Findings of the Chronic Obstructive Pulmonary Disease-Sitting and Exacerbations Trial (COPD-SEAT) in Reducing Sedentary Time Using Wearable and Mobile Technologies With Educational Support: Randomized Controlled Feasibility Trial.

Background: Targeting sedentary time post exacerbation may be more relevant than targeting structured exercise for individuals with chronic obstructive pulmonary disease. Focusing interventions on sitting less and moving more after an exacerbation may act as a stepping stone to increase uptake to pulmonary rehabilitation.

Objective: The aim of this paper was to conduct a randomized trial examining trial feasibility and the acceptability of an education and self-monitoring intervention using wearable technology to reduce sedentary behavior for individuals with chronic obstructive pulmonary disease admitted to hospital for an acute exacerbation.

Study protocol for Chronic Obstructive Pulmonary Disease-Sitting and ExacerbAtions Trial (COPD-SEAT): a randomised controlled feasibility trial of a home-based self-monitoring sedentary behaviour intervention.

Introduction: An acute exacerbation of chronic obstructive pulmonary disease (COPD) marks a critical life event, which can lower patient quality of life and ability to perform daily activities. Patients with COPD tend to lead inactive and highly sedentary lifestyles, which may contribute to reductions in functional capacity. Targeting sedentary behaviour (SB) may be more attainable than exercise (at a moderate-to-vigorous intensity) for behaviour change in patients following an exacerbation.

Metabolism of the cytochrome P450 mechanism-based inhibitor N-benzyl-1-aminobenzotriazole to products that covalently bind with protein in guinea pig liver and lung microsomes: comparative study with 1-aminobenzotriazole.

The metabolism and covalent binding of radioactivity to microsomal protein of the cytochrome P450 (P450) mechanism-based inhibitors 1-amino-[14C]-2,3-benzotriazole ([14C]ABT) and two radiolabeled forms of N-benzyl-1-aminobenzotriazole (BBT), N-benzyl-1-amino-[14C]-2,3-benzotriazole ([14C]-2,3-BBT) and [14C]-N-7-benzyl-1-aminobenzotriazole ([14C]-7-BBT), were examined in hepatic or pulmonary microsomes from untreated and phenobarbital (PB)- or beta-naphthoflavone (betaNF)-induced guinea pigs. [14C]-2,3-BBT and [14C]-7-BBT were converted to multiple metabolites including ABT, benzotriazole, benzaldehyde, 2- or 3-hydroxy-BBT, and 4-hydroxy-BBT by hepatic microsomes, while [14C]ABT, whose primary metabolite was benzotriazole, underwent little biotransformation. Neither ABT nor BBT was extensively metabolized by pulmonary microsomes.

Microsomal cytochrome P450 peroxygenase metabolism of arachidonic acid in guinea pig liver.

Cytochrome P450 (P450) peroxygenase reactions are catalyzed by the ferric form of the enzyme and utilize hydroperoxides as oxidant donors. These reactions involve heterolytic cleavage of the hydroperoxide O-O bond and oxidation of the heme iron of P450 to a ferryl-oxyl complex, with subsequent transfer of the activated oxygen to a substrate. In the present study, we have demonstrated that arachidonic acid (AA) can serve as a substrate for P450 peroxygenase activity in the presence of cumene hydroperoxide (CuOOH) as a cosubstrate.

Evaluation of thrombus detection in a rabbit model using a technetium-99m-labelled anti-fibrin monoclonal antibody.

Technetium-99 m (99mTc)-labelled conjugates of an anti-fibrin monoclonal antibody, DD-3B6/22, have been assessed for their detection of vascular thrombi in a rabbit model. DD-3B6/22 binds to a D-dimer epitope present on cross-linked fibrin but absent from the fibrin monomer or fibrinogen. Injection of a 99mTc-labelled Fab' fragment of DD-3B6/22 allowed delineation of model thrombi as early as 30 min postinjection (p.