A compendium and functional characterization of mammalian genes involved in adaptation to Arctic or Antarctic environments

Many mammals are well adapted to surviving in extremely cold environments. These species have likely accumulated genetic changes that help them efficiently cope with low temperatures. It is not known whether the same genes related to cold adaptation in one species would be under selection in another species. The aims of this study therefore were: to create a compendium of mammalian genes related to adaptations to a low temperature environment; to identify genes related to cold tolerance that have been subjected to independent positive selection in several species; to determine promising candidate genes/pathways/organs for further empirical research on cold adaptation in mammals

Influence of adding multiwalled carbon nanotubes on the adhesive strength of composite epoxy/sol–gel materials

The tensile shear strength of a composite epoxy/sol–gel system modified with different ratios of multiwall carbon nanotubes (MWCNTs) was evaluated using a mechanical testing machine. The experimental results showed that the shear strength increased when lower than ~0.07 wt% of MWCNTs were added in the composite solution. The increase of the shear strength was attributed to both the mechanical load transfer from the matrix to the MWCNTs and the high specific surface area of this material that increased the degree of crosslinking with other inorganic fillers in the formulation. However, a decrease in the adhesive shear strength was observed after more than ~0.07 wt% MWCNTs were added to the composite. The reason for this may be related to the high concentration of MWCNTs within the matrix leading to excessively high viscosity, dewetting of the substrate surfaces, and reduced bonding of MWCNTs with the matrix, thereby limiting the strength. SEM observation of the fracture surfaces for composite epoxy/sol–gel adhesive materials with 0.01 wt% MWCNTs showed a mixed interfacial/cohesive fracture mode. This fracture mode indicated strong links at the adhesive/substrate interface, and interaction between CNTs and the matrix was achieved; therefore, adhesion performance of the composite epoxy/sol–gel material to the substrate was improved. An increase of a strong peak related to the C–O bond at ~1733 cm-1 in the FTIR spectra was observed. This peak represented crosslinking between the CNT surface and the organosilica nanoparticles in the MWCNTs-doped composite adhesive. Raman spectroscopy was also used to identify MWCNTs within the adhesive material. The Raman spectra exhibit peaks at ~1275 cm-1 and in the range of ~1549–1590 cm-1. The former is the graphite G-band, while the latter is the diamond D-band. The D-band and G-band represent the C–C single bond and C=C double bond in carbon nanotubes, respectively

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. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.