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1.
Aging Ment Health ; 28(3): 520-530, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-37139937

RESUMEN

AIM: There is a lack of clarity about therapeutic lying in the context of everyday dementia care. This study provides conceptual clarity on how the term is used and considers the concept in relation to person-centred care. METHODS: Rodgers' (1989) evolutionary framework of concept analysis was employed. A systematic multiple database search was conducted and supplemented with snowballing techniques. Data were analysed thematically through an iterative process of constant comparison. RESULTS: This study highlighted that therapeutic lying is intended to be used in the person's best interests for the purpose of doing good. However, its potential for doing harm is also evident. Its use in the literature has increased with the general trend towards becoming more accepted in the discourse. A continuum emerged depending on the degree to which a lie departs from the truth. Emerging guidelines were also evident as to when a lie could or could not be justified. CONCLUSION: The term therapeutic lying, was contrasted with aspects of person-centred care and was found to be problematic. We conclude that there may be more pragmatic ways of constructing language around the care of people with dementia which could be less stigmatising.


Asunto(s)
Demencia , Humanos , Demencia/terapia , Atención Dirigida al Paciente , Lenguaje , Bases de Datos Factuales
2.
J Chem Ecol ; 47(8-9): 719-731, 2021 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-34402994

RESUMEN

Organisms depend on visual, auditory, and olfactory cues to signal the presence of danger that could impact survival and reproduction. Drosophila melanogaster emits an olfactory alarm signal, termed the Drosophila stress odorant (dSO), in response to mechanical agitation or electric shock. While it has been shown that conspecifics avoid areas previously occupied by stressed individuals, the contextual underpinnings of the emission of, and response to dSO, have received little attention. Using a binary choice assay, we determined that neither age and sex of emitters, nor the time of the day, affected the emission or avoidance of dSO. However, both sex and mating status affected the response to dSO. We also demonstrated that while D. melanogaster, D. simulans, and D. suzukii, have different dSO profiles, its avoidance was not species-specific. Thus, dSO should not be considered a pheromone but a general alarm signal for Drosophila. However, the response levels to both intra- and inter-specific cues differed between Drosophila species and possible reasons for these differences are discussed.


Asunto(s)
Drosophila/química , Odorantes/análisis , Envejecimiento , Animales , Relojes Biológicos , Drosophila/fisiología , Drosophila melanogaster/química , Drosophila melanogaster/fisiología , Estimulación Eléctrica , Femenino , Cromatografía de Gases y Espectrometría de Masas , Factores Sexuales , Conducta Sexual Animal , Especificidad de la Especie , Estrés Mecánico , Compuestos Orgánicos Volátiles/análisis
3.
Sci Rep ; 8(1): 3673, 2018 02 27.
Artículo en Inglés | MEDLINE | ID: mdl-29487349

RESUMEN

We report the effects of aging and parental age in Drosophila melanogaster on two types of responses to social cues: the choice of preferred social spacing in an undisturbed group and the response to the Drosophila stress odorant (dSO) emitted by stressed flies. The patterns of changes during aging were notably different for these two social responses. Flies were initially closer in space and then became further apart. However, the pattern of change in response to dSO followed a more typical decline in performance, similarly to changes in locomotion. Interestingly, the increased social space of old parents, as well as their reduced performance in avoiding dSO, was passed on to their progeny, such that young adults adopted the behavioural characteristic of their old parents. While the response to social cues was inherited, the changes in locomotion were not. We were able to scale the changes in the social space of parents and their progeny by accelerating or decelerating the physiological process of aging by increasing temperatures and exposure to oxidative stress, or via caloric restriction, respectively. Finally, when we aged only one parent, only the male progeny of old fathers and the progeny of very old mothers were more distant.


Asunto(s)
Drosophila melanogaster/fisiología , Envejecimiento/fisiología , Animales , Femenino , Locomoción/fisiología , Masculino , Temperatura
4.
Hum Mol Genet ; 26(21): 4278-4289, 2017 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-28973161

RESUMEN

Defects in neuronal migration cause brain malformations, which are associated with intellectual disability (ID) and epilepsy. Using exome sequencing, we identified compound heterozygous variants (p.Arg71His and p. Leu729ThrfsTer6) in TMTC3, encoding transmembrane and tetratricopeptide repeat containing 3, in four siblings with nocturnal seizures and ID. Three of the four siblings have periventricular nodular heterotopia (PVNH), a common brain malformation caused by failure of neurons to migrate from the ventricular zone to the cortex. Expression analysis using patient-derived cells confirmed reduced TMTC3 transcript levels and loss of the TMTC3 protein compared to parental and control cells. As TMTC3 function is currently unexplored in the brain, we gathered support for a neurobiological role for TMTC3 by generating flies with post-mitotic neuron-specific knockdown of the highly conserved Drosophila melanogaster TMTC3 ortholog, CG4050/tmtc3. Neuron-specific knockdown of tmtc3 in flies resulted in increased susceptibility to induced seizures. Importantly, this phenotype was rescued by neuron-specific expression of human TMTC3, suggesting a role for TMTC3 in seizure biology. In addition, we observed co-localization of TMTC3 in the rat brain with vesicular GABA transporter (VGAT), a presynaptic marker for inhibitory synapses. TMTC3 is localized at VGAT positive pre-synaptic terminals and boutons in the rat hypothalamus and piriform cortex, suggesting a role for TMTC3 in the regulation of GABAergic inhibitory synapses. TMTC3 did not co-localize with Vglut2, a presynaptic marker for excitatory neurons. Our data identified TMTC3 as a synaptic protein that is involved in PVNH with ID and epilepsy, in addition to its previously described association with cobblestone lissencephaly.


Asunto(s)
Proteínas Portadoras/genética , Proteínas Portadoras/metabolismo , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Heterotopia Nodular Periventricular/metabolismo , Adulto , Animales , Encéfalo/anomalías , Corteza Cerebral/metabolismo , Drosophila melanogaster , Epilepsia/genética , Epilepsia/metabolismo , Femenino , Técnicas de Silenciamiento del Gen , Heterocigoto , Humanos , Discapacidad Intelectual/genética , Discapacidad Intelectual/metabolismo , Masculino , Malformaciones del Sistema Nervioso/metabolismo , Neuronas/metabolismo , Linaje , Heterotopia Nodular Periventricular/genética , Terminales Presinápticos , Ratas , Convulsiones/metabolismo , Sinapsis/metabolismo , Secuenciación del Exoma
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