Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven cases of an encephalitic brainstem syndrome are reported. All had an initial flu-like phase, with a febrile state. Then, all had eye movements disturbances and ataxia. Six had a variable dysfunction of other cranial nerves, five had dysmetria of limbs and three had pyramidal signs. In all, the topographic diagnosis was based on clinical, neurophysiological (electromyography, evoked potentials) and neuroradiological (swelled brainstem on CT scan) findings. Analysis of cerebro-spinal fluid revealed pleocytosis (mean; 165 cells/ml), without profile indicative of multiple sclerosis. Serologic tests for Adenovirus or Echovirus were positive in three cases. All recovered spontaneously. With a mean follow-up of three years there was no relapse and the clinical examination remained normal. These seven cases had, after exclusion of other brainstem syndromes, a Bickerstaff's encephalitis. Previous reports are discussed and a post-infectious origin is proposed to this benign syndrome.
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PMID:[Benign encephalitis of the brain stem]. 343 46

Missense mutations in protein kinase Cgamma (gammaPKC) gene have been found in spinocerebellar ataxia type 14 (SCA14), an autosomal dominant neurodegenerative disease. We previously demonstrated that mutant gammaPKC found in SCA14 is susceptible to aggregation and induces apoptosis in cultured cell lines. In the present study, we investigated whether mutant gammaPKC formed aggregates and how mutant gammaPKC affects the morphology and survival of cerebellar Purkinje cells (PCs), which are degenerated in SCA14 patients. Adenovirus-transfected primary cultured PCs expressing mutant gammaPKC-GFP also had aggregates and underwent apoptosis. Long-term time-lapse observation revealed that PCs have a potential to eliminate aggregates of mutant gammaPKC-GFP. Mutant gammaPKC-GFP disturbed the development of PC dendrites and reduced synapse formation, regardless of the presence or absence of its aggregates. In PCs without aggregates, mutant gammaPKC-GFP formed soluble oligomers, resulting in reduced mobility and attenuated translocation of mutant gammaPKC-GFP upon stimulation. These molecular properties of mutant gammaPKC might affect the dendritic morphology in PCs, and be involved in the pathogenesis of SCA14.
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PMID:Mutant gammaPKC found in spinocerebellar ataxia type 14 induces aggregate-independent maldevelopment of dendrites in primary cultured Purkinje cells. 1904 43