Predicting moisture problems in low-slope roofing

Moisture intrusion is the major reason why low-slope roofing systems fail prematurely. With approximately 75% of all roofing activity being reroofing, the roofing professional is faced with deciding what to do with an existing wet roof on almost a daily basis. This paper describes finite-difference computer modeling that has been performed to address moisture control in low-slope roof systems. Based on a large database of finite difference modeling results, algorithms have been developed that allow the roofing practitioners to simply determine if a roofing system design requires a vapor retarder or if the system can be modified to enhance its tolerance for small leaks. This paper illustrates how modeling results were obtained, describes the process employed to develop the algorithms, and demonstrates how these algorithms can be used to design a moisture tolerant low-slope roof. The range of applicability and limitations of these algorithms is also detailed

A new look at moisture control in low slope roofing

One of the criteria for a moisture-tolerant roof is that moisture accumulation in a roofing system must not be large enough to cause condensation within the roof, since this can damage the insulation and reduce its effectiveness. Failing this criterion would require the inclusion of a vapor retarder into the roofing system. We have tested this requirement using computer simulations for a series of new roofing systems and environmental conditions. This paper uses the database from those simulations to develop a simplified method to predict condensation control using only variables associated with the roof and environmental conditions. This method assesses the potential for condensation within the roof assembly without having to perform a computer simulation. Using the computer simulation output data, the moisture accumulation inside each of the roofing systems was calculated. A critical threshold of moisture accumulation was assigned by analyzing the roofing systems which fail to prevent condensation from occurring within the roofing system. An empirical equation for moisture accumulation as a function of roof system and environmental condition variables is developed. The moisture accumulation calculated using this relationship correlates well with the moisture accumulation based on the results of computer simulations. The ability of these two different relationships for moisture accumulation to predict condensation control using the established critical threshold is assessed. Accuracy of both methods is over 95%

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