Performance and operational effectiveness of evacuated flat plate solar collectors compared with conventional thermal, PVT and PV panels

The concept of an evacuated flat plate (EFP) collector was proposed over 40 years ago but, despite its professed advantages, very few manufacturers have developed commercial versions. This situation suggests both technical difficulties in manufacturing a competitively-priced sealed for life panel and a lack of awareness of the bene fits of such panels. This paper demonstrates an evacuated flat plate simulation that closely models experimental efficiency measurements. Having established the validity of the model, it compares published data for a commercial EFP collector with predictions for an optimal design to investigate whether any further efficiency improvement might be possible. The optimised design is then evaluated against alternative solar energy devices by modelling a number of possible applications. These comparisons should inform choices about solar options for delivering heat: EFP collectors are well-suited to some of these applications. Evacuated flat plate collectors are a possible alternative to concentrating collectors for Organic Rankine Cycle power generation. The annual output for all the modelled collectors was found to be a quadratic function of delivery temperature: this enabled a novel optimisation of ORC source temperature. Predictions for concentrating and non-concentrating ORC plant are compared with a PV/thermal alternative. The ORC output is significantly less than a PV panel would achieve; applications needing both heat and power are better served by PVT panels. This is an original and novel result

Z-Pinch Generated X-Rays in Static-Wall Hohlraum Geometry Demonstrate Potential for Indirect-Drive ICF Studies

Hohlraums of full ignition scale (6-mm diameter by 7-mm length) have been heated by x-rays from a z-pinch target on Z to a variety of temperatures and pulse shapes which can be used to simulate the early phases of the National Ignition Facility (NIF) temperature drive. The pulse shape is varied by changing the on-axis target of the z pinch in a static-wall-hohlraum geometry. A 2-{micro}m-thick walled Cu cylindrical target of 8-mm diameter filled with 10 mg/cm{sup 3} CH, for example, produces foot-pulse conditions of {minus}85 eV for a duration of {approximately} 10 ns, while a solid cylindrical target of 5-mm diameter and 14-mg/cm{sup 3} CH generates first-step-pulse conditions of {approximately} 122 eV for a duration of a few ns. Alternatively, reducing the hohlraum size (to 4-mm diameter by 4-mm length) with the latter target has increased the peak temperature to {approximately} 150 eV, which is characteristic of a second-step-pulse temperature. In general, the temperature T of these x-ray driven hohlraums is in agreement with the Planckian relation (T-(P/A){sup 1/4}). P is the measured x-ray input power and A is the surface area of the hohlraum. Fully-integrated 2-D radiation-hydrodynamic simulations of the z pinch and subsequent hohlraum heating show plasma densities within the useful volume of the hohlraums to be on the order of air or less

High-temperature dynamic hohlraums on the pulsed power driver Z

In the concept of the dynamic hohlraum an imploding z-pinch is optically thick to its own radiation. Radiation may be trapped inside the pinch to give a radiation temperature inside the pinch greater than that outside the pinch. The radiation is typically produced by colliding an outer Z-pinch liner onto an inner liner. The collision generates a strongly radiating shock, and the radiation is trapped by the outer liner. As the implosion continues after the collision the radiation temperature may continue to increase due to ongoing PdV (pressure times change in volume) work done by the implosion. In principal the radiation temperature may increase to the point at which the outer liner burns through, becomes optically thin, and no longer traps the radiation. One application of the dynamic hohlraum is to drive an ICF (inertial confinement fusion) pellet with the trapped radiation field. Members of the dynamic hohlraum team at Sandia National Labs have used the pulsed power driver Z (20 LMA, 100 ns) to create a dynamic hohlraum with temperature linearly ramping from 100 to 180 eV over 5 ns. On this shot zp214 a nested tungsten wire array of 4 and 2 cm diameters with masses of 2 and 1 mg imploded onto a 2.5 mg plastic annulus at 5 mm diameter. The current return can on this shot was slotted. It is likely the radiation temperature may be increased to over 200 CV by stabilizing the pinch with a solid current return can. A current return can with 9 slots imprints 9 filaments onto the imploding pinch. This degrades the optical trapping and the quality of the liner collision. A 1.6 mm diameter capsule situated inside this dynamic hohlraum of zp214 would see 15 kJ of radiation impinging on its surface before the pinch itself collapses to a 1.6 mm diameter. Dynamic hohlraum shots including pellets are scheduled to take place on Z in September of 1998

Guidance for the Management of Patients with Vascular Disease or Cardiovascular Risk Factors and COVID-19: Position Paper from VAS-European Independent Foundation in Angiology/Vascular Medicine .

COVID-19 is also manifested with hypercoagulability, pulmonary intravascular coagulation, microangiopathy, and venous thromboembolism (VTE) or arterial thrombosis. Predisposing risk factors to severe COVID-19 are male sex, underlying cardiovascular disease, or cardiovascular risk factors including noncontrolled diabetes mellitus or arterial hypertension, obesity, and advanced age. The VAS-European Independent Foundation in Angiology/Vascular Medicine draws attention to patients with vascular disease (VD) and presents an integral strategy for the management of patients with VD or cardiovascular risk factors (VD-CVR) and COVID-19. VAS recommends (1) a COVID-19-oriented primary health care network for patients with VD-CVR for identification of patients with VD-CVR in the community and patients' education for disease symptoms, use of eHealth technology, adherence to the antithrombotic and vascular regulating treatments, and (2) close medical follow-up for efficacious control of VD progression and prompt application of physical and social distancing measures in case of new epidemic waves. For patients with VD-CVR who receive home treatment for COVID-19, VAS recommends assessment for (1) disease worsening risk and prioritized hospitalization of those at high risk and (2) VTE risk assessment and thromboprophylaxis with rivaroxaban, betrixaban, or low-molecular-weight heparin (LMWH) for those at high risk. For hospitalized patients with VD-CVR and COVID-19, VAS recommends (1) routine thromboprophylaxis with weight-adjusted intermediate doses of LMWH (unless contraindication); (2) LMWH as the drug of choice over unfractionated heparin or direct oral anticoagulants for the treatment of VTE or hypercoagulability; (3) careful evaluation of the risk for disease worsening and prompt application of targeted antiviral or convalescence treatments; (4) monitoring of D-dimer for optimization of the antithrombotic treatment; and (5) evaluation of the risk of VTE before hospital discharge using the IMPROVE-D-dimer score and prolonged post-discharge thromboprophylaxis with rivaroxaban, betrixaban, or LMWH

Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease

BACKGROUND: The cholesteryl ester transfer protein inhibitor evacetrapib substantially raises the high-density lipoprotein (HDL) cholesterol level, reduces the low-density lipoprotein (LDL) cholesterol level, and enhances cellular cholesterol efflux capacity. We sought to determine the effect of evacetrapib on major adverse cardiovascular outcomes in patients with high-risk vascular disease. METHODS: In a multicenter, randomized, double-blind, placebo-controlled phase 3 trial, we enrolled 12,092 patients who had at least one of the following conditions: an acute coronary syndrome within the previous 30 to 365 days, cerebrovascular atherosclerotic disease, peripheral vascular arterial disease, or diabetes mellitus with coronary artery disease. Patients were randomly assigned to receive either evacetrapib at a dose of 130 mg or matching placebo, administered daily, in addition to standard medical therapy. The primary efficacy end point was the first occurrence of any component of the composite of death from cardiovascular causes, myocardial infarction, stroke, coronary revascularization, or hospitalization for unstable angina. RESULTS: At 3 months, a 31.1% decrease in the mean LDL cholesterol level was observed with evacetrapib versus a 6.0% increase with placebo, and a 133.2% increase in the mean HDL cholesterol level was seen with evacetrapib versus a 1.6% increase with placebo. After 1363 of the planned 1670 primary end-point events had occurred, the data and safety monitoring board recommended that the trial be terminated early because of a lack of efficacy. After a median of 26 months of evacetrapib or placebo, a primary end-point event occurred in 12.9% of the patients in the evacetrapib group and in 12.8% of those in the placebo group (hazard ratio, 1.01; 95% confidence interval, 0.91 to 1.11; P=0.91). CONCLUSIONS: Although the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease. (Funded by Eli Lilly; ACCELERATE ClinicalTrials.gov number, NCT01687998 .)

Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial

Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402