Pharmacotherapy Profiles in People with Opioid Use Disorders: Considerations for Relevant Drug-Drug Interactions with Antiviral Treatments for Hepatitis C.

People who inject drugs (PWID) are often affected by physical and psychological diseases and prone to co-medication. In Germany, about 50% of PWID are on opioid substitution therapy (OST). Comprehensive data on pharmacotherapy in these patients may help to select antiviral therapy against hepatitis C virus (HCV) infections and avoid drug-drug interactions (DDIs).

Decreased Time from 9-1-1 Call to PCI among Patients Experiencing STEMI Results in a Decreased One Year Mortality.

Background: The impact on mortality due to prompt recognition of ST-segment Elevation Myocardial Infarction (STEMI) patients by EMS has not been well described. The objective of this study was to describe the association between the time interval, 9-1-1 call to percutaneous intervention (PCI), and mortality at one year.

Methods: This retrospective analysis included patients that were transported by EMS as a "code STEMI" and underwent PCI.

Lysyl oxidases play a causal role in vascular remodeling in clinical and experimental pulmonary arterial hypertension.

Objective: Pulmonary vascular remodeling, the pathological hallmark of pulmonary arterial hypertension, is attributed to proliferation, apoptosis resistance, and migration of vascular cells. A role of dysregulated matrix cross-linking and stability as a pathogenic mechanism has received little attention. We aimed to assess whether matrix cross-linking enzymes played a causal role in experimental pulmonary hypertension (PH).

Transglutaminase 2: a new player in bronchopulmonary dysplasia?

Aberrant remodelling of the extracellular matrix in the developing lung may underlie arrested alveolarisation associated with bronchopulmonary dysplasia (BPD). Transglutaminases are regulators of extracellular matrix remodelling. Therefore, the expression and activity of transglutaminases were assessed in lungs from human neonates with BPD and in a rodent model of BPD.

Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-β signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts.

Glucocorticoids represent the mainstay therapy for many lung diseases, providing outstanding management of asthma but performing surprisingly poorly in patients with acute respiratory distress syndrome, chronic obstructive pulmonary disease, lung fibrosis, and blunted lung development associated with bronchopulmonary dysplasia in preterm infants. TGF-β is a pathogenic mediator of all four of these diseases, prompting us to explore glucocorticoid/TGF-β signaling cross-talk. Glucocorticoids, including dexamethasone, methylprednisolone, budesonide, and fluticasone, potentiated TGF-β signaling by the Acvrl1/Smad1/5/8 signaling axis and blunted signaling by the Tgfbr1/Smad2/3 axis in NIH/3T3 cells, as well as primary lung fibroblasts, smooth muscle cells, and endothelial cells.