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1.
J Clin Ultrasound ; 50(6): 826-831, 2022 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-35018654

RESUMEN

Hepatic epithelioid hemangioendothelioma (HEHE) is a very rare vascular endothelial cell tumor, which lacks typical clinical manifestations and specificity of imaging features. Whether the background of fatty liver and the difference in Contrast enhanced ultrasound (CEUS) characteristics between large and small lesions has not been well defined. In this case reports, we described the ultrasound image features of three patients with HEHE. These three patients with HEHE have certain similar characteristics of conventional ultrasound and CEUS. CEUS imaging features include large nodules show earlier perfusion than liver parenchyma, with rim-enhancement, nonenhancing regions in the center, while small nodules show earlier perfusion than liver parenchyma, with hyperenhancement. All nodules show faster washout than hepatic parenchyma, showing heterogeneous hypoenhancement, and more washout lesions can be found in the PVP and LP. Conventional ultrasound and CEUS not only help to improve the diagnostic confidence of HEHE of rare liver tumors, but also can guide the biopsy area, making it easier to make accurate pathological diagnosis.


Asunto(s)
Hemangioendotelioma Epitelioide , Neoplasias Hepáticas , Medios de Contraste , Hemangioendotelioma Epitelioide/diagnóstico por imagen , Hemangioendotelioma Epitelioide/patología , Humanos , Neoplasias Hepáticas/diagnóstico por imagen , Neoplasias Hepáticas/patología , Estudios Retrospectivos , Ultrasonografía
2.
J Colloid Interface Sci ; 257(2): 244-9, 2003 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-16256476

RESUMEN

The theoretical analysis of the intrinsic ionization constant (K(a2)(int)) of Fe-Al-Mg hydrotalcite-like compounds (HTlc) possessing permanent charges was first performed using the double extrapolation method proposed by James et al. The theoretical permanent charge density (sigma(p,T)) of the HTlc sample was calculated from the crystal structure of HTlc, and the influence of sigma(p,T) on the K(a2)(int) was also examined. From the experimental results, these conclusions can be obtained: the zero point of the charge (pH(ZPC)) of Fe-Al-Mg HTlc increases with decreased Fe3+ content and increases with increased Mg2+ in the HTlc. The pK(a2)(int) of Fe-Al-Mg HTlc also increases with decreased Fe3+ and increased Mg2+ content in the sample; furthermore, the pK(a2)(int) of Fe-Al-Mg HTlc increases with decreased sigma(p,T).

3.
PLoS One ; 9(8): e104135, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25101666

RESUMEN

BACKGROUND: Cardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hyperacetylation and Gata4 over-expression induced by ethanol remain unclear. METHODS AND RESULTS: Pregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol. CONCLUSIONS: Our results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes.


Asunto(s)
Ácidos Anacárdicos/farmacología , Etanol/toxicidad , Desarrollo Fetal/efectos de los fármacos , Factor de Transcripción GATA4/metabolismo , Corazón/embriología , Histonas/metabolismo , Acetilación/efectos de los fármacos , Animales , Secuencia de Bases , Femenino , Factor de Transcripción GATA4/química , Regulación del Desarrollo de la Expresión Génica , Ratones Endogámicos , Datos de Secuencia Molecular , Embarazo , Efectos Tardíos de la Exposición Prenatal , Regiones Promotoras Genéticas , Análisis de Secuencia de ADN
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