8 research outputs found

    Behavioural and neural changes after a “choice” therapy for naming deficits in aphasia: preliminary findings

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    Outcomes & Results: All the individuals demonstrated a significant treatment effect immediately post-treatment and at a 4-week follow-up and four of the five participants at an 8-week follow-up. Three also demonstrated generalisation to untrained items. Unfortunately, no clear-cut patterns emerged to allow us to make claims about the influence of choice, per se, on the behavioural manifestations of improved naming. Interestingly, the participant from the Choice condition showed neural activation changes post-treatment in frontal and parietal regions that were not evident for the participant in the No Choice condition. Moreover, these changes were accompanied by a larger treatment effect for that individual and generalisation to a novel naming task.Background: Anomia, difficulty producing words, is a pervasive symptom of many individuals with aphasia. We have developed a treatment for naming deficits—the Phonological Components Analysis (PCA) protocol—that has proven efficacious in improving word-finding abilities for individuals with post-stroke aphasia.Aims: The aim of this investigation is to present preliminary findings exploring the potential influence of choice—that is the active engagement of a participant in therapy—on our PCA treatment.Methods & Procedures: Five individuals with aphasia were treated in one of two conditions—Choice or No Choice. Potential changes in neural activation as a function of the treatment were also investigated. Two individuals (one from each condition) underwent functional MRI (fMRI) pre- and post-therapy.Conclusion: The efficacy of PCA treatment for naming deficits is further supported. In addition, the neuroimaging data suggest the possibility that active engagement of an individual in his/her therapy (in this case choosing phonological attributes of a target word) may exercise executive functions important for success in treating anomia. Also, continued exploration of task factors that may promote even better treatment effects using this protocol is warranted, as is continued investigation of the neural underpinnings associated with treatment effects

    Apoptotic cell death in disease-Current understanding of the NCCD 2023

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    Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease

    Apoptotic cell death in disease—current understanding of the NCCD 2023

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    Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease

    Apoptotic cell death in disease-Current understanding of the NCCD 2023

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    Targeting tumour hypoxia to prevent cancer metastasis. From biology, biosensing and technology to drug development: the METOXIA consortium

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    Apoptotic cell death in disease—Current understanding of the NCCD 2023

    No full text
    Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease
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