9 research outputs found

    Ampoule sealing apparatus and process

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    An apparatus 10 for effecting sealing of a fused quartz ampoule 24 while maintaining a vacuum on the ampoule via system 12 is disclosed. A plug 28 of fused quartz is lowered into the vertically disposed ampoule 24 (while maintaining the vacuum thereon) and heat sealed therein to prevent any vapor escape from, or contamination of, the contained semiconductor growth charge 29 during subsequent semiconductor crystal growth processes. A rotary vacuum feed-through mechanism 16 selectively rotates axle 34 and spool 32 to unwind wire 30 for lowering of plug 28 into the reduced diameter portion 24b of ampoule 24. Ampoule 24 is hermatically connected to vacuum housing 18 by quick release flange 20 wherein O-ring 22 retains ampoule 24

    Numerical modeling of Bridgman growth of PbSnTe in a magnetic field

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    In this work we study heat and mass transport, fluid motion, and solid/liquid phase change in the process of steady Bridgman growth of Pb(.8)Sn(.2)Te (LTT) in an axially-imposed uniform magnetic field under terrestrial and microgravity conditions. In particular, this research is concerned with the interrelationships among segregation, buoyancy-driven convection, and magnetic damping in the LTT melt. The main objectives are to provide a quantitative understanding of the complex transport phenomena during solidification of the nondilute binary of LTT, to provide estimates of the strength of magnetic field required to achieve the desired diffusion-dominated growth, and to assess the role of magnetic damping for space and earth based control of the buoyancy-induced convection. The problem was solved by using FIDAP and numerical results for both vertical and horizontal growth configurations with respect to the acceleration of gravity vector are presented

    Growth of Compound Semiconductors in a Low Gravity Environment: Microgravity Growth of PbSnTe

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    The growth of the alloy compound semiconductor lead tin telluride (PbSnTe) was chosen for a microgravity flight experiment in the Advanced Automated Directional Solidification Furnace (AADSF), on the United States Microgravity Payload-3 (USMP-3) and on USMP-4 Space Shuttle flights in February, 1996, and November, 1997. The objective of these experiments was to determine the effect of the reduction in convection, during the growth process, brought about by the microgravity environment. The properties of devices made from PbSnTe are dependent on the ratio of the elemental components in the starting crystal. Compositional uniformity in the crystal is only obtained if there is no significant mixing in the liquid during growth. Lead tin telluride is an alloy of PbTe and SnTe. The technological importance of PbSnTe lies in its band gap versus composition diagram which has a zero energy crossing at approximately 40% SnTe. This facilitates the construction of long wavelength (>6 micron) infrared detectors and lasers. Observations and experimental methods of crystal growth of PbSnTe on both Space Shuttle Flights are presented

    Melt Stabilization of PbSnTe in a Magnetic Field

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    Both the experimental observation and numerical simulation indicate that the Bridgman growth of PbSnTe under the microgravity environment in space is still greatly influenced by buoyancy-induced convection. The application of a magnetic field during the semiconductor growth can dampen the convective flow in the metal-like melt. However, for Bridgman growth of PbSnTe on earth (with either vertical or horizontal configuration), both experimental observation and numerical modeling suggest that even with a strong magnetic furnace (5-Tesla constant axial magnetic field), the convective flow in the melt still cannot be sufficiently suppressed to reach the diffusion-controlled level. In order to completely dampen the buoyancy-induced convection on earth, estimates based on scaling analysis indicate that for common experimental conditions, an extremely high magnetic field is required, far beyond the capacity of the experimental apparatus currently available. Therefore, it is proposed that only the combination of microgravity environment and magnetic damping will produce the desired diffusion-controlled growth state for this particular material. The primary objectives of this study are to provide a quantitative understanding of the complex transport phenomena during solidification of non-dilute binarys, to furnish a numerical tool for furnace design and growth condition optimization, to provide estimates of the required magnetic field strength for low gravity growth, and to assess the role of magnetic damping for space and earth control of the double-diffusive convection. As an integral part of a NASA research program, our numerical simulation supports both the flight and ground-based experiments in an effort to bring together a complete picture of the complex physical phenomena involved in the crystal growth process. For Bridgman growth of PbSnTe under microgravity (with both vertical and horizontal configurations), the simulations suggest that a moderate axial magnetic field of only a few kilo-Gauss in strength could effectively eliminate buoyancy-induced convection in the melt and control solute segregation. Therefore, this work confirms the idea that the combination of microgravity environment and the magnetic damping will indeed be sufficient to produce the desired diffusion-controlled growth state for PbSnTe

    Microgravity science at Langley Research Center

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    Although space research is still in an embryonic state, a combination of Earth based and space flight experiments are being coupled to yield a better understanding of the complex interaction of heat and fluid flow on the dynamics of crystal growth. Continued efforts on the ground as well as additional flight opportunities are needed to continue the drive to fully understand the advantages, both scientifically and economically, of microgravity crystal growth

    Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

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    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.

    Antiinflammatory therapy with canakinumab for atherosclerotic disease

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    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

    Rationale and Design for a GRADE Substudy of Continuous Glucose Monitoring

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