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endocarditis/l tyrosine
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Rapid reversion of Loeffler's endocarditis by imatinib in early stage clonal hypereosinophilic syndrome.
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Endomyocardial fibrosis (Loeffler's endocarditis) is the main cause of poor outcome in Hyper Eosinophilic Syndrome (HES) and Eosinophilic Leukemia (EL). Reversion of the cardiac damage has been seldom reported, and thrombi can superimpose on infiltrated walls, originating oembolic complications. The
In-hospital metabolite changes in infective endocarditis-a longitudinal 1H NMR-based study.
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Treatment of infective endocarditis (IE) is a 4-6-week provided course of intravenously administered antibiotics. The aim of this study was to investigate how serum metabolites as measured by proton nuclear magnetic resonance (1H NMR) spectroscopy are changing over time during the active
Loeffler endocarditis in a pediatric patient.
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Loefler endocarditis is a potential fatal adverse event of hypereosinophilic syndrome. We report a case of a 5-year-old girl diagnosed with peripheral hypereosinophilia refractory to corticosteroid therapy who developed eosinophilia-related endocarditis. Echocardiography revealed infiltration of the
[Complete remission of Loeffler's endocarditis with Imatinib in a myeloid and lymphoid neoplasm associated with eosinophilia].
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Severe mitral regurgitation caused by eosinophilic endocarditis.
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We describe a patient with symptoms of heart failure caused by severe mitral regurgitation. Echocardiography revealed an intracardiac mass embedding the posterior mitral valve leaflet, and cardiac magnetic resonance imaging showed two intracardiac thrombi and endomyocardial fibrosis. Eosinophil
Tyrosine tRNA synthetase as a novel extracellular immunomodulatory protein in Streptococcus anginosus
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Streptococcus anginosus is frequently detected in patients with infective endocarditis, abscesses, or oral cancer. Although S. anginosus is considered the causative pathogen of these diseases, the pathogenic mechanisms of the bacterium have remained unclear. Previously, we suggested that an
Endocarditis pathogen promotes vegetation formation by inducing intravascular neutrophil extracellular traps through activated platelets.
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BACKGROUND
Endocarditis-inducing streptococci form multilayered biofilms in complex with aggregated platelets on injured heart valves, but the host factors that interconnect and entrap these bacteria-platelet aggregates to promote vegetation formation were unclear.
RESULTS
In a Streptococcus mutans
Safety and potential risks of enterococci isolated from traditional fermented capers.
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A collection of 17 enterococci isolates obtained from fermentations of capers (the fruits of Capparis sp.) were investigated for incidence of known virulence determinants, antibiotic resistance and production of biogenic amines. Molecular identification revealed the presence of Enterococcus faecium
Safety of Lactobacillus plantarum ST8Sh and Its Bacteriocin.
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Total DNA extracted from Lb. plantarum ST8Sh was screened for the presence of more than 50 genes related to production of biogenic amines (histidine decarboxylase, tyrosine decarboxylase, and ornithine decarboxylase), virulence factors (sex pheromones, gelatinase, cytolysin, hyaluronidase,
Mechanism of outside-in {alpha}IIb{beta}3-mediated activation of human platelets by the colonizing Bacterium, Streptococcus gordonii.
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OBJECTIVE
To better understand the mechanism of platelet recruitment and activation by Streptococcus gordonii. The oral bacterium Streptococcus gordonii, is amongst the most common pathogens isolated from infective endocarditis patients, and has the property of being able to activate platelets,
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