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Macrophage migration inhibition factor (MIF) in drug eruption.

A controlled study was conducted to evaluate the macrophage migration inhibition factor test as a diagnostic aid in 50 patients with drug eruption. Two groups of patients served as controls: group A, 110 patients being treated with drugs without known cutaneous adverse reactions, and group B, 15 patients suffering from dermatologic disorders unrelated to drugs being taken. Positive macrophage migration inhibition factor responses were found toward a variety of drugs in 35 (70%) of the patients with drug eruptions, with no relation to the type of eruption or the duration of drug intake. The percentage of positive macrophage migration inhibition factor responses toward drugs in the patients with drug eruptions was higher than that in the two control groups (4.5% and 6.7%, respectively). The percentage of positive macrophage migration inhibition factor responses recorded for clinically "suspected" drugs was significantly higher than that recorded for the "nonsuspected" drugs.

Cell Migration Inhibition↗

[The effect of prolyl-leucyl-glycine (MIF-1) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on dopamine levels of the striatum].

We report that large dose MPTP-treated mice bring about a reduction in the levels of DA, 5-HT and their metabolites in the striatum. In the mice pretreated with PLG, although the striatal DA level was also reduced, mean DA and 5-HT levels were significantly higher than in mice given MPTP alone. It is concluded that PLG can prevent, at least partially, the neurotoxic effect of MPTP. We assume that the mechanism of action of PLG may directly or indirectly reduce MPTP-induced dopaminergic neurotoxicity in the nigrostriatal system or reduce the affinity of MPP+ to melanin in DA cells.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

[Physiological trials with MIF-I in Parkinson's disease (author's transl)].

The writers present some physiological (and not therapeutic) acute and sub-acute trials with tripeptide: L-propyl-L-leucyl-glycine amide (M.I.F.-I) in Parkinson's Disease. This work confirms the earlier observation that M.I.F.-I employed alone or in combination with Levodopa is active against Parkinson's disease. The writers evoke the hypothesis that this action takes place at the postsynaptic receptors, whose configuration may be modified in the sense of a hypersensitivity. These studies justify undertaking a series of controlled therapeutic trials when the cost of the product permits and as well instituting development work on analogues active orally.

Aged↗