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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Corpus Callosum

 
 
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Disease relevance of Corpus Callosum

 

Psychiatry related information on Corpus Callosum

 

High impact information on Corpus Callosum

  • Developing axons of the corpus callosum of mice are guided across the cerebral midline by a slinglike glial structure that forms transiently between the hemispheres [10].
  • Patients in PVS revealed a significantly higher frequency of corpus callosum, corona radiata, and dorsolateral brainstem injuries than did patients who recovered [11].
  • Surprisingly, many of the axon guidance defects present in the L1 knockout mice, such as abnormal corticospinal tract and corpus callosum, were not observed [12].
  • We show that the GFAP network is disrupted in astrocytes that normally coexpress vimentin and GFAP, e.g., those of the corpus callosum or the Bergmann glia of cerebellum [13].
  • While mice deficient in Nuk exhibit defects in pathfinding of anterior commissure axons, sek4 mutants have defects in corpus callosum formation [14].
 

Chemical compound and disease context of Corpus Callosum

 

Biological context of Corpus Callosum

 

Anatomical context of Corpus Callosum

 

Associations of Corpus Callosum with chemical compounds

  • The corpus callosum atrophy was accompanied by a decreased mean cortical glucose metabolic rate, predominantly in the frontal region of the cortex, and poor performance on the picture arrangement subtest of the Wechsler Adult Intelligence Scale and the verbal fluency task [30].
  • Expression of the dopamine D3 receptor (D3r) was found in primary mixed glial cultures from newborn brain and in the corpus callosum in vivo during the peak of myelination [28].
  • To trace the implanted cells, they were stained with the carbocyanine vital dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate before injecting them into the white matter above the corpus callosum [31].
  • When measurements were compared among 44 patients, whose cerebral speech dominance had been determined by the intracarotid injection of sodium amytal, the area of the corpus callosum was significantly greater in patients with right-hemisphere cerebral speech dominance [32].
  • We observed variations in fractional anisotropy and mean diffusivity over the considered developmental period in most bundles (corpus callosum, cerebellar peduncles, cortico-spinal tract, spino-thalamic tract, capsules, radiations, longitudinal and uncinate fascicles, cingulum) [33].
 

Gene context of Corpus Callosum

  • Newborn Nfia(-/-) animals lack a corpus callosum and show ventricular dilation indicating early hydrocephalus [5].
  • These results are consistent with deficient auditory interhemispheric transfer in patients with a PAX6 mutation, which may be attributable to structural and/or functional abnormalities of the anterior commisure and corpus callosum, although the exact contribution of these two formations to our findings remains unclear [34].
  • The axon guidance defect of the corpus callosum in the jsap1-/- brain was correlated with the misplacement of glial sling cells, which reverted to their normal position after the transgenic expression of JNK interacting protein 1(JIP1) [35].
  • The transgenic JIP1 partially rescued the axon guidance defect of the corpus callosum and the anterior commissure of the jsap1-/- brain [35].
  • Using a multiple tissue expression (MTE) array containing 20 different human brain regions, the highest levels of both SFT/UbcH5A and DMT1 mRNA are detected in the corpus callosum and cerebellum [36].
 

Analytical, diagnostic and therapeutic context of Corpus Callosum

References

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  4. Damage-induced neuronal endopeptidase (DINE) is a unique metallopeptidase expressed in response to neuronal damage and activates superoxide scavengers. Kiryu-Seo, S., Sasaki, M., Yokohama, H., Nakagomi, S., Hirayama, T., Aoki, S., Wada, K., Kiyama, H. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
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  13. Disrupted glial fibrillary acidic protein network in astrocytes from vimentin knockout mice. Galou, M., Colucci-Guyon, E., Ensergueix, D., Ridet, J.L., Gimenez y Ribotta, M., Privat, A., Babinet, C., Dupouey, P. J. Cell Biol. (1996) [Pubmed]
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  15. Insulin-like growth factor-1 inhibits mature oligodendrocyte apoptosis during primary demyelination. Mason, J.L., Ye, P., Suzuki, K., D'Ercole, A.J., Matsushima, G.K. J. Neurosci. (2000) [Pubmed]
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  18. Inappropriate secretion of antiduretic hormone, hypertension, and hypoplastic corpus callosum. Fyhrquist, F., Holmberg, C., Perheentupa, J., Wallenius, M. J. Clin. Endocrinol. Metab. (1977) [Pubmed]
  19. Atrophy of the corpus callosum associated with a decrease in cortical benzodiazepine receptor in large cerebral arterial occlusive diseases. Yamauchi, H., Fukuyama, H., Dong, Y., Nabatame, H., Nagahama, Y., Nishizawa, S., Konishi, J., Shio, H. J. Neurol. Neurosurg. Psychiatr. (2000) [Pubmed]
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  22. Mutation of the Emx-1 homeobox gene disrupts the corpus callosum. Qiu, M., Anderson, S., Chen, S., Meneses, J.J., Hevner, R., Kuwana, E., Pedersen, R.A., Rubenstein, J.L. Dev. Biol. (1996) [Pubmed]
  23. Phosphorylation of cyclic adenosine monophosphate response element binding protein in oligodendrocytes in the corpus callosum after focal cerebral ischemia in the rat. Tanaka, K., Nogawa, S., Ito, D., Suzuki, S., Dembo, T., Kosakai, A., Fukuuchi, Y. J. Cereb. Blood Flow Metab. (2001) [Pubmed]
  24. Differential susceptibility of senile and lesion-induced astrogliosis to phosphatidylserine. Jegliński, W., Pepeu, G., Oderfeld-Nowak, B. Neurobiol. Aging (1997) [Pubmed]
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  35. The axon guidance defect of the telencephalic commissures of the JSAP1-deficient brain was partially rescued by the transgenic expression of JIP1. Ha, H.Y., Cho, I.H., Lee, K.W., Lee, K.W., Song, J.Y., Kim, K.S., Yu, Y.M., Lee, J.K., Song, J.S., Yang, S.D., Shin, H.S., Han, P.L. Dev. Biol. (2005) [Pubmed]
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