WordNet
- of or relating to the cerebrum or brain; "cerebral hemisphere"; "cerebral activity"
- involving intelligence rather than emotions or instinct; "a cerebral approach to the problem"; "cerebral drama" (同)intellectual
- swelling from excessive accumulation of watery fluid in cells, tissues, or serous cavities (同)oedema, hydrops, dropsy
- of or relating to substances that are toxic to cells
PrepTutorEJDIC
- 大脳の,脳の / 頭脳的な,知的な
- 浮腫(ふしゅ),水腫
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- 1. 糖尿病性ケトアシドーシスの小児における脳浮腫 cerebral edema in children with diabetic ketoacidosis
- 2. 虚血性脳卒中の病態生理 pathophysiology of ischemic stroke
- 3. 頸動脈内膜剥離術および頸動脈ステント留置術の麻酔 anesthesia for carotid endarterectomy and carotid stenting
- 4. 急性高山病および高地脳浮腫 acute mountain sickness and high altitude cerebral edema
- 5. 小児における細菌性髄膜炎：神経学的合併症 bacterial meningitis in children neurologic complications
English Journal
- Overexpression of aquaporin‑1 aggravates hippocampal damage in mouse traumatic brain injury models.
- Qiu B1, Li X1, Sun X2, Wang Y1, Jing Z1, Zhang X3, Wang Y1.Author information 1Department of Neurosurgery, First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.2Department of Pharmaceutics, School of Pharmacy, Fudan University, Shanghai 201203, P.R. China.3Liaoning Centers for Diseases Control and Prevention, Shenyang, Liaoning 110005, P.R. China.Abstract'Secondary insult' following primary traumatic brain injury (TBI), including ischemia and edema, may aggravate brain impairments and affect the outcomes. The hippocampus is particularly sensitive to ischemia or edema due to its selective vulnerability, as neural cells of the hippocampus may be more prone to abnormal function or cell death in response to ischemia and edema. Aquaporin‑1 (AQP‑1) was reported to be associated with cerebral edema; however, the expression and role of AQP‑1 in hippocampal edema following TBI have seldom been investigated. In the current study, BALB/c mouse closed craniocerebral injury models were established and the changes of AQP‑1 expression in hippocampi of mouse models following TBI were investigated. Neurological function and edema formation of the models were evaluated and the apoptotic hippocampal cells were then stained in situ and detected, followed by determination of AQP‑1 expression in the hippocampus using immunohistochemistry and western blot analysis. As a result, the majority of mice in the TBI group were severely injured and hippocampal edema was confirmed. The apoptotic cells increased significantly in the hippocampi of mice in the TBI group compared with those in the sham group (P<0.01) and the apoptotic rate increased gradually in a time‑dependent manner. The expression levels of AQP‑1 in the hippocampi of mice were markedly higher in the TBI group than in the sham group (P<0.05) at various time points and AQP‑1 expression levels peaked one day following TBI. These results indicate that upregulation of AQP‑1 may participate in edema formation and delayed cell death of the hippocampus following TBI and may also be a novel therapeutic target to protect the hippocampus from secondary injury following TBI.
- Molecular medicine reports.Mol Med Rep.2014 Mar;9(3):916-22. doi: 10.3892/mmr.2014.1899. Epub 2014 Jan 15.
- 'Secondary insult' following primary traumatic brain injury (TBI), including ischemia and edema, may aggravate brain impairments and affect the outcomes. The hippocampus is particularly sensitive to ischemia or edema due to its selective vulnerability, as neural cells of the hippocampus may be more
- PMID 24430824
- Dexamethasone exacerbates cerebral edema and brain injury following lithium-pilocarpine induced status epilepticus.
- Duffy BA1, Chun KP2, Ma D3, Lythgoe MF4, Scott RC5.Author information 1Centre for Advanced Biomedical Imaging (CABI), Department of Medicine, University College London (UCL), UK. Electronic address: ben.duffy.09@ucl.ac.uk.2School of Environment and Sustainability, University of Saskatchewan, Canada.3Centre for Advanced Biomedical Imaging (CABI), Department of Medicine, University College London (UCL), UK; Centre for Medical Image Computing (CMIC), University College London (UCL), UK.4Centre for Advanced Biomedical Imaging (CABI), Department of Medicine, University College London (UCL), UK. Electronic address: m.lythgoe@ucl.ac.uk.5Department of Neurological Sciences, College of Medicine, University of Vermont, Burlington 05405, VT, USA; UCL Institute of Child Health, University College London, London, UK.AbstractAnti-inflammatory therapies are the current most plausible drug candidates for anti-epileptogenesis and neuroprotection following prolonged seizures. Given that vasogenic edema is widely considered to be detrimental for outcome following status epilepticus, the anti-inflammatory agent dexamethasone is sometimes used in clinic for alleviating cerebral edema. In this study we perform longitudinal magnetic resonance imaging in order to assess the contribution of dexamethasone on cerebral edema and subsequent neuroprotection following status epilepticus. Lithium-pilocarpine was used to induce status epilepticus in rats. Following status epilepticus, rats were either post-treated with saline or with dexamethasone sodium phosphate (10mg/kg or 2mg/kg). Brain edema was assessed by means of magnetic resonance imaging (T2 relaxometry) and hippocampal volumetry was used as a marker of neuronal injury. T2 relaxometry was performed prior to, 48h and 96h following status epilepticus. Volume measurements were performed between 18 and 21days after status epilepticus. Unexpectedly, cerebral edema was worse in rats that were treated with dexamethasone compared to controls. Furthermore, dexamethasone treated rats had lower hippocampal volumes compared to controls 3weeks after the initial insult. The T2 measurements at 2days and 4days in the hippocampus correlated with hippocampal volumes at 3weeks. Finally, the mortality rate in the first week following status epilepticus increased from 14% in untreated rats to 33% and 46% in rats treated with 2mg/kg and 10mg/kg dexamethasone respectively. These findings suggest that dexamethasone can exacerbate the acute cerebral edema and brain injury associated with status epilepticus.
- Neurobiology of disease.Neurobiol Dis.2014 Mar;63:229-36. doi: 10.1016/j.nbd.2013.12.001. Epub 2013 Dec 12.
- Anti-inflammatory therapies are the current most plausible drug candidates for anti-epileptogenesis and neuroprotection following prolonged seizures. Given that vasogenic edema is widely considered to be detrimental for outcome following status epilepticus, the anti-inflammatory agent dexamethasone
- PMID 24333865
- Aquaporin-4 deletion in mice reduces encephalopathy and brain edema in experimental acute liver failure.
- Rama Rao KV1, Verkman AS2, Curtis KM3, Norenberg MD4.Author information 1Department of Pathology, University of Miami Miller School of Medicine, Miami, FL 33101, USA. Electronic address: vkakulavarapu@med.miami.edu.2Department of Medicine, University of California, San Francisco, CA 94143, USA; Department of Physiology, University of California, San Francisco, CA 94143, USA.3Department of Biochemistry & Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33101, USA; Veterans Affairs Medical Center, Miami, FL 33125, USA.4Department of Pathology, University of Miami Miller School of Medicine, Miami, FL 33101, USA; Department of Biochemistry & Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33101, USA; Veterans Affairs Medical Center, Miami, FL 33125, USA. Electronic address: mnorenbe@med.miami.edu.AbstractBrain edema and associated astrocyte swelling leading to increased intracranial pressure are hallmarks of acute liver failure (ALF). Elevated blood and brain levels of ammonia have been implicated in the development of brain edema in ALF. Cultured astrocytes treated with ammonia have been shown to undergo cell swelling and such swelling was associated with an increase in the plasma membrane expression of aquaporin-4 (AQP4) protein. Further, silencing the AQP4 gene in cultured astrocytes was shown to prevent the ammonia-induced cell swelling. Here, we examined the evolution of brain edema in AQP4-null mice and their wild type counterparts (WT-mice) in different models of ALF induced by thioacetamide (TAA) or acetaminophen (APAP). Induction of ALF with TAA or APAP significantly increased brain water content in WT mice (by 1.6%±0.3 and 2.3±0.4%, respectively). AQP4 protein was significantly increased in brain plasma membranes of WT mice with ALF induced by either TAA or APAP. In contrast to WT-mice, brain water content did not increase in AQP4-null mice. Additionally, AQP4-null mice treated with either TAA or APAP showed a remarkably lesser degree of neurological deficits as compared to WT mice; the latter displayed an inability to maintain proper gait, and demonstrated a markedly reduced exploratory behavior, with the mice remaining in one corner of the cage with its head tilted downwards. These results support a central role of AQP4 in the brain edema associated with ALF.
- Neurobiology of disease.Neurobiol Dis.2014 Mar;63:222-8. doi: 10.1016/j.nbd.2013.11.018. Epub 2013 Dec 7.
- Brain edema and associated astrocyte swelling leading to increased intracranial pressure are hallmarks of acute liver failure (ALF). Elevated blood and brain levels of ammonia have been implicated in the development of brain edema in ALF. Cultured astrocytes treated with ammonia have been shown to u
- PMID 24321433
Japanese Journal
- A case of reversible posterior leukoencephalopathy syndrome in a patient on peritoneal dialysis.
- KITAMURA Mineaki,FURUSU Akira,HIROSE Megumi,NISHINO Tomoya,OBATA Yoko,URAMATSU Tadashi,KOHNO Shigeru
- Clinical and experimental nephrology 14(6), 633-636, 2010-12-01
- … The characteristic radiologic findings are bilateral gray and white matter edema in the posterior regions of the cerebral hemispheres. … RPLS most often occurs in the setting of hypertensive crisis, preeclampsia, or with cytotoxic immunosuppressive therapy, but many other clinical settings are described, such as cryoglobulinemia, hemolytic uremic syndrome, systemic lupus erythematosus, and use of erythropoietin. …
- NAID 10029321459
- Hyponatremic Encephalopathy after Excessive Water Ingestion Prior to Pelvic Ultrasound: Neuroimaging Findings
- Yalcin-Cakmakli Gul,Karli Oguz Kader,Shorbagi Ali,Funda Bas Demet,Ergan-Arsava Begum,Kunt Mahir,Akif Topcuoglu Mehmet
- Internal Medicine 49(16), 1807-1811, 2010
- … MR imaging revealed cortical sulcal narrowing, restricted diffusion and sulcal T2 hyperintensity along with diffuse pial enhancement suggesting diffuse cerebral cortical cytotoxic edema and blood-brain barrier breakdown. …
- NAID 130000299648
Related Links
- Cytotoxic. In this type of edema the BBB remains intact. This edema is due to the derangement in cellular metabolism resulting in inadequate functioning of the sodium and potassium pump in the glial cell membrane.
- 脳浮腫（のうふしゅ、英: cerebral edema、独: Hirnödem）は、脳実質内に異常な水分 貯留を生じ、脳容積が増大した状態である。 ... vasogenic edema と、代謝異常により 細胞膜のイオンの出入りが障害され、主として細胞内に水分が溜まる cytotoxic edema ...
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★リンクテーブル★
| リンク元 | 「vasogenic cerebral edema」「vasogenic brain edema」「細胞傷害性脳浮腫」 |
| 関連記事 | 「cerebral」「cytotoxic」 |
「vasogenic cerebral edema」
「vasogenic brain edema」
「細胞傷害性脳浮腫」
「cerebral」
- adj.
- 大脳の、大脳性の、脳性の、脳の
「cytotoxic」
- adj.
- 細胞傷害性の、細胞毒性の、細胞障害性の、細胞傷害の