Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MK-801 induces psychotomimetic behavioural changes in animals. ERKs play an important role in the pathogenesis of schizophrenia and in the action of antipsychotics and psychotomimetics. We observed phosphorylation of ERK-signalling-pathway-associated molecules in the rat frontal cortex and their association with rat behaviour after MK-801 administration. After injecting 0.25-1 mg/kg MK-801, ERK phosphorylation decreased compared to vehicle treatment, and rats showed increased locomotion. After 2 mg/kg treatment, ERK phosphorylation increased and rat motility started to decrease. After treating with 4-8 mg/kg, ERK phosphorylation once again decreased and rats showed hypomotility and ataxia. ERK phosphorylation levels were maintained from 15 min to 90 min after 1 or 2 mg/kg treatment. Ser338-c-Raf and MEK phosphorylation showed similar dose-dependent and temporal patterns to those of ERK. Taken together, Ser338-c-Raf-MEK-ERK phosphorylation by MK-801 in the rat frontal cortex showed a specific pattern and may be associated with behavioural changes induced by MK-801.
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PMID:The effects of MK-801 on the phosphorylation of Ser338-c-Raf-MEK-ERK pathway in the rat frontal cortex. 1607 22

The authors investigated an outbreak of West Nile Fever characterized by severe neurological symptoms and death in a flock of 3600 6-week-old geese. Ataxia, intermittent torticollis and opisthotonus, incoordination, rhythmic side-to-side movement of the head, wriggling of the neck and abnormal head position were features of the disease. Death occurred within 4 to 5 days after the clinical signs appeared. The average daily mortality was 5 to 15, reaching 14% (in total) over a period of 6 weeks. There were no consistent gross pathological lesions, but in a few cases yellowish-grey foci of 3 to 6 mm in diameter were observed on the surface or transection of the brain. Histopathology revealed perivascular lymphohistiocytic infiltration and glia cell proliferation in the brainstem, cerebellum, cortex and spinal cord as well as degeneration of neural fibres in the spinal cord. In addition to the lesions caused by the West Nile Virus in the brain, characteristics of circovirus infection such as lymphocyte depletion, vacuolization and basophilic intra-cytoplasmic inclusion bodies containing circovirus-like particles were seen by light and electron microscopy in the cloacal bursa. West Nile Virus infection was confirmed by reverse transcriptase-polymerase chain reaction amplification of virus-specific nucleic acid from tissue samples of the brain. Based on the nucleotide sequence analysis of the polymerase chain reaction products, 99% identity was found on the tested NS5 region with the IS-98 ST1 strain isolated from a stork in Israel in 1998, and with West Nile Virus stains emerging in the USA in 1999. Using an indirect fluorescent antibody test, high antibody titres against the virus were detected in the serum samples submitted from the affected flock. In selected sera this was confirmed by neutralization antibody test as well.
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PMID:Co-occurrence of West Nile Fever and circovirus infection in a goose flock in Hungary. 1623 74

A neurological disease of young Pekin ducks characterized by ataxia, lameness, and paralysis was observed at several duck farms in Malaysia in 2012. Gross pathological lesions were absent or inconsistent in most of the cases, but severe and consistent microscopic lesions were found in the brain and spinal cord, characterized by non-purulent panencephalomyelitis. Several virus isolates were obtained in embryonated duck eggs and in cell cultures (Vero and DF-1) inoculated with the brain homogenates of affected ducks. After exclusion of other viruses, the isolates were identified as a flavivirus by flavivirus-specific reverse transcription-polymerase chain reaction (RT-PCR) assays. Inoculation of 2-week-old Pekin ducks with a flavivirus isolate by the subcutaneous or intramuscular route resulted in typical clinical signs and histological lesions in the brain and spinal cord. The inoculated virus was detected by RT-PCR from organ samples of ducks with clinical signs and histological lesions. With a few days delay, the disease was also observed among co-mingled contact control birds. Phylogenetic analysis of NS5 and E gene sequences proved that the isolates were representatives of a novel phylogenetic group within clade XI (Ntaya virus group) of the Flavivirus genus. This Malaysian Duck Tembusu Virus (DTMUV), named Perak virus, has moderate genomic RNA sequence similarity to a related DTMUV identified in China. In our experiment the Malaysian strain of DTMUV could be transmitted in the absence of mosquito vectors. These findings may have implications for the control and prevention of this emerging group of flaviviruses.
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PMID:Tembusu-like flavivirus (Perak virus) as the cause of neurological disease outbreaks in young Pekin ducks. 2529 64