opiate

出典: meddic

  • n.
  • オピエート、アヘン剤。(広義)麻酔薬、鎮痛薬。[fig](感覚を)鈍くするもの
  • adj.
  • アヘンの、阿片を含む。アヘン剤の、麻酔薬の。催眠/鎮静の。麻酔する
  • vt.

WordNet   license wordnet

「a narcotic drug that contains opium or an opium derivative」

PrepTutorEJDIC   license prepejdic

「アヘン剤,鎮静剤 / (…にとって)鎮静させるもの《+『to』+『名』》 / アヘンを用いた;鎮静の」

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/06/16 00:14:44」(JST)

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英文文献

  • Extinction of opiate reward reduces dendritic arborization and c-Fos expression in the nucleus accumbens core.
  • Leite-Morris KA1, Kobrin KL2, Guy MD3, Young AJ4, Heinrichs SC5, Kaplan GB6.Author information 1Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Psychiatry, Boston University School of Medicine, 720 Harrison Avenue, Boston, Massachusetts, 02118, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: kleitemo@bu.edu.2Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: kendrak@bu.edu.3Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: marsha.guy@gmail.com.4Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: angela.pieroniyoung@facebook.com.5Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA. Electronic address: Stephen.Heinrichs@va.gov.6Research Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Mental Health Service, VA Boston Healthcare System, 150 South Huntington Ave, Boston, Massachusetts, 02130, USA; Department of Psychiatry, Boston University School of Medicine, 720 Harrison Avenue, Boston, Massachusetts, 02118, USA; Department of Pharmacology and Experimental Therapeutics, 72 East Concord Street, Boston University School of Medicine, Boston, Massachusetts, 02118, USA. Electronic address: Gary.Kaplan@va.gov.AbstractRecurrent opiate use combined with environmental cues, in which the drug was administered, provokes cue-induced drug craving and conditioned drug reward. Drug abuse craving is frequently linked with stimuli from a prior drug-taking environment via classical conditioning and associative learning. We modeled the conditioned morphine reward process by using acquisition and extinction of conditioned place preference (CPP) in C57BL/6 mice. Mice were trained to associate a morphine injection with a drug context using a classical conditioning paradigm. In morphine conditioning (0, 0.25, 0.5, 1, 5, or 10mg/kg) experimental mice acquired a morphine CPP dose response with 10mg/kg as most effective. During morphine CPP extinction experiments, mice were divided into three test groups: morphine CPP followed by extinction training, morphine CPP followed by sham extinction, and saline controls. Extinction of morphine CPP developed within one extinction experiment (4 days) that lasted over two more trials (another 8 days). However, the morphine CPP/sham extinction group retained a place preference that endured through all three extinction trials. Brains were harvested following CPP extinction and processed using Golgi-Cox impregnation. Changes in dendritic morphology and spine quantity were examined in the nucleus accumbens (NAc) Core and Shell neurons. In the NAcCore only, morphine CPP/extinguished mice produced less dendritic arborization, and a decrease in neuronal activity marker c-Fos compared to the morphine CPP/sham extinction group. Extinction of morphine CPP is associated with decreased structural complexity of dendrites in the NAcCore and may represent a substrate for learning induced structural plasticity relevant to addiction.
  • Behavioural brain research.Behav Brain Res.2014 Apr 15;263:51-9. doi: 10.1016/j.bbr.2013.12.041. Epub 2014 Jan 7.
  • Recurrent opiate use combined with environmental cues, in which the drug was administered, provokes cue-induced drug craving and conditioned drug reward. Drug abuse craving is frequently linked with stimuli from a prior drug-taking environment via classical conditioning and associative learning. We
  • PMID 24406724
  • Morphine-induced trafficking of a mu-opioid receptor interacting protein in rat locus coeruleus neurons.
  • Jaremko KM1, Thompson NL Jr1, Reyes BA2, Jin J3, Ebersole B3, Jenney CB4, Grigson PS4, Levenson R3, Berrettini WH5, Van Bockstaele EJ1.Author information 1Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States.2Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States. Electronic address: Beverly.Reyes@drexelmed.edu.3Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033, United States.4Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, PA 17033, United States.5Department of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, United States.AbstractOpiate addiction is a devastating health problem, with approximately 2million people currently addicted to heroin or non-medical prescription opiates in the United States alone. In neurons, adaptations in cell signaling cascades develop following opioid actions at the mu opioid receptor (MOR). A novel putative target for intervention involves interacting proteins that may regulate trafficking of MOR. Morphine has been shown to induce a re-distribution of a MOR-interacting protein Wntless (WLS, a transport molecule necessary for secretion of neurotrophic Wnt proteins), from cytoplasmic to membrane compartments in rat striatal neurons. Given its opiate-sensitivity and its well-characterized molecular and cellular adaptations to morphine exposure, we investigated the anatomical distribution of WLS and MOR in the rat locus coeruleus (LC)-norepinephrine (NE) system. Dual immunofluorescence microscopy was used to test the hypothesis that WLS is localized to noradrenergic neurons of the LC and that WLS and MOR co-exist in common LC somatodendritic processes, providing an anatomical substrate for their putative interactions. We also hypothesized that morphine would influence WLS distribution in the LC. Rats received saline, morphine or the opiate agonist [d-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO), and tissue sections through the LC were processed for immunogold-silver detection of WLS and MOR. Statistical analysis showed a significant re-distribution of WLS to the plasma membrane following morphine treatment in addition to an increase in the proximity of gold-silver labels for MOR and WLS. Following DAMGO treatment, MOR and WLS were predominantly localized within the cytoplasmic compartment when compared to morphine and control. In a separate cohort of rats, brains were obtained from saline-treated or heroin self-administering male rats for pulldown co-immunoprecipitation studies. Results showed an increased association of WLS and MOR following heroin exposure. As the LC-NE system is important for cognition as well as decisions underlying substance abuse, adaptations in WLS trafficking and expression may play a role in modulating MOR function in the LC and contribute to the negative sequelae of opiate exposure on executive function.
  • Progress in neuro-psychopharmacology & biological psychiatry.Prog Neuropsychopharmacol Biol Psychiatry.2014 Apr 3;50:53-65. doi: 10.1016/j.pnpbp.2013.12.003. Epub 2013 Dec 12.
  • Opiate addiction is a devastating health problem, with approximately 2million people currently addicted to heroin or non-medical prescription opiates in the United States alone. In neurons, adaptations in cell signaling cascades develop following opioid actions at the mu opioid receptor (MOR). A nov
  • PMID 24333843
  • Morphine modulates cell proliferation through mir133b &mir128 in the neuroblastoma SH-SY5Y cell line.
  • Gonzalez-Nunez V1, Noriega-Prieto JA2, Rodríguez RE3.Author information 1Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Salamanca, Spain; Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain.2Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain.3Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Salamanca, Spain; Instituto de Neurociencias de Castilla y León (INCyL), University of Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Spain. Electronic address: requelmi@usal.es.AbstractNeuroblastoma is a childhood cancer with high incidence and high mortality rate. Great efforts are made to find new treatments and molecular markers for diagnosis and prognosis. miRNAs stand for novel strategies to modulate tumor growth, as they can act either as tumor suppressors or as oncogenes. Morphine is an opioid agonist widely used to treat severe and chronic pain, as for example cancer pain. Previous studies have revealed that morphine is able to modify cancer progression, by acting on proliferation or on apoptosis; however, up to date, the available results are contradictory, maybe due to the different doses used, routes of administration and model systems. While some studies show that morphine promotes cell proliferation and metastasis, other authors sustain that morphine effect is mainly antiproliferative and pro-apoptotic. In this study we aim to establish the effect of chronic opiate administration on cell proliferation in the neuroblastoma SH-SY5Y cell line. Low doses of morphine (10nM) promoted cell proliferation in undifferentiated cells and reduced the expression levels of miR133b, while higher doses (1μM) inhibited cell proliferation and correlated with decreased levels of miR133b and miR128 without triggering apoptosis. Naloxone, the classical opioid antagonist, could not fully block the effect of morphine on miR128 expression, so that the observed effect may be mediated by non-opioid mechanisms. Our results represent a further contribution to the hypothesis that a joint regulation of miRNA networks and the specific characteristics of the target tissue may determine the effect of morphine on tumor cell growth.
  • Biochimica et biophysica acta.Biochim Biophys Acta.2014 Apr;1842(4):566-72. doi: 10.1016/j.bbadis.2014.01.003. Epub 2014 Jan 14.
  • Neuroblastoma is a childhood cancer with high incidence and high mortality rate. Great efforts are made to find new treatments and molecular markers for diagnosis and prognosis. miRNAs stand for novel strategies to modulate tumor growth, as they can act either as tumor suppressors or as oncogenes. M
  • PMID 24440526
  • Duration of opiate exposure as a determinant of arterial stiffness and vascular age in male opiate dependence: a longitudinal study.
  • Reece AS1, Hulse GK.Author information 1School of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, WA, Australia.AbstractWHAT IS KNOWN AND OBJECTIVE: Despite intriguing initial and associational studies, there remains little research on opiate-related arterial dysfunction and no longitudinal studies. As opiates act potently via P16INK4A/CDKN2A identified on GWAS screens, and as arterial ageing is a surrogate for organismal ageing, this area is of general concern.
  • Journal of clinical pharmacy and therapeutics.J Clin Pharm Ther.2014 Apr;39(2):158-67. doi: 10.1111/jcpt.12121. Epub 2013 Dec 16.
  • WHAT IS KNOWN AND OBJECTIVE: Despite intriguing initial and associational studies, there remains little research on opiate-related arterial dysfunction and no longitudinal studies. As opiates act potently via P16INK4A/CDKN2A identified on GWAS screens, and as arterial ageing is a surrogate for organ
  • PMID 24329809

和文文献

  • A personal view from a long-lasting collaborator on the research strategies of Marshall Nirenberg
  • Higashida Haruhiro
  • Neurochemistry International 61(6), 821-827, 2012-11
  • … Especially he liked his hypothesis for opiate tolerance and dependency as a model of cellular memory. …
  • NAID 120004966606
  • Inhibition of Morphine Glucuronidation in the Liver Microsomes of Rats and Humans by Monoterpenoid Alcohols
  • Ishii Yuji,Iida Naoko,Miyauchi Yuu [他],Mackenzie Peter I.,Yamada Hideyuki
  • Biological and Pharmaceutical Bulletin 35(10), 1811-1817, 2012
  • … This opiate is mainly metabolized by glucuronidation to a non-analgesic metabolite, morphine-3-glucuronide (M-3-G) and an active metabolite morphine-6-glucuronide (M-6-G). …
  • NAID 130001872386
  • Perforation of Peptic Ulcer Following Abrupt Cessation of Long-term Opiate Use
  • KAHROM MAHDI,KAHROM HADI
  • Surgery today : the Japanese journal of surgery 40(9), 836-839, 2010-09-01
  • NAID 10027397617
  • FACT誌収載 鍼灸関係論文(114)耳介鍼療法(auricular acupuncture)はオピエイトの禁断症状のひどさを軽減しない
  • 直本 美知 [訳],濱田 淳 [訳]
  • 医道の日本 69(8), 68-70, 2010-08
  • NAID 40017246802

関連リンク

opiateとは。意味や和訳。[名]アヘン剤;((略式))鎮静剤, 麻酔剤. [形]1 アヘンを混ぜた.2 催眠の;麻酔性の. [動] 〔oupiegrave;it〕 (他)…に麻酔をかける;…を鈍くする, 無感覚にする.[中ラテン語opi#257;tus (opiumアヘンの形容詞 ...
内容(「CDジャーナル」データベースより)ヘヴィ・ロックの新たな指針を示すバンド、トゥールの92年にリリースされたミニ・アルバムを再発。沈んだサウンドと辛辣な歌詞で、悩めるアメリカの若者の病んだ気持ちを完全に ...
Opiate. 1,006 likes · 4 talking about this. The Copenhagen quintet Opiate was formed in 2010 and consists of vocalist Anders Høst, drummer Erik R. Olsson, bassist Thomas Lausen and guitarists Jacob Andersen-Usaj and Martin ...

関連画像

Mandate of Heaven Presents The Opiate ShopThe term opiate refers to the alkaloids 220px-Papaversomniferum.jpgOpiateheroin heroin wurde 1874 erstmals wondering who this is go to the imdb to entersto opiate addicts rather than finding an


★リンクテーブル★
リンク元意識障害」「アヘン」「オピエート
拡張検索μ-opiate receptor」「opiate receptors
関連記事opia

意識障害」

  [★]

consciousness disturbance, disturbance of consciousness
意識


分類

時間による分類

急性/慢性, 持続性/一過性

PSY.38

  • 単純な意識障害
明識困難状態 < 昏蒙 < 傾眠 < 昏眠 < 昏睡
  • 複雑な意識障害
  • せん妄     意識混濁 + (高度)精神運動興奮
  • 夜間せん妄
  • 意識障害に関連した特殊な病態

意識レベルの分類 覚醒度

Mayo Clinicの分類

救急 意識障害をみたら

  • AIUEOTIPS (also see DIF.96)
  症候学プリント DIF.95
A alcohol アルコール関連 accidents, arterial occlusions, arteriosclerosis, aneurysms, autoimmune disorders
I insulin インスリン関連(低血糖、糖尿病性ケトアシドーシス非ケトン性高浸透圧性昏睡) inflammatory, intoxication (encephalitis, cerebral abcess, meningitis, alcoholism, opiates, barbiturates)
U uremia 尿毒症電解質異常、内分泌異常、肝性脳症 undefined disorders (narcolepsy, conversion hysteria)
E encephalopathy, endocrinopathy, electrolyte 脳症(脳炎、脳血管障害)、てんかん後 endocrine disorders(myxedema coma, hyperparathyroidism, diabetic coma, insulin shock), epileptic coma
O opiate, other overdose of O2 & CO2 薬物中毒 organ failure(hepatic coma, respiratory failure, uremia)
T trauma, tumor, temparature 頭部外傷、脳挫傷、硬膜外血腫、硬膜下血腫  
I infection 感染症、髄膜炎
P psychogenic 精神疾患
S syncope, seizure, stroke, shock, senile 失神クモ膜下出血

意識障害を来した患者が来た場合:どのような疾患を鑑別に挙げるべきか(IMD.237)

  • 1. 脳原発の疾患(一次性)
  • a. テント上病変(脳幹の圧迫性病変ないし脳ヘルニアをきたす疾患)
  • 1) 脳血管障害:脳出血、脳梗塞
  • 2) 硬膜下血腫
  • 3) 脳腫瘍:原発性、転移性
  • 4) 脳膿瘍
  • b. テント下病変(脳幹網様体の障害)
  • 1) 脳幹出血、脳幹梗塞、小脳出血、小脳梗塞、脳腫痛、多発性硬化症など
  • c. びまん性病変
  • 1) くも膜下出血、中枢神経感染症:髄膜炎、脳炎、 播種性血管内凝固症候群など
  • 2. 全身疾患に伴う病態(二次性)
  • a. 代謝性またはびまん性病変
  • 1) ショック:心筋梗塞、大出血など
  • 2) 薬物、毒物
  • 3) 無酸素ないし低酸素血症
  • 4) DIC、全身性感染症:敗血症など
  • 5) 肝不全、腎不全、糖尿病性高血糖、重症肝炎、内分泌疾患など
  • 6) 低血糖、ビタミンB1欠乏: Wernicke脳症
  • 7) 脳振盪、てんかん大発作後
  • 8) 酸塩基平衡および電解質異常
  • 9) 栄養障害
  • b. 心因性無反応
  • 1) ヒステリー、統合失調症


意識障害をきたす電解質異常

QB.D-345
カリウムは静止膜電位にかかわるが、ニューロンの活動にはそれほど関わらないから、意識障害はきたしにくいのかもしれない。
pHの異常も局所的に干渉されるため意識障害をきたしにくいのかもしれない。

意識障害の評価法

evaluation of consciousness disturbance



アヘン」

  [★]

opium
あへん阿片、鴉片(中国)
opiate濫用薬物薬物濫用



オピエート」

  [★]

opiate
アヘン剤
アヘン opiumオピオイド opioid
  • アヘンの天然由来の化学的誘導体。


μ-opiate receptor」

  [★] μ-オピエート受容体


opiate receptors」

  [★] オピエート受容体


opia」

  [★]

  • comb form.
  • 視力、視力障害
  • ex.


"http://meddic.jp/opiate" より作成


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