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2.
JBR-BTR ; 90(5): 315-24, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-18085185

RESUMO

Pseudocysts, lipomas, infarcts and simple cysts of the calcaneus are described as different entities in the medical literature. However, some evolutions or associations may suggest a relationship which is not yet demonstrated in all cases. The aim of this article is to describe each lesion and emphasize their different characteristics that may suggest a relationship between them.


Assuntos
Cistos Ósseos/diagnóstico , Neoplasias Ósseas/diagnóstico , Calcâneo , Diagnóstico por Imagem , Infarto/diagnóstico , Lipoma/diagnóstico , Calcâneo/irrigação sanguínea , Calcâneo/patologia , Diagnóstico Diferencial , Fraturas Ósseas/diagnóstico , Humanos , Necrose
3.
J Membr Biol ; 194(1): 21-32, 2003 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-14502440

RESUMO

Extracellular nucleotides exert autocrine/ paracrine effects on ion transport by activating P2 receptors. We studied the effects of extracellular ATP and UTP on the cystic fibrosis transmembrane conductance regulator (CFTR) channel stably expressed in Chinese Hamster Ovary cells (CHO-BQI cells). CFTR activity was measured using the (125I) iodide efflux technique and whole-cell patch-clamp recording in response to either forskolin or xanthine derivatives. Using RT-PCR and intracellular calcium concentration ([Ca2+]i) measurement, we showed that CHO-BQI cells express P2Y2 but not P2Y4 receptors. While ATP and UTP induced similar increases in [Ca2+]i, pre-addition by one of these two agonists desensitized the response for the other, suggesting that ATP- and UTP-induced [Ca2+]i increases were mediated by a common receptor, which was identified as the P2Y2 subtype. CFTR activity was reduced by ATP and UTP but not by ADP or adenosine applications. This inhibitory effect of ATP on CFTR activity was not due to a change in cAMP level. Furthermore, CFTR activation by forskolin or IBMX failed to promote [Ca2+]i increase, suggesting that CFTR activation did not generate an ATP release large enough to stimulate P2Y2 receptors. Taken together, our results show that endogenous P2Y2 receptor activation downregulates CFTR activity in a cAMP-independent manner in CHO cells.


Assuntos
Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia , Receptores Purinérgicos P2/fisiologia , Trifosfato de Adenosina/farmacologia , Animais , Sequência de Bases , Células CHO , Cálcio/metabolismo , Clonagem Molecular , Cricetinae , Regulador de Condutância Transmembrana em Fibrose Cística/efeitos dos fármacos , Regulador de Condutância Transmembrana em Fibrose Cística/genética , Primers do DNA , Iodetos/metabolismo , Técnicas de Patch-Clamp , Receptores Purinérgicos P2/efeitos dos fármacos , Receptores Purinérgicos P2Y2 , Proteínas Recombinantes/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transfecção , Uridina Trifosfato/farmacologia
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