Publications by authors named "Guadalupe Martel-Gallegos"

There is solid epidemiological evidence that arsenic exposure leads to cognitive impairment, while experimental work supports the hypothesis that it also contributes to neurodegeneration. Energy deficit, oxidative stress, demyelination, and defective neurotransmission are demonstrated arsenic effects, but it remains unclear whether synaptic structure is also affected. Employing both a triple-transgenic Alzheimer's disease model and Wistar rats, the cortical microstructure and synapses were analyzed under chronic arsenic exposure.

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Article Synopsis
  • * A study on Wistar rats exposed to 3 ppm of arsenic in drinking water from fetal development showed behavioral deficits and increased levels of amyloid-β (Aβ) linked to higher activity of the enzyme β-secretase (BACE1).
  • * The findings suggest that arsenic exposure disrupts the production and clearance of Aβ, indicating that early metal exposure could play a role in neurodegeneration and amyloid buildup in the brain.
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Inwardly rectifying K (Kir) channel expression signals at an advanced stage of maturation during oligodendroglial differentiation. Knocking down their expression halts the generation of myelin and produces severe abnormalities in the central nervous system. Kir4.

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Plants are considered advantageous platforms for biomanufacturing recombinant vaccines. This constitutes a field of intensive research and some plant-derived vaccines are expected to be marketed in the near future. In particular, plant-based production of immunogens targeting molecules with implications on the pathology of Alzheimer's has been explored over the last decade.

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Background: Activation of ATP-gated P2X7 receptors (P2X7R) in macrophages leads to production of reactive oxygen species (ROS) by a mechanism that is partially characterized. Here we used J774 cells to identify the signaling cascade that couples ROS production to receptor stimulation.

Methods: J774 cells and mP2X7-transfected HEK293 cells were stimulated with Bz-ATP in the presence and absence of extracellular calcium.

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It has been reported that in human neutrophils, external ATP activates plasma membrane purinergic P2X(7) receptors (P2X(7)R) to elicit Ca(2+) entry, production of reactive oxygen species (ROS), processing and release of pro-inflammatory cytokines, shedding of adhesion molecules and uptake of large molecules. However, the expression of P2X(7)R at the plasma membrane of neutrophils has also been questioned since these putative responses are not always reproduced. In this work, we used electrophysiological recordings to measure functional responses associated with the activation of membrane receptors, spectrofluorometric measurements of ROS production and ethidium bromide uptake to asses coupling of P2X(7)R activation to downstream effectors, immune-labelling of P2X(7)R using a fluorescein isothiocyanate-conjugated antibody to detect the receptors at the plasma membrane, RT-PCR to determine mRNA expression of P2X(7)R and Western blot to determine protein expression in neutrophils and HL-60 cells.

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Ischemia-reperfusion injury is a common pathological occurrence causing tissue damage in heart attack and stroke. Entrapment of neutrophils in the vasculature during ischemic events has been implicated in this process. In this study, we examine the effects that lactacidosis and consequent reductions in intracellular pH (pH(i)) have on surface expression of adhesion molecules on neutrophils.

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