The turbulent heat flux in low Mach number flows with large density variations

A transport equation has been derived which is the difference between the volume- and mass-averaged velocities and is simply related to the turbulent heat flux phi sup h. Using this equation and an assumption analogous to the drift flux approximation of two-phase flow modeling, an algebraic closure relation for phi sup h that exibits fluxes due to directed transport proportional to -del anti p and due to gradient transport proportional to -del tau has been obtained

Abstract W P351: Plasma Interleukin-6 and C-reactive Protein Are Associated With Acute Diffusion Hyperintensity After Transient Ischemic Attack

Background: In suspected TIA, DWI hyperintensity confirms the diagnosis of brain ischemia and identifies those with 3-fold risk of early recurrent stroke. However, immediate MRI is expensive and may not be available in many healthcare settings. A simple validated blood test to objectively support the diagnosis of cerebral ischaemia after transient symptoms might have utility in clinical practice. We hypothesised that blood markers of inflammation may be associated with abnormal DWI following TIA. Methods: BIO-TIA was a multi-centre prospective study of consecutive patients with clinically-defined TIA, confirmed by a stroke physician. Phlebotomy and stroke protocol MRI were performed within 72 hours of symptoms. Patients with malignancy, active infection, trauma, surgery, definite transient non-ischaemic symptoms or recurrent stroke before phlebotomy/MRI were excluded. Plasma high-sensitivity CRP and interleukin-6 (IL-6) were measured by mass spectrometry. Results: In 201 included patients, mean age was 68 years (59% male). Carotid stenosis was present in 26.4% and atrial fibrillation in 29.1%. Mean ABCD2 score was 4.2 (SD 1.3). Acute DWI hyperintensity was observed in 37.8% (76/201). Median hsCRP was 1.78mg/L in DWI-negative, compared with 3.01mg/L in DWI-positive TIA (p=0.04). Median IL-6 was 3.76pg/ml (DWI-negative) versus 4.91pg/ml (DWI-positive) (p=0.04). When the highest quartiles of CRP and IL-6 distributions were compared with quartiles 1-3, the prevalence of DWI hyperintensity was 61.5% (Q4) versus 32.9% (Q1-3) for CRP (p=0.001), and 56.4% (Q4) versus 34.9% [Q1-3) for IL-6 (p=0.02). Thresholds of 4.78mg/L for CRP or 6.21pg/ml for IL-6 had at least 80% specificity for identification of abnormal DWI signal. IL-6 was associated with CRP (rho 0.58), age (rho 0.36), and ABCD2 score (rho 0.18) and carotid stenosis (p≤0.01 for all), but not statin use. Conclusion: Our preliminary findings require validation, but suggest that inexpensive, rapidly-measured blood markers are associated with acute DWI hyperintensity after TIA. If validated, blood markers may have utility to support the diagnosis of cerebral ischemia or select patients for early MRI. </jats:p

Evolocumab and clinical outcomes in patients with cardiovascular disease

BACKGROUND Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%). CONCLUSIONS In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets