Publications by authors named "Emily Hess"

Thiamine is a vital co-factor for several anti-inflammatory and antioxidant processes that are critical for mitigation of sepsis-associated inflammation, but pharmacokinetic (PK) analysis has not been reported in horses. We hypothesized that IV thiamine hydrochloride (TH) at increasing dosages would result in corresponding increases in plasma thiamine concentrations without causing adverse effects. A randomized cross-over study was performed in 9 healthy horses that each received TH at 5, 10, and 20 mg/kg IV.

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Background: In metabolically stable horses, alpha-2-agonists suppress insulin secretion with transient hyperglycemia and rebound hyperinsulinemia. In horses with insulin dysregulation (ID), the effect of alpha-2-agonists has not been investigated; however, both the alpha-2-agonist-induced suppression of insulin secretion and rebound hyperinsulinemia could have clinical relevance.

Hypothesis/objectives: In horses with ID, alpha-2-agonists will alter insulin and glucose dynamics.

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Objective: To determine the influence of needle gauge, syringe volume, and syringe size on needle tract leakage after injection in porcine jejunum.

Study Design: Ex vivo experiment.

Sample Population: Three hundred sixty jejunal segments from 20 feedlot pigs.

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Background: People with acute psychiatric illness may be at risk of coercion into informal admission. A lack of capacity assessment (CA) and provision of adequate information (PAI) for informal patients may constitute a risk of coercive admitting practice, resulting in increased use of the mental health act (MHA) in the days following admission. We developed and tested a proforma to aid in ensuring CA and PAI for informal admissions.

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Microvascular endothelial cells maintain a tight barrier to prevent passage of plasma and circulating immune cells into the extravascular tissue compartment, yet endothelial cells respond rapidly to vasoactive substances, including thrombin, allowing transient paracellular permeability. This response is a cornerstone of acute inflammation, but the mechanisms responsible are still incompletely understood. Here, we demonstrate that thrombin triggers MALT1 to proteolytically cleave cylindromatosis (CYLD).

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