Publications by authors named "John Boucher"

The cause of progressive disability in Primary Progressive Multiple Sclerosis (PPMS) is unknown. Pathogenic genes have been described in some MS cases that may contribute to progressive disability, independent of immune - mediated mechanisms (Jia et al., 2018).

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Background: Cognitive decline is a frequent complication of Parkinson's disease (PD) and the identification of predictive biomarkers for it would help in its management.

Objective: Our aim was to analyse whether senescence markers (telomere length, p16 and p21) or their change over time could help to better predict cognitive and motor progression of newly diagnosed PD patients. We also compared these senescence markers to previously analysed markers of inflammation for the same purpose.

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Abnormal hemorheology has been proposed previously as a possible genesis of exercise-induced hypoxemia (EIH) in humans. This study, in support of the hemorheological hypothesis, aims at determining if red blood cell shape changes might be related to EIH. Three groups of subjects: one without EIH (n=5); one developing mild-EIH (n=7); and, one with moderate EIH (n=5).

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Venipuncture procedures are widely thought to influence biochemical, hematological or hemorheological measurements. In line with the preparation of the new Guidelines for the standardization of hemorheological measurement, we compared various blood rheological parameters (i.e.

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The aim of the present study was to test the relationships between hemorheology and autonomic nervous system (ANS) activity in 23 sickle cell trait (SCT) carriers and 17 control subjects. Hemorheological parameters were assessed at rest. Nocturnal ANS activity was calculated from heart rate variability indices.

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The contribution of accessory toxins to the acute inflammatory response to Vibrio cholerae was assessed in a murine pulmonary model. Intranasal administration of an El Tor O1 V. cholerae strain deleted of cholera toxin genes (ctxAB) caused diffuse pneumonia characterized by infiltration of PMNs, tissue damage, and hemorrhage.

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The cystic fibrosis transmembrane conductance regulator (CFTR), which is aberrant in patients with cystic fibrosis, normally functions both as a chloride channel and as a pleiotropic regulator of other ion transporters. Here we show, by ratiometric imaging with luminally exposed pH-sensitive green fluorescent protein, that CFTR affects the pH of cellubrevin-labeled endosomal organelles resulting in hyperacidification of these compartments in cystic fibrosis lung epithelial cells. The excessive acidification of intracellular organelles was corrected with low concentrations of weak base.

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