WordNet
- the 20th letter of the Roman alphabet (同)t
PrepTutorEJDIC
- technical knockout
- tritiumの化学記号
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/01/16 18:25:26」(JST)
[Wiki ja表示]
TKO
- テクニカルノックアウト (Technical Knock Out) の略。
- TKO (お笑いコンビ) - 松竹芸能所属のお笑いコンビ
- TKO (格闘技団体) - カナダを中心に活動する総合格闘技の団体
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[Wiki en表示]
TKO may refer to:
In sports
- Technical knockout, a professional fighting term.
- Takeo Spikes, linebacker in the NFL
- A variation of cutter, a professional wrestling move
In music
- "T.K.O. (Boxing Day)", a song from Elvis Costello's Punch the Clock album
- "TKO" (Le Tigre song), a song from Le Tigre's This Island
- "T.K.O." (Giant Panda song), single by Giant Panda
- "TKO", a song from Jesse Malin's The Fine Art of Self Destruction album
- TKO (band) a rock band from Seattle, Washington
- TKO, a pop group led by Katie White
- TKO-HQ, a jam band based in Dublin, Ireland
- "Love T.K.O.", a song by Teddy Pendergrass
- "TKO", a track on the Sam & Max Season Two Soundtrack
- "TKO" (Justin Timberlake song), a 2013 song by Justin Timberlake
- "TKO" (Motion City Soundtrack), a 2015 song by Motion City Soundtrack.
Other
- "TKO" (Babylon 5), an episode of Babylon 5
- T.K.O. (film), a 2007 film starring Dianna Agron
- The Kindness Offensive, a North London group known for random acts of kindness
- Taylor KO Factor, a measurement of the stopping power of a firearms cartridge
- The Kill Order, the prequel to The Maze Runner series
- TKO Software, a defunct software company
- Tseung Kwan O, a new town in Hong Kong
- MTR station code for Tseung Kwan O Station
- Triple knockout, in molecular biology
- "To keep open", a medical acronym for an intravenous drip that is flowing just enough to keep the IV open for future use (sometimes written as KVO - "keep vein open")
- Three Kingdoms Online, a browser based strategy game
- "Test Kit Obsolescence", a term used to describe the process of establishing equivalence between existing and new diagnostic test kit performance
English Journal
- Iliosacral screw insertion using CT-3D-fluoroscopy matching navigation.
- Takao M1, Nishii T2, Sakai T3, Yoshikawa H3, Sugano N2.Author information 1Department of Orthopaedic Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address: masaki-tko@umin.ac.jp.2Department of Orthopaedic Medical Engineering, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.3Department of Orthopaedic Surgery, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.AbstractBACKGROUND: Percutaneous iliosacral screw insertion requires substantial experience and detailed anatomical knowledge to find the proper entry point and trajectory even with the use of a navigation system. Our hypothesis was that three-dimensional (3D) fluoroscopic navigation combined with a preoperative computed tomography (CT)-based plan could enable surgeons to perform safe and reliable iliosacral screw insertion. The purpose of the current study is two-fold: (1) to demonstrate the navigation accuracy for sacral fractures and sacroiliac dislocations on widely displaced cadaveric pelves; and (2) to report the technical and clinical aspects of percutaneous iliosacral screw insertion using the CT-3D-fluoroscopy matching navigation system.
- Injury.Injury.2014 Jun;45(6):988-94. doi: 10.1016/j.injury.2014.01.015. Epub 2014 Jan 19.
- BACKGROUND: Percutaneous iliosacral screw insertion requires substantial experience and detailed anatomical knowledge to find the proper entry point and trajectory even with the use of a navigation system. Our hypothesis was that three-dimensional (3D) fluoroscopic navigation combined with a preoper
- PMID 24507831
- Loss of tet enzymes compromises proper differentiation of embryonic stem cells.
- Dawlaty MM1, Breiling A2, Le T3, Barrasa MI1, Raddatz G2, Gao Q1, Powell BE1, Cheng AW4, Faull KF5, Lyko F2, Jaenisch R6.Author information 1Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.2Division of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, 69120 Heidelberg, Germany.3Pasarow Mass Spectrometry Laboratory, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Ahmanson Translational Imaging Division, University of California, Los Angeles, Los Angeles, CA 90095, USA.4Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Computational and Systems Biology Program, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.5Pasarow Mass Spectrometry Laboratory, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.6Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Electronic address: jaenisch@wi.mit.edu.AbstractTet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and are dynamically expressed during development. Whereas loss of individual Tet enzymes or combined deficiency of Tet1/2 allows for embryogenesis, the effect of complete loss of Tet activity and 5hmC marks in development is not established. We have generated Tet1/2/3 triple-knockout (TKO) mouse embryonic stem cells (ESCs) and examined their developmental potential. Combined deficiency of all three Tets depleted 5hmC and impaired ESC differentiation, as seen in poorly differentiated TKO embryoid bodies (EBs) and teratomas. Consistent with impaired differentiation, TKO ESCs contributed poorly to chimeric embryos, a defect rescued by Tet1 reexpression, and could not support embryonic development. Global gene-expression and methylome analyses of TKO EBs revealed promoter hypermethylation and deregulation of genes implicated in embryonic development and differentiation. These findings suggest a requirement for Tet- and 5hmC-mediated DNA demethylation in proper regulation of gene expression during ESC differentiation and development.
- Developmental cell.Dev Cell.2014 Apr 14;29(1):102-11. doi: 10.1016/j.devcel.2014.03.003.
- Tet enzymes (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) and are dynamically expressed during development. Whereas loss of individual Tet enzymes or combined deficiency of Tet1/2 allows for embryogenesis, the effect of complete loss of Tet activity and 5hmC marks in d
- PMID 24735881
- Liver Tumor Promotion by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin is Dependent on the Aryl Hydrocarbon Receptor and TNF/IL-1 Receptors.
- Kennedy GD1, Nukaya M, Moran SM, Glover E, Weinberg S, Balbo S, Hecht SS, Pitot HC, Drinkwater NR, Bradfield CA.Author information 1Department of Surgery, University of Wisconsin, School of Medicine and Public Health, Madison, WI.AbstractWe set out to better understand the signal transduction pathways that mediate liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxn ("dioxin"). To this end, we first employed congenic mice homozygous for either the Ahrb1 or Ahrd alleles (encoding an aryl hydrocarbon receptor, AHR, with high or low binding affinity for dioxin, respectively) and demonstrated that hepatocellular tumor promotion in response to dioxin segregated with the Ahr locus. Once we had genetic evidence for the importance of AHR signaling, we then asked if tumor promotion by dioxin was influenced by "interleukin1 (IL-1)-like" inflammatory cytokines. The importance of this question arose from our earlier observation that aspects of the acute hepatocellular toxicity of dioxin are dependent upon IL1-like cytokine signaling. To address this issue, we employed a triple knock-out (TKO) mouse model with null alleles at the loci encoding the three relevant receptors for tumor necrosis factor α and β and IL-1α and β (i.e., null alleles at the Tnfrsf1a, Tnfrsf1b and Il-1r1 loci). The observation that TKO mice were resistant to the tumor promoting effects of dioxin in liver suggests that inflammatory cytokines play an important step in dioxin mediated liver tumor promotion in the mouse. Collectively, these data support the idea that the mechanism of dioxin acute hepatotoxicity and its activity as a promoter in a mouse two stage liver cancer model may be similar, i.e., tumor promotion by dioxin, like acute hepatotoxicity, are mediated by the linked action of two receptor systems, the AHR and the receptors for the "IL-1-like" cytokines.
- Toxicological sciences : an official journal of the Society of Toxicology.Toxicol Sci.2014 Apr 9. [Epub ahead of print]
- We set out to better understand the signal transduction pathways that mediate liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxn ("dioxin"). To this end, we first employed congenic mice homozygous for either the Ahrb1 or Ahrd alleles (encoding an aryl hydrocarbon receptor, AHR, with high or
- PMID 24718703
Japanese Journal
- 9203 カナダにおけるコンバージョン建築の調査研究(その3) : バンクーバーにおける転用事例に見られるデザイン手法(意匠論:形態(3),建築歴史・意匠,学術講演会・建築デザイン発表会)
- 9202 カナダにおけるコンバージョン建築の調査研究(その2) : トロント、オタワの転用事例に見られるデザイン手法(意匠論:形態(3),建築歴史・意匠,学術講演会・建築デザイン発表会)
- 9201 カナダにおけるコンバージョン建築の調査研究(その1) : モントリオール、ケベック・シティにおける転用事例にみられるデザイン手法(意匠論:形態(3),建築歴史・意匠,学術講演会・建築デザイン発表会)
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