Unexpected high diversity of galling insects in the Amazonian upper canopy: The savanna out there

A relatively large number of studies reassert the strong relationship between galling insect diversity and extreme hydric and thermal status in some habitats, and an overall pattern of a greater number of galling species in the understory of scleromorphic vegetation. We compared galling insect diversity in the forest canopy and its relationship with tree richness among upland terra firme, várzea, and igapó floodplains in Amazonia, Brazil. The soils of these forest types have highly different hydric and nutritional status. Overall, we examined the upper layer of 1,091 tree crowns. Galling species richness and abundance were higher in terra firme forests compared to várzea and igapó forests. GLM-ANCOVA models revealed that the number of tree species sampled in each forest type was determinant in the gall-forming insect diversity. The ratio between galling insect richness and number of tree species sampled (GIR/TSS ratio) was higher in the terra firme forest and in seasonally flooded igapó, while the várzea presented the lowest GIR/TSS ratio. In this study, we recorded unprecedented values of galling species diversity and abundance per sampling point. The GIR/TSS ratio from várzea was approximately 2.5 times higher than the highest value of this ratio ever reported in the literature. Based on this fact, we ascertained that várzea and igapó floodplain forests (with lower GIA and GIR), together with the speciose terra firme galling community emerge as the gall diversity apex landscape among all biogeographic regions already investigated. Contrary to expectation, our results also support the "harsh environment hypothesis", and unveil the Amazonian upper canopy as similar to vegetation habitats, hygrothermically stressed environments with temperature at lethal limits and high levels of leaf sclerophylly. © 2014 Julião et al

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.

Insect galls of Itamonte (Minas Gerais, Brazil): characterization and occurrence

Computer systems that are dependable in the presence of faults are increasingly in demand. Among available fault tolerance mechanisms, software-implemented hardware fault tolerance (SIHFT) is constantly gaining in popularity, because of its cost efficiency and flexibility. Fault tolerance mechanisms are often validated using fault injection, comprising a variety of techniques for introducing faults into a system. Traditional fault injection techniques, however, suffer from a number of drawbacks, notably lack of coverage (impossibility to exhaust all test cases) and the failure to activate enough injected faults. In this paper we present a new approach called symbolic fault injection which is targeted at validation of SIHFT mechanisms and is based on the concept of symbolic execution of programs. It can be seen as the extension of a formal technique for formal program verification that makes it possible to evaluate the consequences of all possible faults (of a certain kind) in given memory locations for all possible system inputs. This makes it possible to formally prove properties of fault tolerance mechanisms. The new method for symbolic fault injection has been prototypically implemented on the basis of an industrial-strength formal verification system and we demonstrate its viability by proving that a CRC implementation detects all possible single bit-flips