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1.
Ann Vasc Surg ; 93: 71-78, 2023 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-36805426

RESUMEN

BACKGROUND: Most studies on focusing on the prevalence of vascular anomalies are either aimed to determine the individual occurrence of a specific type among known bearers of abnormalities or propose an estimation of prevalence for the general population by extrapolating from the paediatric population. In this scenario, we intended to assess the profile of vascular anomalies in a group of patients subjected to imaging studies, throughout a long period of time, to evaluate the frequency of abnormal findings in a consecutive, nonselected population. METHODS: This is a retrospective review of 996,569 computed tomography and magnetic resonance studies between 2009 and 2019. Findings were grouped as vascular tumours (hemangiomas; vascular tumours), cavernomas, and vascular malformations. Positive findings were evaluated with regard to patients' demographic characteristics and anatomic distribution and the subset of vascular malformations was also evaluated with regard to size, classification in accordance to flow pattern, and Hamburg Classification. RESULTS: Eighteen thousand four hundred thirty positive examinations were evaluated (mean age, 55.82 ± 15.43 years; 8,188 men). Vascular anomalies were present in 18.49 per 1,000 examinations (17.41 hemangiomas; 0.69 cavernomas and 0.39 vascular malformations per 1,000 examinations). Hemangiomas and cavernomas were homogeneous in anatomic location between sexes throughout the age groups. Complex malformations were heterogeneous in anatomic distribution between the sexes in each age group, with intracranial findings decreasing for female patients in older groups. CONCLUSIONS: Vascular anomalies were found in 18.49 per 1,000 examinations. Hemangiomas and cavernomas were homogenously distributed, whereas complex malformations displayed a heterogeneous anatomic distribution pattern between sexes in each age group.


Asunto(s)
Hemangioma Cavernoso , Hemangioma , Malformaciones Vasculares , Neoplasias Vasculares , Niño , Masculino , Humanos , Adulto , Femenino , Anciano , Persona de Mediana Edad , Incidencia , Resultado del Tratamiento , Malformaciones Vasculares/diagnóstico por imagen , Malformaciones Vasculares/epidemiología
2.
J Neurochem ; 106(1): 231-43, 2008 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-18363831

RESUMEN

Na(+)/H(+) exchanger (NHE) proteins are involved in intracellular pH and volume regulation and may indirectly influence neurotransmission. The abundant NHE isoform 1 (NHE1) has also been linked to brain cell damage during metabolic stress. It is not known, however, whether NHE1 or other NHE isoforms play a role in striatal dopamine (DA) neurotransmission under normal or metabolic stress conditions. Our study tested the hypothesis that NHE inhibition with cariporide mesilate (HOE-642) modifies striatal DA overflow and DAergic terminal damage in mice caused by the mitochondrial inhibitor malonate. We also explored the expression of NHE1-5 in the striatum and substantia nigra. Reverse microdialysis of HOE-642 elicited a transient elevation followed by a reduction in DA overflow accompanied by a decline in striatal DA content. HOE-642 pre-treatment diminished the malonate-induced DA overflow without reducing the intensity of the metabolic stress or subsequent DAergic axonal damage. Although NHE isoforms 1-5 are expressed in the striatum and midbrain, NHE1 protein was not co-located on nigrostriatal DAergic neurons. The absence of NHE1 co-location on DAergic neurons suggests that the effects of HOE-642 on striatal DA overflow are either mediated via NHE1 located on other cell types or that HOE-642 is acting through multiple NHE isoforms.


Asunto(s)
Encefalopatías Metabólicas/metabolismo , Proteínas de Transporte de Catión/metabolismo , Cuerpo Estriado/metabolismo , Dopamina/metabolismo , Estrés Oxidativo/fisiología , Intercambiadores de Sodio-Hidrógeno/metabolismo , Transmisión Sináptica/efectos de los fármacos , Animales , Antiarrítmicos/farmacología , Encefalopatías Metabólicas/fisiopatología , Proteínas de Transporte de Catión/antagonistas & inhibidores , Cuerpo Estriado/efectos de los fármacos , Cuerpo Estriado/fisiopatología , Metabolismo Energético/efectos de los fármacos , Metabolismo Energético/fisiología , Guanidinas/farmacología , Masculino , Malonatos/farmacología , Ratones , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Enfermedades Mitocondriales/inducido químicamente , Enfermedades Mitocondriales/metabolismo , Enfermedades Mitocondriales/fisiopatología , Terminales Presinápticos/efectos de los fármacos , Terminales Presinápticos/metabolismo , Terminales Presinápticos/patología , Isoformas de Proteínas/antagonistas & inhibidores , Isoformas de Proteínas/metabolismo , Intercambiador 1 de Sodio-Hidrógeno , Intercambiadores de Sodio-Hidrógeno/antagonistas & inhibidores , Sustancia Negra/efectos de los fármacos , Sustancia Negra/metabolismo , Sulfonas/farmacología , Transmisión Sináptica/fisiología , Degeneración Walleriana/inducido químicamente , Degeneración Walleriana/metabolismo , Degeneración Walleriana/fisiopatología
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