Pharmacokinetic and Pharmacological Aspects of a Papain-Based Enzyme Solution for Rescuing Clogged Enteral Feeding Tubes.

Successful enteral feeding depends on patent enteral feeding tubes to permit trouble-free entry of nutritional formula into the alimentary tract. However, tube clogs can be a challenging complication of enteral feeding. This report addresses questions about using a papain-based enzyme solution to unclog enteral feeding tubes, including any effects that papain may have on patients and if solution use should be contraindicated in patients on ketogenic diets.

Hand hygiene feedback impacts compliance.

Background: Health care-acquired infections are one of the top causes of mortality in the United States (Stone, 2009; Scott, 2009). Hand hygiene (HH) can reduce the incidence of such infections. Adherence to HH practices remains challenging for health care workers (World Health Organization, 2014).

Antirestenotic mechanisms of everolimus on human coronary artery smooth muscle cells: inhibition of human coronary artery smooth muscle cell proliferation, but not migration.

Everolimus, a pharmaceutical component of drug-eluting stents, inhibits coronary vessel restenosis, but the antirestenotic mechanisms of action remain unclear. Here, we describe the effects of everolimus on key contributors to vessel restenosis, smooth muscle cell proliferation, and migration. In a dose-dependent fashion, everolimus reduced human coronary artery smooth muscle cell (HCASMC) proliferation without toxicity in a bimodal fashion, with accentuated potency occurring at 10 μM.

Anti-proliferative compounds for the prevention of restenosis.

Coronary artery disease is commonly characterized by atherosclerotic obstruction of vessels responsible for providing adequate blood supply to the myocardium. Disruption of atheromatous plaques can promote thrombosis, significant reductions in cardiac perfusion, and devastating acute (i.e, death) or chronic (i.

The K-562 cell model for analysis of neutrophil NADPH oxidase function.

Polymorphonuclear neutrophils (PMN) have a remarkable capacity for generation of large amounts of reactive oxygen species in response to a variety of infectious or inflammatory stimuli, a process known as the respiratory burst that involves activation of a multicomponent NADPH oxidase. Given their short life span, PMN are not amenable to most molecular biology methods for studying activation of this oxidant-generating system. We have explored a variety of methods for introduction of components of the phagocytic oxidase (phox system) into the promyelocytic erythroleukemia cell line, K-562.

Cigarette smoke condensate induces MMP-12 gene expression in airway-like epithelia.

Cigarette smoke (CS)-induced emphysema is attributable to matrix metalloproteinase-12 (MMP-12) in mice, however, a relationship between CS and MMP-12 is absent in human emphysema. Here, we show that cigarette smoke condensate (CSC) induces MMP-12 gene expression in airway-like epithelia through a hydrogen peroxide (H(2)O(2))-dependent pathway involving NADPH oxidase, AP-1, and TNF-alpha. Cigarette smoke condensate-induced H(2)O(2) production and MMP-12 gene expression were inhibited by apocynin, a specific inhibitor of NADPH oxidases, while 3-aminobenzamide, an inhibitor of AP-1, attenuated CSC-induced MMP-12 gene expression.

Relative contributions of alpha4 and alphaL integrins to IL-4-induced leukocyte rolling and adhesion.

Objective: To delineate the relative contributions of alpha4 and alphaL to mediate interleukin-4 (IL-4) induced leukocyte rolling, and the subsets of leukocytes that use these pathways to adhere.

Methods: Intravital microscopy was used to examine leukocytes in venules of cremaster muscles of mice receiving intrascrotal injections of IL-4. alpha4 and alphaL monoclonal antibodies (mAbs) were administrated either prior to (prophylactic) or 24 h following (therapeutic) treatment with IL-4.

Human bronchial epithelial cells express and secrete MMP-12.

Matrix metalloproteinases (MMPs) degrade extracellular matrix proteins, which may be responsible for enlargement of alveoli in chronic obstructive pulmonary disease (COPD) and remodeling of pulmonary tissue associated with chronic asthma. Here, we provide novel evidence that MMP-12 is expressed and secreted by normal human bronchial epithelial cell cultures (NHBECs) and reveal the regulation of MMP-12 gene expression by tumor necrosis factor-alpha (TNF-alpha), epidermal growth factor (EGF), and interferon gamma (IFN-gamma). Reverse transcription-polymerase chain reaction analyses demonstrated MMP-12 mRNA presence in unstimulated differentiated NHBEC cultures.

The N-formylpeptide receptor (FPR) and a second G(i)-coupled receptor mediate fMet-Leu-Phe-stimulated activation of NADPH oxidase in murine neutrophils.

N-Formylypeptides such as fMet-Leu-Phe (fMLF) potently induce superoxide production through NADPH oxidase activation. The receptors that mediate this response have not been defined. Here, we provide definitive proof using a mouse model that formyl peptide receptor (FPR) is a receptor, but not the only receptor, that mediates fMLF-induced oxidase activation.