The immunological basis of glutamatergic disturbance in schizophrenia: towards an integrated view.

This overview presents a hypothesis to bridge the gap between psychoneuroimmunological findings and recent results from pharmacological, neurochemical and genetic studies in schizophrenia. In schizophrenia, a glutamatergic hypofunction is discussed to be crucially involved in dopaminergic dysfunction. This view is supported by findings of the neuregulin- and dysbindin genes, which have functional impact on the glutamatergic system.

[Some characteristics of the biological action of D, L-1,4-dibromo-1,4-dideoxy-2,3-butanediol].

In tests conducted on mice and rats with transplantable tumours the antineoplastic activity of the racemic agent D, L-1,4-dibromo-1, 4-didesoxy-2, 3-butandiol is shown. With chronic administration of the drug in subtherapeutic and therapeutic doses a higher leucocytes count was in evidence in the blood of the animals with and without tumours.