Publications by authors named "B W Gallaher"

Introduction: The electronic health record (EHR) has greatly expanded healthcare communication between patients and health workers. However, the volume and complexity of EHR messages have increased health workers' cognitive load, impeding effective care delivery and contributing to burnout.

Methods: To understand these potential detriments resulting from EHR communication, we analyzed EHR messages sent between patients and health workers at Emory Healthcare, a large academic healthcare system in Atlanta, Georgia.

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is the causative agent of Q fever and an obligate intracellular pathogen in nature that survives and grows in a parasitophorous vacuole (PV) within eukaryotic host cells. promotes intracellular survival by subverting apoptotic and pro-inflammatory signaling pathways that are typically regulated by nuclear transcription factor-κB (NF-κB). We and others have demonstrated that NMII proteins inhibit expression of pro-inflammatory cytokines and induce expression of anti-apoptotic genes during infection.

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Helicobacter pylori is the major cause of peptic ulcers and gastric cancer in humans. Treatment involves a two or three drug cocktail, typically including amoxicillin. Increasing levels of resistance to amoxicillin contribute to treatment failures, and higher levels of resistance are believed to be due to multiple genetic mutations.

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Exposure of the fetus to excess maternal glucocorticoids has been postulated to alter fetal growth and development, and thus provide a possible mechanism for the link between impaired fetal growth and altered postnatal physiology. However, the effects of exposure to excess maternal glucocorticoids on fetal physiology and metabolism in utero have not been described. We therefore studied the effects of chronic maternal cortisol infusion on fetal growth, blood pressure, metabolism and endocrine status in chronically catheterised fetal sheep.

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This review presents a brief overview of the cell's apoptotic machinery, including specific and indirect death signals. Specific death signals are transferred via death ligands, death receptors, and their intracellular signalling pathways. Indirect death signals cumulate a wide range of stimuli that potentially harm survival of cells.

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