Objectives: Cardiac surgery is associated with perioperative complications, some of which might be attributable to hypotension. The Hypotension Prediction Index (HPI), a machine-learning-derived early warning tool for hypotension, has only been evaluated in noncardiac surgery. We investigated whether using HPI with diagnostic guidance reduced hypotension during cardiac surgery and in the ICU.
View Article and Find Full Text PDFMethylerythritol cyclodiphosphate (MEcPP) is an intermediate in the biosynthesis of isoprenoids in plant plastids and in bacteria, and acts as a stress signal in plants. Here, we show that MEcPP regulates biofilm formation in Escherichia coli K-12 MG1655. Increased MEcPP levels, triggered by genetic manipulation or oxidative stress, inhibit biofilm development and production of fimbriae.
View Article and Find Full Text PDFStudy Objectives: To identify the influence of modifiable factors in anesthesia induction strategy on post-induction hypotension (PIH), specifically the type, dosage and speed of administration of induction agents. A secondary aim was to identify patient related non-modifiable factors associated with PIH.
Design: Single-center, prospective observational cohort study.
Background: Postinduction hypotension (PIH) may be associated with increased morbidity and mortality. In earlier studies, the definition of PIH is solely based on different absolute or relative thresholds. However, the time-course (eg, how fast blood pressure drops during induction) is rarely incorporated, whereas it might represent the hemodynamic instability of a patient.
View Article and Find Full Text PDFUnlabelled: The intricate communication between plastids and the nucleus, shaping stress-responsive gene expression, has long intrigued researchers. This study combines genetics, biochemical analysis, cellular biology, and protein modeling to uncover how the plastidial metabolite MEcPP activates the stress-response regulatory hub known as the Rapid Stress Response Element (RSRE). Specifically, we identify the HAT1/TPL/IMPα- 9 suppressor complex, where HAT1 directly binds to RSRE and its activator, CAMTA3, masking RSRE and sequestering the activator.
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