Microbial induced calcium carbonate precipitation (miccp) for road construction

The growing concern over climate change has led the drive for the development of alternative building materials in several industries, including road construction. Bio-based construction, using Microbial Induced Calcium Carbonate Precipitation (MICCP) has been investigated in recent years as a potential cost-effective and environmentally friendly alternative engineering approach. The Council for Scientific and Industrial Research (CSIR) developed a research program looking at MICCP. Several barriers to using MICCP in road construction was found, a potential biohazard using exotic bacteria and the current technique used for treatment. In this paper, in situ cultivation of indigenous urease positive bacteria was investigated and compared to a CSIR designed biological prototype. The objective of this paper is to present the results of Unconfined Compressive Strength (UCS) tests performed on a marginal G5 (COLTO, 1985) material treated with the prototype and in situ cultivated bacteria. The work showed that it was possible to cultivate urease positive bacteria present within the G5 material. It was found that the cementation solution could act as a stimulation and cementation media when the pH is reduced to give the bacteria time to cultivate and buffer the pH upward for Calcium Carbonate Precipitation to take place. Lastly, the CSIR prototype performed better in terms of UCS and treatment technique. The treatment consists of only one application of the prototype, which is more consistent with current road construction practice, as compared with the multiple application needed for in situ cultivation.Papers presented at the 40th International Southern African Transport Conference on 04 -08 July 202

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