Cooling Characteristics of the V-1650-7 Engine. II - Effect of Coolant Conditions on Cylinder Temperatures and Heat Rejection at Several Engine Powers

An investigation has been conducted on a V-1650-7 engine to determine the cylinder temperatures and the coolant and oil heat rejections over a range of coolant flows (50 to 200 gal/min) and oil inlet temperatures (160 to 2150 F) for two values of coolant outlet temperature (250 deg and 275 F) at each of four power conditions ranging from approximately 1100 to 2000 brake horsepower. Data were obtained for several values of block-outlet pressure at each of the two coolant outlet temperatures. A mixture of 30 percent by volume of ethylene glycol and 70-percent water was used as the coolant. The effect of varying coolant flow, coolant outlet temperature, and coolant outlet pressure over the ranges investigated on cylinder-head temperatures was small (0 deg to 25 F) whereas the effect of increasing the engine power condition from ll00 to 2000 brake horsepower was large (maximum head-temperature increase, 110 F)

Correlation of cylinder-head temperatures and coolant heat rejections of a multicylinder, liquid-cooled engine of 1710-cubic-inch displacement

Data obtained from an extensive investigation of the cooling characteristics of four multicylinder, liquid-cooled engines have been analyzed and a correlation of both the cylinder-head temperatures and the coolant heat rejections with the primary engine and coolant variables was obtained. The method of correlation was previously developed by the NACA from an analysis of the cooling processes involved in a liquid-cooled-engine cylinder and is based on the theory of nonboiling, forced-convection heat transfer. The data correlated included engine power outputs from 275 to 1860 brake horsepower; coolant flows from 50 to 320 gallons per minute; coolants varying in composition from 100 percent water to 97 percent ethylene glycol and 3 percent water; and ranges of engine speed, manifold pressure, carburetor-air temperature, fuel-air ratio, exhaust-gas pressure, ignition timing, and coolant temperature. The effect on engine cooling of scale formation on the coolant passages of the engine and of boiling of the coolant under various operating conditions is also discussed

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.

Fructan and its relationship to abiotic stress tolerance in plants

Numerous studies have been published that attempted to correlate fructan concentrations with freezing and drought tolerance. Studies investigating the effect of fructan on liposomes indicated that a direct interaction between membranes and fructan was possible. This new area of research began to move fructan and its association with stress beyond mere correlation by confirming that fructan has the capacity to stabilize membranes during drying by inserting at least part of the polysaccharide into the lipid headgroup region of the membrane. This helps prevent leakage when water is removed from the system either during freezing or drought. When plants were transformed with the ability to synthesize fructan, a concomitant increase in drought and/or freezing tolerance was confirmed. These experiments indicate that besides an indirect effect of supplying tissues with hexose sugars, fructan has a direct protective effect that can be demonstrated by both model systems and genetic transformation