Cooperative pathogenicity in cystic fibrosis: Stenotrophomonas maltophilia modulates Pseudomonas aeruginosa virulence in mixed biofilm.

The present study was undertaken in order to understand more about the interaction occurring between S. maltophilia and P. aeruginosa, which are frequently co-isolated from CF airways.

Ascertainment bias in dementias: a secondary to tertiary centre analysis in Central Italy and conceptual review.

Background And Aims: Ascertainment bias (AB) indicates a bias of an evaluation centre in estimating the prevalence/incidence of a disease due to the specific expertise of the centre. The aim of our study was to evaluate classification of different types of dementia in new cases appearing in secondary and tertiary centres, in order to evidence possible occurrence of AB in the various (secondary to tertiary) dementia centres.

Methods: To assess the mechanism of AB, the rates of new cases of the different forms of dementia reported by different centres were compared.

Sequential activation of human oculomotor centers during planning of visually-guided eye movements: a combined fMRI-MEG study.

We used magneto-encephalography (MEG) to measure visually evoked activity in healthy volunteers performing saccadic eye movements to visual targets. The neuromagnetic activity was analyzed from regions of cortical activation identified in separate functional magnetic resonance imaging (fMRI) studies. The latency of visual responses significantly increased from the Middle Temporal region (MT+) to the Intraparietal Sulcus (IPS) to the Frontal Eye Field (FEF), and their amplitude was greater in the hemisphere contralateral to the visual target.

Segmental conduction abnormalities and myelin thickenings in Val102/fs null mutation of MPZ gene.

The authors report in patients with Val102/fs null mutation a possibly age dependent variability of clinical and electrophysiologic phenotype, segmental conduction abnormalities mainly in ulnar nerves at the elbow, and excessive myelin foldings and thickenings. The authors hypothesize that myelin thickenings at the paranodal region, in concurrence with compression at usual entrapment sites or minor repetitive trauma, may induce segmental conduction abnormalities.