ABSTRACT
Left atrial (LA) masses are known to be associated with peripheral embolization. Accurate identification of etiology is crucial because treatment strategies may differ. We present the case of a young woman, who was initially diagnosed with a LA thrombus and anticoagulated. The diagnosis was revised to a primary cardiac tumor after review of the echocardiographic findings. Surgical excision revealed an atrial myxoma in an unusual location.
Subject(s)
Atrial Appendage/diagnostic imaging , Echocardiography, Doppler/methods , Echocardiography, Transesophageal/methods , Heart Neoplasms/diagnosis , Myxoma/diagnosis , Adult , Female , Humans , Tomography, X-Ray ComputedSubject(s)
Adenocarcinoma/secondary , Breast Neoplasms/pathology , Carcinoma, Squamous Cell/secondary , Gastrointestinal Neoplasms/pathology , Melanoma/secondary , Skin Neoplasms/secondary , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Retrospective Studies , Singapore , Tertiary Care CentersABSTRACT
GPR40 is a member of a subfamily of homologous G protein-coupled receptors that include GPR41 and GPR43 and that have no current function or ligand ascribed. Ligand fishing experiments in HEK293 cells expressing human GPR40 revealed that a range of saturated and unsaturated carboxylic acids with carbon chain lengths greater than six were able to induce an elevation of [Ca(2+)](i), measured using a fluorometric imaging plate reader. 5,8,11-Eicosatriynoic acid was the most potent fatty acid tested, with a pEC(50) of 5.7. G protein coupling of GPR40 was examined in Chinese hamster ovary cells expressing the G alpha(q/i)-responsive Gal4-Elk1 reporter system. Expression of human GPR40 led to a constitutive induction of luciferase activity, which was further increased by exposure of the cells to eicosatriynoic acid. Neither the constitutive nor ligand-mediated luciferase induction was inhibited by pertussis toxin treatment, suggesting that GPR40 was coupled to G alpha(q/11.) Expression analysis by quantitative reverse transcription-PCR showed that GPR40 was specifically expressed in brain and pancreas, with expression in rodent pancreas being localized to insulin-producing beta-cells. These data suggest that some of the physiological effects of fatty acids in pancreatic islets and brain may be mediated through a cell-surface receptor.
