Neurobiology of DiseaseElsevier, 6. sep. 2011 - 1104 sider Neurobiology of Disease is aimed at any basic scientist or clinician scientist teaching a course or conducting research on the basic science underlying the major neurological diseases. It provides an excellent overview of cutting-edge research on the fundamental disorders of the nervous system, including physiological and molecular aspects of dysfunction. The major categories of neurological disease are covered, and the chapters provide specific information about particular diseases exemplifying each of these categories. Sufficient clinical information is included to put into perspective the basic mechanisms discussed. The book assembles a world-class team of section editors and chapters written by acknowledged experts in their respective fields.
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Side 16
... loss of neurons occurs very early in the cerebral cortex, leading to conspicuous cortical atrophy, but similar changes are less prominent in other brain regions. In NPC disease, loss of neurons in the cerebral cortex is less prominent ...
... loss of neurons occurs very early in the cerebral cortex, leading to conspicuous cortical atrophy, but similar changes are less prominent in other brain regions. In NPC disease, loss of neurons in the cerebral cortex is less prominent ...
Side 22
... loss of PEX1p will impair both PTS1 and PTS2 import, whereas the loss of PEX7p will only interfere with PTS2 import. Consequently, in CG1, elevations in VLCFA, DHCA, THCA, l-pipecolic acid, and to a variable degree due to the dietary ...
... loss of PEX1p will impair both PTS1 and PTS2 import, whereas the loss of PEX7p will only interfere with PTS2 import. Consequently, in CG1, elevations in VLCFA, DHCA, THCA, l-pipecolic acid, and to a variable degree due to the dietary ...
Side 23
... loss). Neuropathologically, these foci consist of myelin pallor, variable axonal and oligodendrocytic loss, periodic acid– Schiff (PAS)–positive macrophages, a few reactive astrocytes and few or no detectable lymphocytes (Fig. 4). On ...
... loss). Neuropathologically, these foci consist of myelin pallor, variable axonal and oligodendrocytic loss, periodic acid– Schiff (PAS)–positive macrophages, a few reactive astrocytes and few or no detectable lymphocytes (Fig. 4). On ...
Side 26
... loss of myelin exceeds that of axons, but there is considerable axonal loss. The earliest change at the advancing edge appears to be enlargement of the extracellular space with a few astrocytes and macrophages at the ultrastructural ...
... loss of myelin exceeds that of axons, but there is considerable axonal loss. The earliest change at the advancing edge appears to be enlargement of the extracellular space with a few astrocytes and macrophages at the ultrastructural ...
Side 28
... loss of hearing that has been classified as sensorineural in type. It can be seen in ZS, NALD, IRD, ARD, RCDP, acyl ... loss, gliosis of the nerve fiber layer and optic nerve, optic atrophy, extensive loss of outer and inner segments of ...
... loss of hearing that has been classified as sensorineural in type. It can be seen in ZS, NALD, IRD, ARD, RCDP, acyl ... loss, gliosis of the nerve fiber layer and optic nerve, optic atrophy, extensive loss of outer and inner segments of ...
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abnormalities acid activity amyotrophic lateral sclerosis animal models antibodies antigens associated ataxia atrophy autism autoimmune axonal brain calcium cancer cause cellular central nervous system cerebellar cerebral chromosome Clin clinical cognitive cortex cortical creatine deficiency dementia dendritic diagnosis disorders dysfunction effects enzyme expression factors function gene genetic gliomas granule cell hippocampal human identified immune impairment increased infarction infection inflammatory involved lesions loss lymphoma lysosomal mechanisms medulloblastoma membrane meningiomas metabolism metastasis mice migraine mitochondrial molecular motor neuron mouse model multiple muscle mutations myelin myoclonus nerve neurological neuropathy Neurosci normal nucleus occur onset Parkinson’s disease pathogenesis pathology Pathophysiology pathways patients PCNSL phenotype potential primary prion progressive protein Purkinje cells receptor region response result role SCA1 seizures sodium channel spinal stroke studies subunit suggest symptoms syndrome synuclein systemic lupus erythematosus temporal lobe epilepsy therapy tion tissue transgenic treatment tumor vascular virus white matter
Populære passager
Side 410 - Alizadeh, AA, Eisen, MB, Davis, RE, Ma, C., Lossos, I. S., Rosenwald, A., Boldrick, JC, Sabet, H., Tran, T., Yu, X., Powell, JI, Yang, L., Marti, GE, Moore, T., Hudson, J.
Side 583 - ... marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction b. failure to develop peer relationships appropriate to developmental level c. a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (eg, by a lack of showing, bringing, or pointing out objects of interest) d.
Side 583 - A. Qualitative impairment in social interaction, as manifested by at least two of the following: (1) marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction (2) failure to develop peer relationships appropriate to developmental level (3) a lack of spontaneous seeking to share enjoyment...
Side 583 - ... play appropriate to developmental level (3) restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following: (a) encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus (b) apparently inflexible adherence to specific, nonfunctional routines or rituals (c) stereotyped and repetitive motor mannerisms (eg, hand or finger flapping or twisting, or...
Side 532 - Gurney, ME, Pu, H., Chiu, AY, Dal Canto, MC, Polchow, CY, Alexander, DD, Caliendo, J., Hentati, A., Kwon, YW, Deng, HX, Chen, W., Zhai, P., Sufit, RL, and Siddique, T.
Side 533 - K. (1997). Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1. Science 276, 1699-1702.
Side 240 - Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation: analysis of pooled data from five randomized controlled trials.
Side 121 - Kruger R, Kuhn W, Muller T, Woitalla D, Graeber M, Kosel S, Przuntek H, Epplen JT, Schols L, Riess O.
Side 431 - Pomeroy SL, Tamayo P, Gaasenbeek M. Sturla LM, Angelo M, McLaughlin ME, Kim JY. Goumnerova LC, Black PM, Lau C. Allen JC. Zagzag D, Olson JM, Curran T, Wetmore C, Biegel JA. Poggio T. Mukherjee S. Rifkin R. Califano A, Stolovitzky G. Louis DN, Mesirov JP, Lander ES.
Side 533 - Oosthuyse, B., Moons, L., Storkebaum, E., Beck, H., Nuyens, D., Brusselmans, K., Van Dorpe, J., Hellings, P., Gorselink, M., Heymans, S., Theilmeier, G., Dewerchin, M., Laudenbach, V., Vermylen...