出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/10/09 17:00:01」(JST)[Wiki en表示]
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- 1. 止血の概要 overview of hemostasis
- 2. 凝固検査の臨床使用 clinical use of coagulation tests
- 3. 悪性腫瘍に関連した凝固亢進状態の病因 pathogenesis of the hypercoagulable state associated with malignancy
- 4. 敗血症に対する治験剤および無効剤 investigational and ineffective therapies for sepsis
- 5. 成人における播種性血管内凝固の臨床的特徴、診断、および治療 clinical features diagnosis and treatment of disseminated intravascular coagulation in adults
- Resveratrol Restores Sirtuin 1 (SIRT1) Activity and Pyruvate Dehydrogenase Kinase 1 (PDK1) Expression after Hemorrhagic Injury in a Rat Model.
- Jian B, Yang S, Chaudry IH, Raju R.Author information Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.AbstractSevere hemorrhage leads to decreased blood flow to tissues resulting in decreased oxygen and nutrient availability affecting mitochondrial function. A mitoscriptome profiling study demonstrated alteration in several genes related to mitochondria, consistent with the mitochondrial functional decline observed after trauma hemorrhage (T-H). Our experiments led to the identification of sirtuin 1 (SIRT1) as a potential target in T-H. Administration of resveratrol (a naturally occurring polyphenol and activator of SIRT1) after T-H improved left ventricular function and tissue ATP levels. Our hypothesis was that mitochondrial function after T-H depends on SIRT1 activity. In this study, we evaluated the activity of SIRT1, a mitochondrial functional modulator, and the mitochondrial-glycolytic balance after T-H. We determined the changes in protein levels of pyruvate dehydrogenase kinase (PDK)-1 and nuclear c-Myc, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and NF-E2-related factor (NRF)2 after T-H and after treatment with resveratrol or a combination of sirtinol (a SIRT1 inhibitor) and resveratrol. We have also tested the activity of mitochondrial complex 1. SIRT1 enzyme activity was significantly decreased after T-H, whereas resveratrol treatment restored the activity. We found elevated PDK1 and c-Myc levels and decreased PGC-1α, NRF2 and mitochondrial complex I activity after T-H. The reduced SIRT1 activity after T-H may be related to declining mitochondrial function, since resveratrol was able to reinstate SIRT1 activity and mitochondrial function. The elevated level of PDK1 (an inhibitor of pyruvate dehydrogenase complex) after T-H indicates a possible shift in cellular energetics from mitochondria to glycolysis. In conclusion, SIRT1 modulation alters left ventricular function after T-H through regulation of cellular energetics.
- Molecular medicine (Cambridge, Mass.).Mol Med.2014 Dec 24;20(1):10-6. doi: 10.2119/molmed.2013.00077.
- Severe hemorrhage leads to decreased blood flow to tissues resulting in decreased oxygen and nutrient availability affecting mitochondrial function. A mitoscriptome profiling study demonstrated alteration in several genes related to mitochondria, consistent with the mitochondrial functional decline
- PMID 24395567
- Toxicity and bio-accumulation of inhaled cerium oxide nanoparticles in CD1 mice.
- Aalapati S1, Ganapathy S, Manapuram S, Anumolu G, Prakya BM.Author information 1Department of Toxicology, International Institute of Biotechnology and Toxicology [IIBAT] , Chennai , India.AbstractMale CD1 mice were subjected to nose-inhalation exposure of CeO2 nanoparticles (NPs) for 0, 7, 14 or 28 days with 14 or 28 days of recovery time at an aerosol concentration of 2 mg/m(3). Markers of lung injury and pro-inflammatory cytokines (interleukin-1beta, tumour necrosis factor-alpha, interleukin-6 and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid (BALF), oxidative stress in lungs, bio-accumulation, and histopathology of pulmonary and extrapulmonary tissues were assessed. BALF analysis revealed the induction of pulmonary inflammation, as evident by an increase in the influx of neutrophils with a significant secretion of pro-inflammatory cytokines that lead to generation of oxidative stress and cytotoxicity, as is evident by induction of lipid peroxidation, depletion of glutathione and increased BALF lactate dehydrogenase and protein. The histopathological examination revealed that these inhaled CeO2 NPs were located all over the pulmonary parenchyma, inducing a severe, chronic, active inflammatory response characterised by necrosis, proteinosis, fibrosis and well-formed discrete granulomas in the pulmonary tissue and tubular degeneration leading to coagulative necrosis in kidneys. Inductively coupled plasma optical emission spectrometer results showed a significant bio-accumulation of these particles in the pulmonary and extrapulmonary tissues, even after one month of post-inhalation exposure. Together, these findings suggest that inhalation exposure of CeO2 NPs can induce pulmonary and extrapulmonary toxicity.
- Nanotoxicology.Nanotoxicology.2014 Nov;8(7):786-98. doi: 10.3109/17435390.2013.829877. Epub 2013 Aug 22.
- Male CD1 mice were subjected to nose-inhalation exposure of CeO2 nanoparticles (NPs) for 0, 7, 14 or 28 days with 14 or 28 days of recovery time at an aerosol concentration of 2 mg/m(3). Markers of lung injury and pro-inflammatory cytokines (interleukin-1beta, tumour necrosis factor-alpha, interleuk
- PMID 23914771
- A murine model of airway fibrosis induced by repeated naphthalene exposure.
- Aoshiba K1, Tsuji T2, Itoh M2, Semba S2, Yamaguchi K3, Nakamura H2, Watanabe H2.Author information 1Department of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, Japan. Electronic address: email@example.comDepartment of Respiratory Medicine, Tokyo Medical University Ibaraki Medical Center, Japan.3Comprehensive and Internal Medicine, Tokyo Women's Medical University Medical Center East, Japan.AbstractThe airway epithelium serves as a biological barrier essential for host defense against inhaled pollutants. While chronic epithelial injury, commonly associated with chronic obstructive pulmonary disease and bronchiolitis obliterans syndrome, often results in airway fibrosis, limited animal models of airway fibrosis have been established. Club cells (Clara cells) in the small airways represent an important population of epithelial progenitor cells and also the principal site of localization of the cytochrome P-450 monooxygenase system, which metabolically activates xenobiotic chemicals such as naphthalene by converting them to toxic epoxide intermediates. We hypothesized that repeated exposure to naphthalene may cause prolonged loss of club cells, triggering aberrant local epithelial repair mechanisms that lead to peribronchial fibrosis. We administered intraperitoneal injections of naphthalene to C57/BL6J mice once a week for 14 consecutive weeks. Repeated club cell injury caused by naphthalene triggered regional hyperproliferation of epithelial progenitor cells, while other regions remained denuded or squamated, resulting in fibroblast proliferation and peribronchial collagen deposition associated with upregulation of the fibrogenic cytokines transforming growth factor-β and connective tissue growth factor. The total collagen content of the lung assessed by measurement of the hydroxyproline content was also increased after repeated exposure to naphthalene. These results lend support to the relevance of repeated injury of airway epithelial cells as a trigger for resting fibroblast proliferation and airway fibrosis. This model of airway fibrosis is simple and easy to reproduce, and may be expected to advance our understanding of the pathogenesis and potential treatment of airway fibrotic disorders.
- Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie.Exp Toxicol Pathol.2014 Jul;66(4):169-77. doi: 10.1016/j.etp.2014.01.001. Epub 2014 Jan 28.
- The airway epithelium serves as a biological barrier essential for host defense against inhaled pollutants. While chronic epithelial injury, commonly associated with chronic obstructive pulmonary disease and bronchiolitis obliterans syndrome, often results in airway fibrosis, limited animal models o
- PMID 24480153
- The Use of Bone Marrow Stromal Cells (Bone Marrow-Derived Multipotent Mesenchymal Stromal Cells) for Alveolar Bone Tissue Engineering: Basic Science to Clinical Translation
- Kagami Hideaki,Agata Hideki,Inoue Minoru,Asahina Izumi,Tojo Arinobu,Yamashita Naohide,Imai Kohzoh
- … Bone tissue engineering is a promising field of regenerative medicine in which cultured cells, scaffolds, and osteogenic inductive signals are used to regenerate bone. … Human bone marrow stromal cells (BMSCs) are the most commonly used cell source for bone tissue engineering. … Application of basic fibroblast growth factor helped to maintain the in vivo osteogenic ability of BMSCs. …
- NAID 120005447068
- Ki-67 is a strong prognostic marker of non-small cell lung cancer when tissue heterogeneity is considered
- Tabata Kazuhiro,Tanaka Tomonori,Hayashi Tomayoshi,Hori Takashi,Nunomura Sayuri,Yonezawa Suguru,Fukuoka Junya
- BMC Clinical Pathology 14(1), 23, 2014-05-13
- … Cox multivariate analysis of Ki-67 showed that HS was an independent risk factor affecting overall survival. …
- NAID 120005451798
- CCN2 as a Novel Molecule Supporting Energy Metabolism of Chondrocytes
- Maeda-Uematsu Aya,Kubota Satoshi,Kawaki Harumi,Kawata Kazumi,Miyake Yoshiaki,Hattori Takako,Nishida Takashi,Moritani Norifumi,Lyons Karen M.,Iida Seiji,Takigawa Masaharu
- Journal of Cellular Biochemistry 115(5), 854-865, 2014-05
- … CCN2/connective tissue growth factor (CTGF) is a unique molecule that promotes both chondrocytic differentiation and proliferation through its matricellular interaction with a number of extracellular biomolecules. …
- NAID 120005468290
- rheumatoid factor (RF) antibodies directed against antigenic determinants on IgG molecules, found in the serum of about 80 per cent of patients with classic or definite rheumatoid arthritis; but in only about 20 per cent of patients with ...
- 組織因子（tissue factor: TF）は細胞膜結合型の1本鎖糖蛋白質で，外因系血液凝固反応の開始因子である．TFは細胞表面のリン脂質層上でⅦ因子または活性化Ⅶ（Ⅶa）因子と複合体を形成し，Ⅸ因子およびⅩ因子を活性化させ ...
|リンク元||「第VIII因子」「組織因子」「prothrombinase」「TF」「coagulation factor III」|
|拡張検索||「tissue factor pathway inhibitor」|
- Thromboplastin, Tissue factor
- also Tissue factor
- factor VIII, FVIII
- 血漿トロンボプラスチン因子 plasma thromboplastin factor PTF
- 抗血友病グロブリン antihemophilic globulin、抗血友病因子A antihemophilic factor A platelet cofactor I、抗血友病因子
- 12 hr
- factor in, factor out
- factor in, factor out