Journal of immunological methods, 54(3), 355-360 (1982-11-12)
In the past, the lesions of experimental allergic encephalomyelitis (EAE) have been induced to localize around brain tissue damaged by anoxia or direct physical or chemical attack. The procedure for producing the requisite antecedent brain injury has been simplified by
Gold thioglucose, mimpa and lesions of the ventromedial hypothalamus.
D F Brown
Journal of neuropathology and experimental neurology, 43(4), 455-457 (1984-07-01)
An aliphatic triamine has been reported to cause lesions in rats in the vicinity of the area postrema and the median eminence of the hypothalamus, sites known to lack a blood-brain barrier. The present study revealed that some of the
Journal of neuropathology and experimental neurology, 41(2), 233-240 (1982-03-01)
The administration of an aliphatic triamine, 3,3'-methylimino-bis-(N-methylpropylamine), was used to produce non-necrotizing lesions in the hypothalamus and medulla oblongata of rats. The distribution of the lesions in the hypothalamus was similar to that produced by goldthioglucose, and consisted ultrastructurally of
It has been demonstrated that the ventromedial hypothalamus (VMH) of alloxan-induced diabetic mice is protected from subsequent gold thioglucose (GTG)-induced lesions. Another compound, 3,3'-methyliminobis-(N-methylpropylamine) (MIMPA), a triamine structurally unrelated to GTG, has been shown to cause similar VMH lesions in
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