Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
1.
Clin Neurol Neurosurg ; 214: 107167, 2022 03.
Artículo en Inglés | MEDLINE | ID: mdl-35176633

RESUMEN

BACKGROUND: Hypopituitarism seems to be rather common following aneurysmal subarachnoid haemorrhage (aSAH), even though its real prevalence remains unclear and the effects on six-month patient functional outcomes are debatable. This study correlated hypopituitarism after aSAH and cognitive performances using neuropsychological tests. METHODS: In a prospective cohort of patients with aSAH, basal pituitary hormone testing was undergone and two neuropsychological tests, Montreal Cognitive Assessment (MoCA) and Mini Mental Status Examination (MMSE), were administered in three phases: in the subacute phase (2 weeks), the chronic phase (3-6 months) and the follow-up phase (6-12 months) post aSAH. RESULTS: Twenty-five patients were enrolled in the study. Considering the median values of MMSE and MoCA in the subacute phase there was an association with hypo-free triiodothyronine (fT3) (p = 0.03, p = 0.03), hypo-luteinizing hormone (LH) (p = 0.002, p = 0.0002), hypo-follicle stimulating hormone (FSH) (p = 0.002, p = 0.002) and hypo-testosterone (p = 0.02, p = 0.05) respectively. Similarly, in the chronic phase we found an association of median values of MMSE and MoCA with hypo-free thyroxine (fT4) (p = 0.03, p = 0.03), hypo-LH (p = 0.03, p = 0.03) and hypo-FSH (p = 0.03, p = 0.03), respectively. Finally, in the follow-up phase, MMSE and MoCA correlated with hypo-fT4 (p = 0.03, p = 0.03), hypo-LH (p = 0.05, p = 0.05) and hypo-FSH (p = 0.05, p = 0.05), respectively. CONCLUSIONS: For aSAH patients in the post-acute phase, neuropsychological tests can represent an inexpensive tool to confirm cognitive impairment, which can be associated with neuroendocrine dysfunction.


Asunto(s)
Disfunción Cognitiva , Hipopituitarismo , Hemorragia Subaracnoidea , Cognición , Disfunción Cognitiva/complicaciones , Disfunción Cognitiva/etiología , Hormona Folículo Estimulante , Humanos , Hipopituitarismo/complicaciones , Hipopituitarismo/etiología , Hormona Luteinizante , Pruebas Neuropsicológicas , Proyectos Piloto , Estudios Prospectivos , Hemorragia Subaracnoidea/complicaciones , Hemorragia Subaracnoidea/diagnóstico , Hemorragia Subaracnoidea/epidemiología
2.
Cancer Lett ; 288(2): 170-6, 2010 Feb 28.
Artículo en Inglés | MEDLINE | ID: mdl-19619936

RESUMEN

The study investigated the effects of the dopamine-somatostatin chimeric compound BIM-23A760 on cell proliferation and apoptosis in cultured cells from human non-functioning pituitary tumors (NFPTs). Both BIM-23A760 and the dopaminergic agonist BIM-53097 induced a significant inhibition of cell proliferation associated with increased p27 expression, together with a significant increase in caspase-3 activity. Conversely, null or marginal effects were elicited by somatostatin analogs. Moreover, BIM-23A760 and BIM-53097 induced ERK1/2 and p38 phosphorylation and the blockade of these pathways prevented both the antiproliferative and the pro-apoptotic effects of these drugs. In conclusions the chimeric compound BIM-23A760 is able to exert cytostatic and cytotoxic effects in NFPTs, these phenomena being mainly mediated by DR2D and involving ERK1/2 and p38 pathways activation.


Asunto(s)
Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Dopamina/análogos & derivados , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Neoplasias Hipofisarias/enzimología , Somatostatina/análogos & derivados , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo , Adulto , Anciano , Caspasa 3/metabolismo , Inhibidor p27 de las Quinasas Dependientes de la Ciclina , Dopamina/farmacología , Agonistas de Dopamina/farmacología , Activación Enzimática , Femenino , Humanos , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Masculino , Persona de Mediana Edad , Proteína Quinasa 3 Activada por Mitógenos/antagonistas & inhibidores , Fosforilación , Neoplasias Hipofisarias/patología , Inhibidores de Proteínas Quinasas/farmacología , Receptores de Dopamina D2/agonistas , Receptores de Dopamina D2/metabolismo , Receptores de Somatostatina/efectos de los fármacos , Receptores de Somatostatina/metabolismo , Somatostatina/farmacología , Células Tumorales Cultivadas , Proteínas Quinasas p38 Activadas por Mitógenos/antagonistas & inhibidores
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA