Narcolepsy with cataplexy as presenting symptom of occult neuroblastoma.

Neuroblastoma associated with the paraneoplastic syndrome of opsoclonus-myoclonus is well-described. However, presentation with narcolepsy-cataplexy is not well-documented in the literature. Narcolepsy with cataplexy is also rare in children younger than 5 years of age.

A novel FKRP mutation in congenital muscular dystrophy disrupts the dystrophin glycoprotein complex.

Mutations in the gene encoding fukutin related protein (FKRP) produce a spectrum of disease including congenital muscular dystrophy and limb girdle muscular dystrophy. FKRP is one member of a class of molecules thought to be glycosyltransferases that mediate O-linked glycosylation. The primary target of these glycosyltransferases is thought to be dystroglycan.

Immunoaugmenting effect of FK 506 on experimental allergic encephalomyelitis in Lewis rats.

The effect of the immunosuppressive drug FK 506 on encephalomyelitis (EAE) in Lewis rats was studied. Treatment that began during EAE induction delayed EAE onset, but when the disease started it was chronic/progressive and of unusual severity and duration, leading to death in many animals. Treatment started after onset of EAE shortened the disease.

Experimental allergic encephalomyelitis, beta-adrenergic receptors and interferon gamma-secreting cells in beta-adrenergic agonist-treated rats.

Treatment with the beta 2-adrenergic agonist terbutaline or the beta-adrenergic agonist isoproterenol suppresses experimental allergic encephalomyelitis, decreases the number of IFN gamma-producing splenic cells, and decreases the number of beta-adrenergic receptors on splenic lymphocytes in Lewis rats. The effects of terbutaline are greater when the drug is given from the day of immunization through the acute phase of the illness or from day 15 postimmunization until recovery, than when given for the first 12 days after immunization.

Beta-adrenergic agonists suppress chronic/relapsing experimental allergic encephalomyelitis (CREAE) in Lewis rats.

Chronic/relapsing experimental allergic encephalomyelitis (CREAE) serves as an animal model for relapsing/remitting multiple sclerosis. Treatment with the beta-adrenergic agonist isoproterenol or the beta 2-adrenergic agonist terbutaline significantly suppressed both the first acute attack and the number of relapses in CREAE Lewis rats. The number of relapses was decreased even when treatment with beta-adrenergic agonist was started after the onset of the first acute attack of CREAE.