Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unilateral labyrinthectomy (UL) in rats is used as a human vertigo model. In this model, spontaneous nystagmus and dysequilibrium caused by UL are ameliorated within 48-72 hours. The amelioration, termed vestibular compensation (VC), is long lasting. Although cerebellar flocculi have been reported to be involved in VC, the molecular mechanisms behind VC are unknown. In this study, we used 2D-DIGE to detect protein changes in flocculi during acute (48 hours) and chronic (1 week) stages of VC. We found 99 out of 967 protein spots that showed significant changes in their intensities. Of the 99 spots, 45 spots (ipsilateral side, 15; contralateral side, 30) changed unilaterally during the acute stage, whereas 46 spots (ipsilateral side, 21; contralateral side, 25) changed unilaterally during the chronic stage. Thus, the acute compensation mechanism is more complicated in the contralateral flocculus than in the ipsilateral flocculus. Using MALDI-TOF MS, we identified 10 proteins out of the 12 protein spots. Of these, 3 proteins involved in synaptic transmission, neuronal filament formation and vesicular transport, respectively, demonstrated altered expression only in the acute stage. Our results enhance the understanding of the role of the cerebellar flocculi in VC generation.
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PMID:Proteomic analysis of the rat cerebellar flocculus during vestibular compensation. 2044 35

The study aimed to evaluate the correlations between the clinical and paraclinical data in the lateral bulbar infarction, benefiting from the access to the semiologic characteristics of a group studied and the MRI angiography, without a contrast agent, through the 3D TOF technique combined with MIP, as an imaging technique for the evaluation of the arterial lesion. The study group included 20 patients with lateral bulbar infarction, 14 men, and 6 women aged between 21 and 80 years, the mean age being 56, 9 years, who were enrolled in the study in the period 2012 and 2014, following the admission in the National Institute of Neurology and Neurovascular Diseases. All the patients enrolled in this stage study, performed brain MRI - in the Medinst laboratory, which included the following sequences T1, T2, Flair, DWI, MRI angiography without contrast agent (3D TOF combined with MIP). The study was retrospective. Following the analysis of the 3D TOF sequences combined with MIP, it was found that in the group studied, 8 patients had damage at the level of the vertebral artery, 2 at the level of the posterior inferior cerebellar artery and 10 patients presented mixed lesions of both the vertebral artery and of the PICA artery. In terms of the mechanism involved, most of the lateral bulbar infarctions were generated by arterial dissection (9 cases) and 6 cases had atheroma as etiology. Regarding the risk factors, dyslipidemia and smoking predominated in the studied group and the most common signs and symptoms were gait abnormalities, the ataxia of the limbs, dysphonia, and Horner syndrome. Abbreviations: 3D TOF = 3D time of flight angiography, MIP = maximum intensity projection, MRI = magnetic resonance imaging, CT = computed tomography, FLAIR = fluid attenuated inversion recovery, DWI = diffusion weighted imaging, HTA = hypertension, DZ II = diabetes mellitus, VA = vertebral artery, PICA = posterior inferior cerebellar artery, VG = vertigo, NT = nystagmus, N/ E = nausea/ emesis, DP = dysphagia, PVP = pharyngeal/ vocal cord paresis, HS = Horner syndrome, PTH = pain/ temperature hypesthesia, LA = ipsilateral limb ataxia, GA = Gait ataxia, C-R-F = Cardiovascular risk factors, L = left, R = right.
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PMID:Correlations between the semiologic changes and the imaging aspects in the lateral bulbar infarction. 2797 32