DEVELOPMENT AND STUDY OF THE UNK SUPERCONDUCTING DIPOLE MODELS

L'expérience acquise lors de l'étude de modèles courts a permis de réaliser et d'essayer deux dipôles longs de 6 m. Les essais se sont déroulés dans le cryostat à immersion sans fer. La première transition a révélé un courant de l'ordre de 6 kA ce qui correspond au champ dans un aimant de 5 T avec le fer. Le courant maximum est de 6,5 kA. Les pertes totales pour le courant de 6 kA et à la vitesse de l'injection de 100 A/s sont de 750 j/c. Les valeurs absolues des composantes harmoniques du champ dans la partie centrale du dipôle correspondent aux valeurs théoriques et sont proches des valeurs admissibles. Elles dépendent peu du niveau du champ ce qui prouve une bonne stabilité mécanique et une faible déformation de la bobine à l'échelle 1.Two full-scale dipole models, 6 m long each, have been manufactured in the scope of the programme on development of superconducting dipoles for the UNK. Results of their tests in a bath cryostat are reported. A number of short models have been manufactured and tested with view to improve the integral characteristics of the magnetic field. The results of magnetic measurements of the central and edge field are presented. Also reported are the results of study of training and dynamic characteristics of dipoles

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society