Venous thromboembolism is a clot inside a vein. ... 心臟科專科醫生李樹堅指,醫學研究數據顯示一至兩成中風患者都是曾經有過房顫的 ...

接下來讓我們看這些論文和書籍都說些什麼吧:

除了clot醫學,大家也想知道這些:

Mechanisms of Vascular Defects in Diabetes Mellitus

為了解決clot醫學的問題,作者Kartha, C. C. (EDT)/ Ramachandran, Surya (EDT)/ Pillai, Radhakri 這樣論述:

This book intends to bring together, a panel of renowned experts in the field of vascular biology and diabetology, to integrate the current understanding of the pathogenesis and pathophysiology of vascular diseases in diabetes mellitus. This attempt is significant given the increasing interest in

this area as the prevalence of vascular diseases continues to escalate globally. Patients with diabetes are at a higher risk of structural and functional changes in all vessel walls of the human body. Vascular complications of diabetes are leading causes for both morbidity and mortality.In recent y

ears, several articles have focused on advancing our knowledge on the profound effect of hyperglycemia and insulin resistance on building up vascular wall inflammation leading to endothelial dysfunction in patients with diabetes mellitus Other reports have elaborated on the various disorders, hyperg

lycemia can lead to, their therapies, adverse effects and complications. There are also studies that highlight the role of factors that induce vascular wall alterations in hyperglycemia. In this book, we attempt to discuss vascular disease progression in diabetes with a unique approach. We attempt t

o provide a complete perspective of the pathophysiology of vascular complications and then dissect each of the factors that play a key role in accelerating vascular wall alterations in diabetes. Each of these factors has been adversely implicated in the initiation and progression of disease to a lar

ge extent. In this collection for the first time all these factors would be described under a common canopy. Further, the text would emphasize on pathogenesis of micro vascular complications of diabetes, such as retinopathy, neuropathy and nephropathy. Pharmacological therapies for treating vascular

dysfunction in diabetes mellitus would also be reviewed. This compendium hopefully would be an invaluable replacement to scores of literature on diabetic vascular disease and would be of great interest to clinicians, academicians, medical students and researchers.The book will be divided into seven

sections, each emphasizing a common incentive to development of vascular disease in diabetes. Section I deals with pathophysiology of diabetic vascular disease, beginning with an update on the global burden of diabetes mellitus and its vascular complications. The pathophysiology and pathogenesis of

diabetes associated macrovasculopathy, how hyperglycemia functions as an atherogenic factor, effects of hyperglycemia on smooth muscle accumulation in vascular lesions and genetic susceptibility for increased risk of vascular disease in diabetes will be discussed in the following chapters of this s

ection.The next section (Section II) surveys the process of endothelial dysfunction under hyperglycaemia and hyperinsulinemia and their effects on angiogenesis, vascular remodeling and wound healing. A chapter is also dedicated to the endothelial progenitor cell population and its dysfunction during

development of vascular complications in diabetes.Section III will highlight the molecular mechanisms underlying endothelial dysfunction, various pathways such as nitric oxide synthase pathway, oxidative stress pathway, renin - angiotensin system and increased vascular superoxide production in the

initiation and progression of vascular disease in diabetes. This section also covers role of endothelin, monocyte derived cytokines, peroxynitrate and adipokines in macrovascular complications of diabetes.Metabolic factors such as advanced glycation end products, atherogenic dyslipoproteinaemia, and

homocysteine will be reviewed in Section IV, whereas an overview of the hemostatic factors such as platelet dysfunction, hyperglycaemia induced thrombin formation and aberrant clot lysis will be dwelled upon in Section V.Section VI includes chapters on microvascular complications of diabetes which

encompasses long term complications of diabetes affecting small blood vessels of the eye, kidneys and nervous system. The pathogenesis and mechanisms of these complications would be detailed here.The final section (Section VII) of the book will consider mechanism of action of drugs for treating endo

thelial dysfunction in diabetes mellitus which would elaborate on lipid regulating therapies such as statins, as well as other therapies such as ACE inhibitors, Angiotensin II receptors, insulin, metformin and their effects on enhancing vascular function in diabetes.We intend to invite authors who s

ymbolize a multidisciplinary approach to this complicated disease. The proposed authors include clinicians who understand the trend of vascular complications in their long term clientele, epidemiologists with a holistic view, basic and experimental researchers with years of experience in dissecting

the factors leading to endothelial dysfunction and clinical researchers with the skill of translating bench work to the bedside. We expect this book will be of significant value and interest to the same group of clinicians, researchers, post doctoral fellows and medical and non medical graduate stud

ents. The novel assimilated insights could stimulate development of mechanism based prevention and therapeutic strategies providing a promising option to limit cardiovascular complications in diabetes mellitus.

水飛薊素對熱中暑導致大鼠多重器官功能不良及發炎反應的保護作用

為了解決clot醫學的問題,作者謝銘城 這樣論述:

全球暖化增加了與熱相關的疾病發生和死亡的風險。與熱有關的疾病包括:熱痙攣、熱暈厥、熱衰竭和熱中暑。在熱中暑期間,熱壓力會引起氧化壓力和全身性炎症反應,導致多器官功能障礙。水飛薊素 (silymarin; SM) 是從水飛薊中提取的類黃酮混合物,具抗氧化和抗炎作用。因此,本研究評估預處理SM是否可改善大鼠熱中暑引起的多重器官功能不良和死亡。雄性Wistar大鼠分成四組:(1)對照組 (control; CTL) 組:給予大鼠carboxymethylcellulose (CMC;~0.3 cc,口服管餵) 每天一次,持續 7 天,未給予熱壓力;(2) 單獨SM:每天1次給予大鼠SM (

100 mg/kg,口服管餵),連續7天,未給予熱壓力; (3) 熱中暑 (heat stroke; HS) 組:大鼠用CMC預處理7天,再置於烘箱中(42 ℃),使核心體溫升高至42.5 ℃;(4) SM+HS組:大鼠給以SM (100 mg/kg,口服管餵) 持續7天,再置於烘箱中 (42 ℃),使核心體溫升高至42.5 ℃。移出烘箱後,將大鼠置於室溫 (24 ℃) 監測大鼠核心體溫、血壓及心跳變化。實驗結果顯示,與HS 組相比,SM預處理 (SM+HS 組) 顯著提高了熱中暑後六小時大鼠的存活率;於第六小時,HS和SM+HS組存活大鼠之核心體溫和平均動脈血壓無顯著差異,但 SM顯著降低血

漿中 CK-MB、GPT、creatinine、CPK和LDH 濃度,改善器官功能。SM可以減少肺臟的iNOS、NLRP3、ASC-1、IL-18、NF-κB等促發炎相關蛋白,並降低細胞凋亡蛋白cleaved caspase 3含量;SM未明顯誘導產生細胞保護蛋白HSP70 及HO-1,以及自噬作用相關蛋白beclin-1和LC3B。在肝臟,SM亦可以減少促發炎相關蛋白iNOS及NF-κB 表現量,降低細胞凋亡蛋白 Bax 及cleaved caspase 3,並增加抗凋亡Bcl-2含量;SM 可顯著誘導產生細胞保護蛋白HSP70 及HO-1,但不影響自噬蛋白p62 及LC3B 之表現量。由以

上實驗結果可知:預先給予SM可以提高熱中暑存活率並改善多重器官功能不良,也可降低熱中暑後肺臟及肝臟之發炎反應,抑制細胞凋亡,但不影響自噬作用;可在肝臟組織誘發保護性蛋白HSP70 及HO-1產生,可以藉此減輕熱傷害而產生肝臟保護作用。

Von Willebrand Disease: Causes, Tests, and Treatment Options

為了解決clot醫學的問題,作者Smithson, J. P./ Wetzel, Brian, M.d. 這樣論述:

Von Willebrand disease (VWD) is a type of bleeding disorder that interferes with your body's ability to clot blood. Normally, your blood clots to prevent excessive bleeding if you suffer from a cut or a scrape. If your blood doesn't clot, the bleeding may not stop and may be heavy or severe. In s

ome rare cases, the excessive bleeding may lead to death. Early diagnosis of von Willebrand disease is vital. With proper treatment plan, people with all types of von Willebrand disease are able to live normal, full lives.

Mechanisms of Anticancer Activities of Surfactin from Bacillus subtilis in Oral Squamous Cell Carcinoma

為了解決clot醫學的問題,作者VO THI THUY TIEN 這樣論述:

背景:口腔癌是全球各個地區,特別是南亞地區日益嚴重的健康問題。口腔鱗狀細胞癌(OSCC)是一種侵襲性惡性腫瘤,具有較高的局部轉移現象和不良癒後特性,佔所有口腔癌病例的90%。先前研究發現,來自枯草芽孢桿菌的表面活性素是一種有效的生物表面活性劑,能夠對多種癌症產生細胞毒性作用。雖然一些研究數據顯示,在一些頭頸部癌細胞模型中,枯草芽孢桿菌的代謝物具有抗癌活性,但沒有一個研究數據是有關於枯草芽孢桿菌的表面活性素。此外,其抗癌作用背後的潛在機制仍須進一步釐清和探討。目的:本論文研究目的是探討有關枯草芽孢桿菌表面活性素在OSCC治療中的抗癌潛力。此外,我們也探討了表面活性素的抗癌作用之訊息傳遞路徑,以

促使未來能應用於臨床上。方法:使用兩種人類OSCC細胞株(SCC4和SCC25)進行研究。首先,透過使用PrestoBlueTM細胞活性試劑來評估細胞存活性,偵測枯草芽孢桿菌表面活性素在不同濃度(5,10,15和30 uM)下對OSCC細胞的細胞毒性作用,同時也與人類牙齦纖維母細胞和人類口腔角質細胞相比較。根據細胞活性測定的數據,我們證明30 uM的表面活性素對OSCC細胞具有抗癌作用。為了探討其潛在機制,在表面活性素處理細胞前,先使用特定的藥理性抑製劑或小分子干擾核糖核酸來處理OSCC細胞,然後進行多項實驗以評估各個訊息傳遞分子的表現量,並釐清各分子間的上下游關係。另外,我們也透過DAPI染

色來檢測細胞凋亡現象、使用吖啶橙染色觀察自噬作用、透過西方墨點法、酵素結合免疫吸附分析法和即時聚合酶連鎖反應等方法來分析表面活性素的抗癌機制、使用JC-1染劑來測定粒線體膜電位的變化,及用Fluo-3 / AM探針鑒定鈣離子濃度。最後,我們透過測量細胞內及粒線體ROS的生成和NADPH氧化酶的活性來評估ROS的整體概況。結果:枯草芽孢桿菌的表面活性素可以有效地殺死OSCC細胞,呈劑量和時間依賴性趨勢。表面活性素對OSCC細胞存活的抑制是由細胞凋亡,自噬和細胞週期停滯之間的相互作用引起的,其中ROS和NADPH氧化酶扮演非常重要的角色,因為我們的研究結果證明表面活性素是透過誘發大量的ROS來造成

細胞凋亡的。此外,我們也進一步發現另一條抗癌途徑,即NADPH氧化酶/ROS/內質網壓力/鈣離子,透過該訊息傳遞路徑,表面活性素也能有效地殺死OSCC細胞。有趣的是,表面活性素還可能導致OSCC細胞的自噬作用,最後,我們證明表面活性素可以藉由影響細胞週期相關蛋白來造成OSCC的細胞凋亡現象。結論和相關性:來自枯草芽孢桿菌中的表現活性素是一種非常有前途的抗癌藥物,具有多方面的抗癌機制。儘管如此,我們未來還需要更多詳細的細胞及動物實驗來釐清更多的機轉,以確保表面活性素應用於臨床上的可能性,但是現階段,我們至少已經為許多口腔癌患者提供了一個新的治療策略。