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3.
Tex Heart Inst J ; 47(4): 311-314, 2020 08 01.
Article in English | MEDLINE | ID: mdl-33472227

ABSTRACT

Infective endocarditis of a fully endothelialized cardiac prosthesis, and especially the late presentation of endocarditis, challenges our current understanding of device-related complications. Late bacterial endocarditis associated with the Amplatzer Septal Occluder, a device frequently used to close atrial septal defects, has been documented only rarely. We report the case of an intravenous drug user who had late infective endocarditis associated with his Amplatzer Septal Occluder, secondary to methicillin-sensitive Staphylococcus aureus bacteremia nearly 14 years after device insertion. The patient recovered after surgical excision and débridement of the vegetative mass, which may be the first time that a surgical approach has been taken to treat this condition. This report corroborates the need for late screening of high-risk patients who have septal occluder devices.


Subject(s)
Endocarditis, Bacterial/etiology , Septal Occluder Device , Staphylococcal Infections/etiology , Substance Abuse, Intravenous/complications , Adult , Cardiac Catheterization/methods , Echocardiography, Transesophageal , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/microbiology , Humans , Male , Staphylococcal Infections/diagnosis , Staphylococcal Infections/microbiology
4.
FASEB J ; 27(12): 5022-33, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24043261

ABSTRACT

It has been hypothesized that the peripheral taste system may be modulated in the context of an animal's metabolic state. One purported mechanism for this phenomenon is that circulating gastrointestinal peptides modulate the functioning of the peripheral gustatory system. Recent evidence suggests endocrine signaling in the oral cavity can influence food intake (FI) and satiety. We hypothesized that these hormones may be affecting FI by influencing taste perception. We used immunohistochemistry along with genetic knockout models and the specific reconstitution of peptide YY (PYY) in saliva using gene therapy protocols to identify a role for PYY signaling in taste. We show that PYY is expressed in subsets of taste cells in murine taste buds. We also show, using brief-access testing with PYY knockouts, that PYY signaling modulates responsiveness to bitter-tasting stimuli, as well as to lipid emulsions. We show that salivary PYY augmentation, via viral vector therapy, rescues behavioral responsiveness to a lipid emulsion but not to bitter stimuli and that this response is likely mediated via activation of Y2 receptors localized apically in taste cells. Our findings suggest distinct functions for PYY produced locally in taste cells vs. that circulating systemically.


Subject(s)
Peptide YY/metabolism , Satiety Response , Taste , Animals , Eating , Mice , Mice, Knockout , Peptide YY/genetics , Receptors, Neuropeptide Y/genetics , Receptors, Neuropeptide Y/metabolism , Taste Buds/metabolism
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