The effect of hydrogeological and hydrochemical dynamics on landslide triggering in the central highlands of Ethiopia

The volcanic terrain at the western margin of the Main Ethiopian Rift in the Debre Sina area is known for its slope stability problems. This report describes research on the effects of the hydrogeological and hydrochemical dynamics on landslide triggering by using converging evidence from geological, geomorphological, geophysical, hydrogeochemical and isotopic investigations. The chemical characterization indicates that shallow to intermediate aquifers cause groundwater flow into the landslide mass, influencing long-term groundwater-level fluctuations underneath the landslide and, as a consequence, its stability. The low content of total dissolved solids and the bicarbonate types (Ca–Mg–HCO3 and Ca–HCO3) of the groundwater, and the dominantly depleted isotopic signature, indicate a fast groundwater flow regime that receives a high amount of precipitation. The main causes of the landslide are the steep slope topography and the pressure formed during precipitation, which leads to an increased weight of the loose and weathered materials. The geophysical data indicate that the area is covered by unconsolidated sediments and highly decomposed and weak volcanic rocks, which are susceptible to sliding when they get moist. The heterogeneity of the geological materials and the presence of impermeable layers embodied within the highly permeable volcanic rocks can result in the build-up of hydrostatic pressure at their interface, which can trigger landslides. Intense fracturing in the tilted basalt and ignimbrite beds can also accelerate infiltration of water, resulting to the build-up of high hydrostatic pressure causing low effective normal stress in the rock mass, giving rise to landslides

The influence of Karst Aquifer mineralogy and geochemistry on groundwater characteristics: West Bank, Palestine

This work reports, for the first time, the mineralogical and geochemical characteristics of karst aquifers in the Central West Bank (CWB) catchment in Palestine. It provides an integrated study approach by correlating the geochemistry of the lithology and hydrochemical data of groundwater samples. Mineralogical analysis showed that all of the samples were dominantly composed of either calcite CaCO3 (5–100 wt. %) or dolomite CaMg(CO3)2 (4–100 wt. %), with minor amounts of quartz and feldspar, which is supported by the inorganic carbon content (9–13 wt. %) and hydrochemical composition of the spring water samples. The whole-rock geochemical data indicated that the samples have low contents of trace elements and transition metals. In contrast, the concentrations of alkaline earth elements (Mg, Ca, Sr, Ba) and Mn were high in the rock and groundwater samples. Generally, the trace elements of rock samples with concentrations >10 ppm included Sr (17–330 ppm), Mn (17–367 ppm), Ba (2–32 ppm), W (5–37 ppm), Cr (3–23 ppm), Zn (1.7–28 ppm), V (4–23 ppm), and Zr (1–22 ppm), while the concentrations of all the other trace elements was below 10 ppm. Ionic ratios and hierarchical cluster analysis (HCA) suggested that the chemical evolution of groundwater was mainly related to the geogenic (rock–water) interaction in the study area. This is clear in the alkaline earth elements (Mg, Ca, Sr, Ba) ratios, especially regarding the Sr values. The calcite rock samples had higher Sr (mean 160 ppm, n = 11) than those of the dolomite rocks (mean 76 ppm, n = 9)

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.