WordNet

kill by smashing someones skull
mental ability; "hes got plenty of brains but no common sense" (同)brainpower, learning_ability, mental capacity, mentality, wit
that part of the central nervous system that includes all the higher nervous centers; enclosed within the skull; continuous with the spinal cord (同)encephalon
the brain of certain animals used as meat
hit on the head
examination of tissues or liquids from the living body to determine the existence or cause of a disease

PrepTutorEJDIC

『脳』,脳髄 / 《しばしば複数形で》『頭脳』,『知力』 / 《話》秀才,知的指導者 / …‘の'頭を打ち砕く
=brassiere,　brassiere

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1. 高グレードの神経膠腫患者の臨床症状および初回外科的アプローチ clinical manifestations and initial surgical approach to patients with high grade gliomas
2. 中枢神経系病変を有するHIV感染患者に対するアプローチ approach to hiv infected patients with central nervous system lesions
3. 慢性髄膜炎患者へのアプローチ approach to the patient with chronic meningitis
4. 小児期の中枢神経系原発性血管炎 childhood primary angiitis of the central nervous system
5. 進行性多巣性白質脳症：疫学、臨床症状、および診断 progressive multifocal leukoencephalopathy epidemiology clinical manifestations and diagnosis

English Journal

TDP-43 causes differential pathology in neuronal versus glial cells in the mouse brain.

Yan S1, Wang CE, Wei W, Gaertig MA, Lai L, Li S, Li XJ.Author information 1Department of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, USA.AbstractMutations in TAR DNA-binding protein 43 (TDP-43) are associated with familial forms of amyotrophic lateral sclerosis and frontotemporal lobar degeneration. Although recent studies have revealed that mutant TDP-43 in neuronal and glial cells is toxic, how mutant TDP-43 causes primarily neuronal degeneration in an age-dependent manner remains unclear. Using adeno-associated virus (AAV) that expresses mutant TDP-43 (M337V) ubiquitously, we found that mutant TDP-43 accumulates preferentially in neuronal cells in the postnatal mouse brain. We then ubiquitously or selectively expressed mutant TDP-43 in neuronal and glial cells in the striatum of adult mouse brains via stereotaxic injection of AAV vectors and found that it also preferentially accumulates in neuronal cells. Expression of mutant TDP-43 in neurons in the striatum causes more severe degeneration, earlier death and more robust symptoms in mice than expression of mutant TDP-43 in glial cells; however, aging increases the expression of mutant TDP-43 in glial cells, and expression of mutant TDP-43 in older mice caused earlier onset of phenotypes and more severe neuropathology than that in younger mice. Although expression of mutant TDP-43 in glial cells via stereotaxic injection does not lead to robust neurological phenotypes, systemic inhibition of the proteasome activity via MG132 in postnatal mice could exacerbate glial TDP-43-mediated toxicity and cause mice to die earlier. Consistently, this inhibition increases the expression of mutant TDP-43 in glial cells in mouse brains. Thus, the differential accumulation of mutant TDP-43 in neuronal versus glial cells contributes to the preferential toxicity of mutant TDP-43 in neuronal cells and age-dependent pathology.
Human molecular genetics.Hum Mol Genet.2014 May 15;23(10):2678-93. doi: 10.1093/hmg/ddt662. Epub 2013 Dec 30.
Mutations in TAR DNA-binding protein 43 (TDP-43) are associated with familial forms of amyotrophic lateral sclerosis and frontotemporal lobar degeneration. Although recent studies have revealed that mutant TDP-43 in neuronal and glial cells is toxic, how mutant TDP-43 causes primarily neuronal degen
PMID 24381309

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging.

Paveliev M1, Kislin M1, Molotkov D1, Yuryev M1, Rauvala H1, Khiroug L2.Author information 1Neuroscience Center, University of Helsinki.2Neuroscience Center, University of Helsinki; Leonard.Khirug@helsinki.fi.AbstractAlthough acute brain trauma often results from head damage in different accidents and affects a substantial fraction of the population, there is no effective treatment for it yet. Limitations of currently used animal models impede understanding of the pathology mechanism. Multiphoton microscopy allows studying cells and tissues within intact animal brains longitudinally under physiological and pathological conditions. Here, we describe two models of acute brain injury studied by means of two-photon imaging of brain cell behavior under posttraumatic conditions. A selected brain region is injured with a sharp needle to produce a trauma of a controlled width and depth in the brain parenchyma. Our method uses stereotaxic prick with a syringe needle, which can be combined with simultaneous drug application. We propose that this method can be used as an advanced tool to study cellular mechanisms of pathophysiological consequences of acute trauma in mammalian brain in vivo. In this video, we combine acute brain injury with two preparations: cranial window and skull thinning. We also discuss advantages and limitations of both preparations for multisession imaging of brain regeneration after trauma.
Journal of visualized experiments : JoVE.J Vis Exp.2014 Apr 6;(86). doi: 10.3791/51559.
Although acute brain trauma often results from head damage in different accidents and affects a substantial fraction of the population, there is no effective treatment for it yet. Limitations of currently used animal models impede understanding of the pathology mechanism. Multiphoton microscopy allo
PMID 24748024

Fractalkine activates NRF2/NFE2L2 and heme oxygenase 1 to restrain tauopathy-induced microgliosis.

Lastres-Becker I1, Innamorato NG, Jaworski T, Rábano A, Kügler S, Van Leuven F, Cuadrado A.Author information 11 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Investigación Sanitaria La Paz (IdiPaz), Instituto de Investigaciones Biomédicas Alberto Sols UAM-CSIC, and Department of Biochemistry, Faculty of Medicine, Autonomous University of Madrid, Madrid, Spain.AbstractThe chemokine fractalkine modulates microglial responses in neurodegenerative diseases, including tauopathies, but the mechanistic processes and their relevance in human brain pathologies is not yet known. Here, we show that hippocampal HT22 cells expressing human TAU(P301L) mutant protein produce fractalkine, which in microglia activates AKT, inhibits glycogen synthase kinase-3β and upregulates the transcription factor NRF2/NFE2L2 and its target genes including heme oxygenase 1. In a mouse model of tauopathy based on stereotaxic delivery in hippocampus of an adeno-associated viral vector for expression of TAU(P301L), we confirmed that tau-injured neurons express fractalkine. NRF2- and fractalkine receptor-knockout mice did not express heme oxygenase 1 in microglia and exhibited increased microgliosis and astrogliosis in response to neuronal TAU(P301L) expression, demonstrating a crucial role of the fractalkine/NRF2/heme oxygenase 1 pathway in attenuation of the pro-inflammatory phenotype. The hippocampus of patients with Alzheimer's disease also exhibits increased expression of fractalkine in TAU-injured neurons that recruit microglia. These events correlated with increased levels of NRF2 and heme oxygenase 1 proteins, suggesting an attempt of the diseased brain to limit microgliosis. Our combined results indicate that fractalkine mobilizes NRF2 to limit over-activation of microglia and identify this new target to control unremitting neuroinflammation in tauopathies.
Brain : a journal of neurology.Brain.2014 Jan;137(Pt 1):78-91. doi: 10.1093/brain/awt323. Epub 2013 Nov 25.
The chemokine fractalkine modulates microglial responses in neurodegenerative diseases, including tauopathies, but the mechanistic processes and their relevance in human brain pathologies is not yet known. Here, we show that hippocampal HT22 cells expressing human TAU(P301L) mutant protein produce f
PMID 24277722