No abstract

Summary: Endocarditis caused by Fusobacterium nucleatum is exceedingly rare. We report a case of E nucleatum right-sided endocarditis in a patient with no known intravenous drug abuse. A detailed computer and manual search of the literature using Med-Line and Index Medicus, respectively, revealed a total of five cases of endocarditis due to this species. The clinical characteristics and the patient's hospital course are summarized and reviewed.Key words: endocarditis, tricuspid valve, Fusobacterium nucleatum revealed a total of five previously reported cases of endocarditis in which this species has been identified as a single causative agent,3*4 or as part of a polymicrobial infect i~n .~+~ The total number of cases of endocarditis due to the genus Fusobacterium included 15 cases: 7 of these were E necrophor~m,~ 5 were E n~c l e a t u m ,~-~ and 3 were unidentified Fusobacterium species."* Our case brings the total number of cases of identified E nucleatum endocarditis to six. The clinical features and hospital course of our patient, as well as those documented for E nucleatum, are reviewed and summarized (Table I). Case Report IntroductionInfections due to anaerobic gram-negative nonsporeforming bacilli, including the genera Bacteroides and Fusobacterium, have been well documented.' However, endocarditis caused by these organisms remains relatively uncommon and is mostly due to Bacteroidesfragilis.* Endocarditis caused by the Fusobacterium genus is exceedingly rare. We report a case of right-sided endocarditis due to Fusobacterium nucleatum (previously known as E fisiform).

Clinical use of glucocorticoids is associated with increased intraocular pressure (IOP), a major risk factor for glaucoma. Glucocorticoids have been reported to induce changes in actin cytoskeletal organization, cell adhesion, extracellular matrix, fibrogenic activity, and mechanical properties of trabecular meshwork (TM) tissue, which plays a crucial role in aqueous humor dynamics and IOP homeostasis. However, we have a limited understanding of the molecular underpinnings regulating these myriad processes in TM cells. To understand how proteins, including cytoskeletal and cell adhesion proteins that are recognized to shuttle between the cytosolic and nuclear regions, influence gene expression and other cellular activities, we used proteomic analysis to characterize the nuclear protein fraction of dexamethasone (Dex) treated human TM cells. Treatment of human TM cells with Dex for 1, 5, or 7 days led to consistent increases (by ≥ two-fold) in the levels of various actin cytoskeletal regulatory, cell adhesive, and vesicle trafficking proteins. Increases (≥two-fold) were also observed in levels of Wnt signaling regulator (glypican-4), actin-binding chromatin modulator (BRG1) and nuclear actin filament depolymerizing protein (MICAL2; microtubule-associated monooxygenase, calponin and LIM domain containing), together with a decrease in tissue plasminogen activator. These changes were independently further confirmed by immunoblotting analysis. Interestingly, deficiency of BRG1 expression blunted the Dex-induced increases in the levels of some of these proteins in TM cells. In summary, these findings indicate that the widely recognized changes in actin cytoskeletal and cell adhesive attributes of TM cells by glucocorticoids involve actin regulated BRG1 chromatin remodeling, nuclear MICAL2, and glypican-4 regulated Wnt signaling upstream of the serum response factor/myocardin controlled transcriptional activity.