無酸素性脳症
- 関
- anoxic brain injury、brain anoxia、brain hypoxia、cerebral anoxia、cerebral hypoxia、hypoxic brain damage、hypoxic encephalopathy
WordNet
- relating to or marked by a severe deficiency of oxygen in tissues or organs
UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
English Journal
- Plasmalemmal VDAC controversies and maxi-anion channel puzzle.
- Sabirov RZ, Merzlyak PG.AbstractThe maxi-anion channel has been observed in many cell types from the very beginning of the patch-clamp era. The channel is highly conductive for chloride and thus can modulate the resting membrane potential and play a role in fluid secretion/absorption and cell volume regulation. A wide nanoscopic pore of the maxi-anion channel permits passage of excitatory amino acids and nucleotides. The channel-mediated release of these signaling molecules is associated with kidney tubuloglomerular feedback, cardiac ischemia/hypoxia, as well as brain ischemia/hypoxia and excitotoxic neurodegeneration. Despite the ubiquitous expression and physiological/pathophysiological significance, the molecular identity of the maxi-anion channel is still obscure. VDAC is primarily a mitochondrial protein; however several groups detected it on the cellular surface. VDAC in lipid bilayers reproduced the most important biophysical properties of the maxi-anion channel, such as a wide nano-sized pore, closure in response to moderately high voltages, ATP-block and ATP-permeability. However, these similarities turned out to be superficial, and the hypothesis of plasmalemmal VDAC as the maxi-anion channel did not withstand the test by genetic manipulations of VDAC protein expression. VDAC on the cellular surface could also function as a ferricyanide reductase or a receptor for plasminogen kringle 5 and for neuroactive steroids. These ideas, as well as the very presence of VDAC on plasmalemma, remain to be scrutinized by genetic manipulations of the VDAC protein expression. This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism.
- Biochimica et biophysica acta.Biochim Biophys Acta.2012 Jun;1818(6):1570-80. Epub 2011 Oct 1.
- The maxi-anion channel has been observed in many cell types from the very beginning of the patch-clamp era. The channel is highly conductive for chloride and thus can modulate the resting membrane potential and play a role in fluid secretion/absorption and cell volume regulation. A wide nanoscopic p
- PMID 21986486
- Histological study of the protective effect of melatonin on neural cells after neonatal hypoxia-ischemia.
- Alonso-Alconada D, Alvarez A, Lacalle J, Hilario E.SourceDepartment of Cell Biology and Histology, School of Medicine and Dentistry, University of the Basque Country, Leioa, Vizcaya, Spain.
- Histology and histopathology.Histol Histopathol.2012 Jun;27(6):771-83.
- To minimize as much as possible the neurological consequences from hypoxic-ischemic (HI) brain injury, neuroprotective strategies are urgently required. In this sense, there is growing interest in the neuroprotective potential of melatonin after perinatal asphyxia, due to its high efficacy, low toxi
- PMID 22473697
Japanese Journal
- 症例報告 視野障害を呈した扼頸後遅発性低酸素脳症の1例
- 無酸素脳症後の高次脳機能障害により日常生活が困難となった患者の1例 : 社会生活自立に向けての援助の試み : 透析看護の立場から
- 西出 るみ子,西 徹也,西出 憲和,上之園 康久,喜田 裕也,藤井 良一,射手矢 巌
- 日本透析医学会雑誌 = Journal of Japanese Society for Dialysis Therapy 41(1), 77-80, 2008-01-28
- 今回,私たちは高カリウム血症による心肺停止に由来する無酸素脳症を発症し,その結果として高次脳機能障害症状を呈した症例を経験した.患者の行動と言動は一見,正常にみえるため私たちは最初高次脳機能障害の存在を認識できなかった.しかし,患者の注意,行動障害は著しく,それを確診した後はMSWスタッフ(Medical Social Worker Staff)と協力しながら医療,福祉両面からの援助を行った.その …
- NAID 10025192622
Related Links
- encephalopathy /en·ceph·a·lop·a·thy/ (en-sef″ah-lop´ah-the) any degenerative brain disease. AIDS encephalopathy HIV e. anoxic encephalopathy hypoxic e. biliary encephalopathy , bilirubin encephalopathy kernicterus. bovine ...
- en·ceph·a·lop·a·thy (n-s f-l p-th) n. pl. en·ceph·a·lop·a·thies Any of various diseases of the brain. en·ceph a·lo·path ic (-l-p th k) adj. encephalopathy (ɛnˌsɛfəˈlɒpəθɪ) n 1. (Pathology) any degenerative disease of the brain, often ...
★リンクテーブル★
[★]
無酸素脳症、脳無酸素症
- 関
- anoxic encephalopathy、brain hypoxia、cerebral anoxia、cerebral hypoxia、hypoxic brain damage、hypoxic encephalopathy
[★]
低酸素脳症、脳低酸素症
- 関
- anoxic encephalopathy、brain anoxia、cerebral anoxia、cerebral hypoxia、hypoxic brain damage、hypoxic encephalopathy
[★]
無酸素脳症、脳無酸素症
- 関
- anoxic encephalopathy、brain anoxia、brain hypoxia、cerebral hypoxia、hypoxic brain damage、hypoxic encephalopathy
[★]
低酸素脳症、脳低酸素症
- 関
- anoxic encephalopathy、brain anoxia、brain hypoxia、cerebral anoxia、hypoxic brain damage、hypoxic encephalopathy
[★]
- 英
- anoxic brain injury、anoxic encephalopathy
- 関
- 脳低酸素症、低酸素脳症、低酸素性脳障害、脳無酸素症、無酸素性脳傷害
[★]
- 関
- 一酸化炭素中毒
- CO中毒やcyanide中毒で起こりうる。遅発性の脳症。
- 低酸素虚血状態から回復後、apathy, confusion, and agitationが起こってくる。進行性の神経障害にはshuffling gait, diffuse rigidity and spasticity, persistent parkinsonism or myoclonus, and , on occasion, coma and death after 1-2 weeksがある.(HIM.1724)
- 広範な脱髄が見られることがある。(HIM.1724)
[★]
- 関
- anaerobic、anoxia、oxygen-free