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1.
J Clin Ethics ; 24(4): 343-52, 2013.
Artículo en Inglés | MEDLINE | ID: mdl-24597422

RESUMEN

Physicians and medical institutions in the United States are placing increasing emphasis on providing culturally sensitive care for patients, such as implementing a Confucian family-based model of medical decision making when caring for elderly Chinese patients. In this article, I articulate various reasons why deferring to the family is not a guarantee of culturally sensitive care, particularly when family members are first-generation Chinese-Americans. Nonetheless, I offer several suggestions to help physicians, medical institutions, and family members to provide more culturally sensitive care for elderly Chinese patients.


Asunto(s)
Asiático , Confucionismo , Características Culturales , Toma de Decisiones , Atención a la Salud/ética , Familia , Anciano , Anciano de 80 o más Años , Toma de Decisiones/ética , Emigración e Inmigración , Teoría Ética , Familia/etnología , Familia/psicología , Humanos , Estados Unidos
2.
Elife ; 52016 07 26.
Artículo en Inglés | MEDLINE | ID: mdl-27458797

RESUMEN

Dravet Syndrome is an intractable form of childhood epilepsy associated with deleterious mutations in SCN1A, the gene encoding neuronal sodium channel Nav1.1. Earlier studies using human induced pluripotent stem cells (iPSCs) have produced mixed results regarding the importance of Nav1.1 in human inhibitory versus excitatory neurons. We studied a Nav1.1 mutation (p.S1328P) identified in a pair of twins with Dravet Syndrome and generated iPSC-derived neurons from these patients. Characterization of the mutant channel revealed a decrease in current amplitude and hypersensitivity to steady-state inactivation. We then differentiated Dravet-Syndrome and control iPSCs into telencephalic excitatory neurons or medial ganglionic eminence (MGE)-like inhibitory neurons. Dravet inhibitory neurons showed deficits in sodium currents and action potential firing, which were rescued by a Nav1.1 transgene, whereas Dravet excitatory neurons were normal. Our study identifies biophysical impairments underlying a deleterious Nav1.1 mutation and supports the hypothesis that Dravet Syndrome arises from defective inhibitory neurons.


Asunto(s)
Epilepsias Mioclónicas/genética , Epilepsias Mioclónicas/patología , Mutación , Canal de Sodio Activado por Voltaje NAV1.1/deficiencia , Neuronas/fisiología , Telencéfalo/fisiología , Células Cultivadas , Humanos , Células Madre Pluripotentes Inducidas/fisiología
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