Publications by authors named "M A Baltrons"

Aim: To analyse the potential usefulness and clinical relevance of the assessment by echocardiography with left atrial strain, based on the myocardial atrial deformation curves with speckle-tracking velocity vector imaging (VVI), in the analysis of short-form recurrent atrial extra systoles in ambulatory patients not suffering from organic cardiopathy.

Methods: We designed a descriptive, prospective, and observational study including 270 patients between the ages of 18 and 75 assessed during an outpatient cardiology consultation attended due to palpitations over a period of two years. Using ambulatory electrocardiographic monitoring, we selected cases with short forms of repetitive atrial extrasystole, isolated or recurrentatrial fibrillation and a control group formed by those patients without repetitive ectopia.

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Glioblastoma (GBM) is a highly aggressive brain tumor and almost all patients die because of relapses. GBM-derived cells undergo cell death without nuclear fragmentation upon treatment with different apoptotic agents. Nuclear dismantling determines the point-of-no-return in the apoptotic process.

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Article Synopsis
  • The "Amyloid Cascade Hypothesis," which links increased amyloid-β (Aβ) to Alzheimer's disease progression, has been the leading theory for 25 years but has not led to successful treatments.
  • Research highlights significant connections between Aβ and tau in impairing synaptic function and memory loss, suggesting both proteins may work together in the disease's development.
  • The authors advocate for a new perspective on Alzheimer's pathogenesis that focuses on the role of amyloid-β protein precursor (AβPP) and the need for new therapeutic strategies targeting AβPP rather than just Aβ and tau.
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The Akt kinase has been widely assumed for years as a key downstream effector of the PI3K signaling pathway in promoting neuronal survival. This notion was however challenged by the finding that neuronal survival responses were still preserved in mice with reduced Akt activity. Moreover, here we show that the Akt signaling is elevated in the aged brain of two different mice models of Alzheimer Disease.

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