Daclizumab was effective in reducing contrast enhancing lesions and improving clinical scores in patients with relapsing and remitting multiple sclerosis with active disease not controlled by interferon therapy. These results provide evidence for long-term efficacy and support further clinical development of daclizumab.

BackgroundDispatch of basic life support–trained first responders equipped with automated external defibrillators in addition to advanced life support–trained emergency medical services personnel in out‐of‐hospital cardiac arrest (OHCA) has, in some minor cohort studies, been associated with improved survival. The aim of this study was to evaluate the association between basic life support plus advanced life support response and survival in OHCA at a national level.Methods and ResultsThis prospective cohort study was conducted from January 1, 2012, to December 31, 2014. People who experienced OHCA in 9 Swedish counties covered by basic life support plus advanced life support response were compared with a propensity‐matched contemporary control group of people who experienced OHCA in 12 counties where only emergency medical services was dispatched, providing advanced life support. Primary outcome was survival to 30 days. The analytic sample consisted of 2786 pairs (n=5572) derived from the total cohort of 7308 complete cases. The median time from emergency call to arrival of emergency medical services or first responder was 9 minutes in the intervention group versus 10 minutes in the controls (P<0.001). The proportion of patients admitted alive to the hospital after resuscitation was 31.4% (875/2786) in the intervention group versus 24.9% (694/2786) in the controls (conditional odds ratio, 1.40; 95% confidence interval, 1.24–1.57). Thirty‐day survival was 9.5% (266/2786) in the intervention group versus 7.7% (214/2786) in the controls (conditional odds ratio, 1.27; 95% confidence interval, 1.05–1.54).ConclusionsIn this nationwide interventional trial, using propensity score matching, dispatch of first responders in addition to emergency medical services in OHCA was associated with a moderate, but significant, increase in 30‐day survival.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02184468.

BackgroundProstacyclin analogs are potent vasodilators and possess anti-inflammatory properties. However, the effect of prostacyclin on extracellular matrix (ECM) in COPD is not well known. Collagen fibrils and proteoglycans are essential ECM components in the lung and fibroblasts are key players in regulating the homeostasis of ECM proteins. The aim was to study the synthesis of prostacyclin and its effect on fibroblast activity and ECM production, and in particular collagen I and the collagen-associated proteoglycans biglycan and decorin.MethodsParenchymal lung fibroblasts were isolated from lungs from COPD patients (GOLD stage IV) and from lungs and transbronchial biopsies from control subjects. The prostacyclin analog iloprost was used to study the effect of prostacyclin on ECM protein synthesis, migration, proliferation and contractile capacity of fibroblasts.ResultsTGF-β1 stimulation significantly increased prostacyclin synthesis in fibroblasts from COPD patients (p < 0.01), but showed no effect on fibroblasts from control subjects. Collagen I synthesis was decreased by iloprost in both control and COPD fibroblasts (p < 0.05). Conversely, iloprost significantly altered biglycan and decorin synthesis in control fibroblasts, but iloprost displayed no effect on these proteoglycans in COPD fibroblasts. Proliferation rate was reduced (p < 0.05) and contractile capacity was increased in COPD fibroblasts (p < 0.05) compared to control fibroblasts. Iloprost decreased proliferative rate in control fibroblasts (p < 0.05), whereas iloprost attenuated contraction capacity in both COPD (p < 0.01) and control fibroblasts (p < 0.05).ConclusionsIloprost reduced collagen I synthesis and fibroblast contractility but did not affect the collagen-associated proteoglycans or proliferation rate in fibroblasts from COPD patients. Enhanced prostacyclin production could lead to improper collagen network fibrillogenesis and a more emphysematous lung structure in severe COPD patients.

No abstract