1,720,968 research outputs found
Jugular tubercle and vertebral artery/posterior inferior cerebellar artery anatomic relationship: a 3-dimensional angiography computed tomography anthropometric study
No full textExtracranial aneurysm of the posterior inferior cerebellar artery. Literature review and report of a new case
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Extracranial aneurysms of the posterior inferior cerebellar artery. Literature review and report of a new case
No full textRetrospective protein expression and epigenetic inactivation studies of CDH1 in patients affected by low-grade glioma.
No full textAberrant methylation of CpG islands in the promoter regions of tumour cells results in loss of gene function. In addition to genetic lesions, changes in the methylation profile of the promoters may be considered a factor for tumour-specific aberrant expression of the genes.We investigated the methylation status of E-cadherin gene (CDH1) promoter in low-grade glioma and correlated it with clinical outcome. Eighty-four cases of low-grade glioma (43 diffuse astrocytomas, 27 oligodendrogliomas and 14 oligoastrocytomas) with assessable paraffin-embedded tumour blocks and normal brain tissue, derived from non-cancerous tissue adjacent to tumour and commercially normal brain tissue, were collected, from which we determined CDH1 promoter methylation status and E-cadherin protein expression by methylation-specific polymerase chain reaction (MSP) and immunohistochemistry, respectively. CDH1 promoter was found hypermethylated in 54 out of 84 low grade gliomas (64%) compared with 84 normal brain tissue. CDH1 hypermethylation was found in 65% astrocytomas, 66% oligodendrogliomas and 57% oligoastrocytomas. A significant correlation between hypermethylation status, patient survival and progression-free survival was found (P = 0.04). Survival and progression-free survival were lower in patients with hypermethylated CDH1 promoter. We found that 15 astrocytomas, 9 oligodendrogliomas and 6 oligoastrocytomas were immunoreactive for E-cadherin. The incidence of loss of immunoreactivity for E-cadherin decreased significantly with age, overall survival and progression-free survival (P = 0.001, Kaplan-Meier test). We have demonstrated that CDH1 promoter hypermethylation significantly associated with down-regulated E-cadherin expression and overall survival of patients. This may have a bearing on the prognosis of low-grade glioma
Levodopa effect on electromyographic activation patterns of tibialis anterior muscle during walking in Parkinson's disease
No full textPrevious studies have reported that patients with Parkinson's disease (PD) show, in the " off medication" state, a reduced activation of tibialis anterior (TA) in the late swing-early stance phase of the gait cycle. In PD patients the pathophysiological picture may cause differences among the stride cycles. Our aims were to evaluate how frequently TA activity is reduced in the late swing-early stance phase and if there is a relationship between the TA pattern and the clinical picture.Thirty PD patients were studied 2. h after Levodopa administration (" on-med" ) and 12. h after Levodopa wash-out (" off-med" ). They were evaluated by the Unified Parkinson's Disease Rating Scale (UPDRS III) and surface electromyography of TA and gastrocnemius medialis (GM). The root mean square (RMS) of the TA activity in late swing-early stance phase (RMS-A) was normalized as a percent of the RMS of the TA activity in late stance-early swing (RMS-B).RMS-A was reduced in 30% of patients in the " off-med" condition. Within these patients, the percentage of stride cycles with reduced RMS-A, ranged between 28% and 83%. After Levodopa intake, no stride cycle showed reduced RMS-A. Patients with reduced RMS-A had a lower UPDRS III total score in the " on-med" rather than in the " off-med" condition (p=0.02).Our data confirm and extend previous observations indicating that, in " off-med" the function of TA is impaired in those patients clinically more responsive to Levodopa. TA activation is reduced in a relatively high percent of gait cycles in the " off-med" state. Since the variability of TA activation disappears after Levodopa administration, this phenomenon could be the expression of an abnormal dopaminergic drive. © 2010 Elsevier B.V
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