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"Escapes."
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Chicken break! : a counting book
Illustrations and easy-to-read, rhyming text invite the reader to count chickens, from one standing guard to ten drooping and dragging their way back to the coop after breaking out for a night of fun.
Book
Digital Escape Rooms as Innovative Pedagogical Tools in Education: A Systematic Literature Review
This paper aims to present a systematic literature review on state-of-the-art Educational Escape Rooms (EERs) with the use of digital technologies. More specifically, the focus of the study is to present the current developments and trends concerning Digital Educational Escape Rooms (DEERs) and investigate how they foster learning outcomes for online learners. Additionally, the present study provides insights into the design process of such technology enhanced EERs. This review is attributed to identifying and covering research gaps since the current literature has focused on the pedagogical aspects of Escape Rooms (ERs) in education, but no studies seem to have been conducted in regard to the pedagogical implications of Digital Escape Rooms (DERs) in educational environments. Based on the exhaustive literature review, an agenda for future research is promised and the implications for designing innovative ER approaches have been highlighted. The anatomy of the fundamental components of conducting systematic literature reviews was followed. The results of the review could be addressed to multidisciplinary teams related to education, game researchers, educational researchers, faculty members, scholars, instructors, and protagonists of educational systems to encourage them to thoroughly study the core elements of DEERs and how they can be applied in virtual educational contexts to facilitate students’ learning achievements.
Journal Article
Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation
A better understanding of the mechanisms underlying the action of antidepressants is urgently needed. Moda-Sava et al. explored a possible mode of action for the drug ketamine, which has recently been shown to help patients recover from depression (see the Perspective by Beyeler). Ketamine rescued behavior in mice that was associated with depression-like phenotypes by selectively reversing stress-induced spine loss and restoring coordinated multicellular ensemble activity in prefrontal microcircuits. The initial induction of ketamine's antidepressant effect on mouse behavior occurred independently of effects on spine formation. Instead, synaptogenesis in the prefrontal region played a critical role in nourishing these effects over time. Interventions aimed at enhancing the survival of restored synapses may thus be useful for sustaining the behavioral effects of fast-acting antidepressants. Science , this issue p. eaat8078 ; see also p. 129 Spine formation in the prefrontal cortex is central to the long-term antidepressant effects of ketamine. The neurobiological mechanisms underlying the induction and remission of depressive episodes over time are not well understood. Through repeated longitudinal imaging of medial prefrontal microcircuits in the living brain, we found that prefrontal spinogenesis plays a critical role in sustaining specific antidepressant behavioral effects and maintaining long-term behavioral remission. Depression-related behavior was associated with targeted, branch-specific elimination of postsynaptic dendritic spines on prefrontal projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predict motivated escape behavior. Prefrontal spinogenesis was required for the long-term maintenance of antidepressant effects on motivated escape behavior but not for their initial induction.
Journal Article
The Rig
\"Fifteen-year-old Will Drake has made a career of breaking out from high-security prisons. His talents have landed him at the Rig, a specialist juvenile holding facility in the middle of the Arctic Ocean. No one can escape from the Rig. No one except for Drake.\"-- Provided by publisher.
Book
Solitary
Imprisoned for a murder he did not commit, fourteen-year-old Alex Sawyer thinks that he has escaped the hellish Furnace Penitentiary, but instead he winds up in solitary confinement, where new horrors await him.
Book
You can't hide
Poppy, Marcus, Dash, Dylan, and Azumi are trapped inside of Larkspur House, a sinister estate haunted by the ghosts of the orphaned children who have gone before, and the house is using their fears and secrets to pick them off one by one--because nobody gets out of the shadow house alive.
Book
In vivo CRISPR screening identifies Ptpn2 as a cancer immunotherapy target
Immunotherapy with PD-1 checkpoint blockade is effective in only a minority of patients with cancer, suggesting that additional treatment strategies are needed. Here we use a pooled
in vivo
genetic screening approach using CRISPR–Cas9 genome editing in transplantable tumours in mice treated with immunotherapy to discover previously undescribed immunotherapy targets. We tested 2,368 genes expressed by melanoma cells to identify those that synergize with or cause resistance to checkpoint blockade. We recovered the known immune evasion molecules PD-L1 and CD47, and confirmed that defects in interferon-γ signalling caused resistance to immunotherapy. Tumours were sensitized to immunotherapy by deletion of genes involved in several diverse pathways, including NF-κB signalling, antigen presentation and the unfolded protein response. In addition, deletion of the protein tyrosine phosphatase PTPN2 in tumour cells increased the efficacy of immunotherapy by enhancing interferon-γ-mediated effects on antigen presentation and growth suppression.
In vivo
genetic screens in tumour models can identify new immunotherapy targets in unanticipated pathways.
In vivo
CRISPR screening reveals that loss of
Ptpn2
increases the response of tumour cells to immunotherapy and increases IFNγ signalling, suggesting that
PTPN2
inhibition may potentiate the effect of immunotherapies that invoke an IFNγ response.
Ptpn2 deletion enhances tumour suppression
Cancer immunotherapy treatments, such as PD-1 checkpoint blockade, are only effective in a minority of patients, suggesting the need to investigate new treatment strategies. Nicholas Haining and colleagues describe a functional genomics approach using the CRISPR–Cas9 system to identify genes that affect the response to immune checkpoint blockade in the B16 mouse transplantable tumour model. They show that loss of function of the phosphatase PTPN2 in tumour cells enhances interferon-γ-mediated effects on antigen presentation and growth suppression. This finding suggests that PTPN2 is a potential target for cancer immunotherapy and that
in vivo
genetic screenings of tumour models could help identify other possible targets.
Journal Article