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Ramirez-Peinado S.,IDIBELL Bellvitge Biomedical Research Institute | Leon-Annicchiarico C.L.,IDIBELL Bellvitge Biomedical Research Institute | Galindo-Moreno J.,IDIBELL Bellvitge Biomedical Research Institute | Iurlaro R.,IDIBELL Bellvitge Biomedical Research Institute | And 5 more authors.
Journal of Biological Chemistry | Year: 2013

Background: Autophagy is a response to nutrient deprivation. Results: Inhibition of autophagy does not sensitize cells to apoptotic or necrotic cell death induced by glucose starvation. Moreover, glucose deprivation inhibits autophagy. Conclusion: 2-Deoxyglucose, but not glucose deprivation, induces autophagy. Significance: Not all forms of starvation induce cytoprotective autophagy in mammalian cells. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.


Background: Advances in cognitive load theory have led to greater understanding of how we process verbal and visual material during learning, but the evidence base with regard to the use of images within written assessments is still sparse. This study examines whether the inclusion of images within the stimulus format of multiple choice questions (MCQs) has a predictable or consistent influence on psychometric item properties, such as difficulty or discrimination. Methods: Item analysis data from three consecutive years of histology multiple choice examinations were included in this study. All items were reviewed and categorised according to whether their stem, or stimulus format, was purely textual or included an associated image. Results: A total of 195 MCQs were identified for inclusion and analysed using classical test theory; 95 used text alone and 100 included an image within the question stem. The number of students per examination ranged from 277 to 347, with a total of 60,850 student-question interactions. We initially examined whether the inclusion of an image within the item stem altered the item difficulty using Mann-Whitney U. The median item difficulty for images with purely textual stems was 0.77, while that for items incorporating an appropriate image was 0.80; this difference was not significant (0.77 vs. 0.80; p∈=∈0.862, Mann-Whitney-U∈=∈4818.5). Mean values showed that the Item Discrimination Index appeared unaffected by the inclusion of an image within the stem, and Item point biserial correlation also showed no difference in means between these two groups (Independent samples t-test; 2-tailed). Conclusion: We demonstrate that the addition of illustrations within undergraduate histology Multiple Choice Question stems has no overall influence on item difficulty, or measures of item discrimination. We conclude that the use of images in this context is statistically uncritical, and suggest that their inclusion within item stems should be based upon the principles of constructive alignment. However, further research with respect to the effect of images within item stems on cognitive processing, particularly with regard to image complexity or type, would enable the development of more informed guidelines for their use. © 2015 Holland et al.


Connolly N.M.C.,23 St. Stephens Green | Connolly N.M.C.,Royal College of Surgeons in Ireland | Prehn J.H.M.,23 St. Stephens Green | Prehn J.H.M.,Royal College of Surgeons in Ireland
Journal of Bioenergetics and Biomembranes | Year: 2014

Excitotoxicity is a pathological process implicated in neuronal death during ischaemia, traumatic brain injuries and neurodegenerative diseases. Excitotoxicity is caused by excess levels of glutamate and over-activation of NMDA or calcium-permeable AMPA receptors on neuronal membranes, leading to ionic influx, energetic stress and potential neuronal death. The metabolic response of neurons to excitotoxicity is complex and plays a key role in the ability of the neuron to adapt and recover from such an insult. Single-cell imaging is a powerful experimental technique that can be used to study the neuronal metabolic response to excitotoxicity in vitro and, increasingly, in vivo. Here, we review some of the knowledge of the neuronal metabolic response to excitotoxicity gained from in vitro single-cell imaging, including calcium and ATP dynamics and their effects on mitochondrial function, along with the contribution of glucose metabolism, oxidative stress and additional neuroprotective signalling mechanisms. Future work will combine knowledge gained from single-cell imaging with data from biochemical and computational techniques to garner holistic information about the metabolic response to excitotoxicity at the whole brain level and transfer this knowledge to a clinical setting. © 2014, Springer Science+Business Media New York.


Moran C.,23 St. Stephens Green | Moran C.,National Center for Neurosurgery | Sanz-Rodriguez A.,23 St. Stephens Green | Sanz-Rodriguez A.,Center for the Study of Neurological Disorders | And 17 more authors.
Cell Death and Disease | Year: 2013

Prolonged seizures (status epilepticus, SE) can cause neuronal death within brain regions such as the hippocampus. This may contribute to impairments in cognitive functioning and trigger or exacerbate epilepsy. Seizure-induced neuronal death is mediated, at least in part, by apoptosis-associated signaling pathways. Indeed, mice lacking certain members of the potently proapoptotic BH3-only subfamily of Bcl-2 proteins are protected against hippocampal damage caused by status epilepticus. The recently identified BH3-only protein Bcl-2-modifying factor (Bmf) normally interacts with the cytoskeleton, but upon certain cellular stresses, such as loss of extracellular matrix adhesion or energy crisis, Bmf relocalizes to mitochondria, where it can promote Bax activation and mitochondrial dysfunction. Although Bmf has been widely reported in the hematopoietic system to exert a proapoptotic effect, no studies have been undertaken in models of neurological disorders. To examine whether Bmf is important for seizure-induced neuronal death, we studied Bmf induction after prolonged seizures induced by intra-amygdala kainic acid (KA) in mice, and examined the effect of Bmf-deficiency on seizures and damage caused by SE. Seizures triggered an early (1-8 h) transcriptional activation and accumulation of Bax in the cell death-susceptible hippocampal CA3 subfield. Bmf mRNA was biphasically upregulated beginning at 1 h after SE and returning to normal by 8 h, while again being found elevated in the hippocampus of epileptic mice. Bmf upregulation was prevented by Compound C, an inhibitor of adenosine monophosphate-activated protein kinase, indicating Bmf expression may be induced in response to bioenergetic stress. Bmf-deficient mice showed normal sensitivity to the convulsant effects of KA, but, surprisingly, displayed significantly more neuronal death in the hippocampal CA1 and CA3 subfields after SE. These are the first studies investigating Bmf in a model of neurologic injury, and suggest that Bmf may protect neurons against seizure-induced neuronal death in vivo. © 2013 Macmillan Publishers Limited All rights reserved.

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