First report of Triassic vertebrate assemblages from the Villány Hills (Southern Hungary)

Abstract Remains of Triassic vertebrates discovered in the Villány Hills (SW Hungary) are described here. After the well-documented Late Cretaceous Iharkút locality, this material represents the second systematically collected assemblage of Mesozoic vertebrates from Hungary. Fossils were collected from both the classical abandoned road-cut at Templom Hill (Templom-hegy) and a newly discovered site at a construction zone located 200 meters west of the road-cut. Macrofossils of the construction site are mainly isolated bones and teeth of nothosaurs from the Templomhegy Dolomite, including a fragmentary mandible referred to as Nothosaurus sp. and placodont teeth tentatively assigned here to cf. Cyamodus sp. Affinities of these fossils suggest a Middle Triassic (Ladinian) age of these shallow marine deposits. New palynological data prove for the first time a Late Triassic (Carnian) age of the lower part of the Mészhegy Sandstone Formation. Vertebrate remains discovered in this formation clearly represent a typical Late Triassic shallow-marine fauna including both chondrichthyan (Lissodus, Palaeobates, Hybodus) and osteichthyan (cf. Saurichthys, ?Sphaerodus sp.) fish fossils. The presence of reworked nothosaur and placodont tooth fragments as well as of possible archosauriform teeth, suggest an increase of terrestrial influence and the erosion of underlying Triassic deposits during the Late Triassic. A belemnite rostrum collected from the lowermost beds of the Somssichhegy Limestone Formation proves that this Lower Jurassic (Pliensbachian) layer was deposited in a marine environment. Most of the vertebrate remains (nothosaurs, placodonts, hybodont shark teeth, perhaps Palaeobates, Lissodus) recovered from these beds are also reworked Triassic elements strongly supporting an erosive, nearshore depositional environment

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