Here, we report on the development of a genetic system for Marinobacter sp. strain CP1, previously isolated from the Biocathode MCL community and shown to oxidize iron and grow as a cathodic biofilm. Sequence analysis of the small and large subunits of the 16S rRNA gene of CP1, as well as comparison of select conserved proteins, indicate that it is most closely related to Marinobacter adhaerens HP15 and Marinobacter sp. ES.042. In silico DNA–DNA hybridization using the genome-to-genome distance calculator (GGDC) predicts CP1 to be a new species of Marinobacter described here as Marinobacter atlanticus. CP1 is competent for transformation with plasmid DNA using conjugation with Escherichia coli donor strain WM3064 and constitutive expression of green fluorescent protein (GFP) is stable in the absence of antibiotic selection. Targeted double deletion mutagenesis of homologs for the M. aquaeoli fatty acyl-CoA reductase (acrB) and fatty aldehyde reductase (farA) genes resulted in a loss of production of wax esters; however, single deletion mutants for either gene resulted in an increase in total wax esters recovered. Genetic tools presented here for CP1 will enable further exploration of wax ester synthesis for biotechnological applications, as well as furthering our efforts to understand the role of CP1 within the Biocathode MCL community.
Background: Drug-induced pericarditis is an important cause of pericarditis and if un-noticed and un-managed can lead to constrictive pericarditis, pericardial effusion and cardiac tamponade. Objective: The objective of this analysis was to determine if a significant signal exists between Azacitidine use and pericarditis. Methods: A pharmacovigilance analysis was performed using the FDA Adverse Event Database. Results: 48 reports of Azacitidine induced pericarditis with Azacitidine as the suspect drug were identified. The most common indications for Azacitidine use in the adverse event reports were myelodysplastic syndrome (48%) and acute myelogenous leukemia (27%). Physicians reported 44% of the Azacitidine induced pericarditis reports while other health professional reported 52% of the reports. The disproportionality analysis showed a PRR of 5.0, chi-squared of 149.8, ROR of 5.0 and IC025 of 1.8. Literature review found three case reports of Azacitidine induced pericarditis. Conclusion: The signal between Azacitidine and pericarditis was found to be statistically significant. Clinicians should be aware of the possible risk of pericarditis when prescribing Azacitidine. If there is suspicion for Azacitidine induced pericarditis, clinicians should consider discontinuation of Azacitidine to improve patient’s symptoms and reduce the likelihood of the development of constrictive pericarditis, pericardial effusion and cardiac tamponade.
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