114 research outputs found

    Layered Metals Fabrication Technology Development for Support of Lunar Exploration at NASA/MSFC

    Get PDF
    NASA's human exploration initiative poses great opportunity and risk for missions to the Moon and beyond. In support of these missions, engineers and scientists at the Marshall Space Flight Center are developing technologies for ground-based and in-situ fabrication capabilities utilizing provisioned and locally-refined materials. Development efforts are pushing state-of-the art fabrication technologies to support habitat structure development, tools and mechanical part fabrication, as well as repair and replacement of ground support and space mission hardware such as life support items, launch vehicle components and crew exercise equipment. This paper addresses current fabrication technologies relative to meeting targeted capabilities, near term advancement goals, and process certification of fabrication methods

    Evaluation of ARCAM Deposited Ti-6Al-4V

    Get PDF
    A wide range of Metal Additive Manufacturing (MAM) technologies are becoming available. One of the challenges in using new technologies for aerospace systems is demonstrating that the process and system has the ability to manufacture components that meet the high quality requirements on a statistically significant basis. The widest-used system for small to medium sized components is the ARCAM system manufactured in Gothenburg, Sweden. This system features a 4kW electron-beam gun, and has a chamber volume of 250mm long x 250mm wide x 250mm to 400mm tall. This paper will describe the basis for the quality and consistency requirements, the experimental and evaluation procedures used for the evaluation, and an analysis of the results for Ti-6Al-4V

    Sustainable Human Presence on the Moon using In Situ Resources

    Get PDF
    New capabilities, technologies and infrastructure must be developed to enable a sustained human presence on the moon and beyond. The key to having this permanent presence is the utilization of in situ resources. To this end, NASA is investigating how in situ resources can be utilized to improve mission success by reducing up-mass, improving safety, reducing risk, and bringing down costs for the overall mission. To ensure that this capability is available when needed, technology development is required now. NASA/Marshall Space Flight Center (MSFC) is supporting this endeavor, along with other NASA centers, by exploring how lunar regolith can be mined for uses such as construction, life support, propulsion, power, and fabrication. Efforts at MSFC include development of lunar regolith simulant for hardware testing and development, extraction of oxygen and other materials from the lunar regolith, production of parts and tools on the moon from local materials or from provisioned feedstocks, and capabilities to show that produced parts are "ready for use". This paper discusses the lunar regolith, how the regolith is being replicated in the development of simulants and possible uses of the regolith

    Developing Fabrication Technologies to Provide On Demand Manufacturing for Exploration of the Moon and Mars

    Get PDF
    NASA's human exploration initiative poses great opportunity and risk for manned and robotic missions to the Moon, Mars, and beyond. Engineers and scientists at the Marshall Space Flight Center (MSFC) are developing technologies for in situ fabrication capabilities during lunar and Martian surface operations utilizing provisioned and locally refined materials. Current fabrication technologies must be advanced to support the special demands and applications of the space exploration initiative such as power, weight and volume constraints. In Situ Fabrication and Repair (ISFR) will advance state-of-the-art technologies in support of habitat structure development, tools, and mechanical part fabrication. The repair and replacement of space mission components, such as life support items or crew exercise equipment, fall within the ISFR scope. This paper will address current fabrication technologies relative to meeting ISFR targeted capabilities, near-term advancement goals, and systematic evaluation of various fabrication methods

    Activity-dependent degeneration of axotomized neuromuscular synapses in Wld(S) mice

    Get PDF
    AbstractActivity and disuse of synapses are thought to influence progression of several neurodegenerative diseases in which synaptic degeneration is an early sign. Here we tested whether stimulation or disuse renders neuromuscular synapses more or less vulnerable to degeneration, using axotomy as a robust trigger. We took advantage of the slow synaptic degeneration phenotype of axotomized neuromuscular junctions in flexor digitorum brevis (FDB) and deep lumbrical (DL) muscles of Wallerian degeneration-Slow (WldS) mutant mice. First, we maintained ex vivo FDB and DL nerve-muscle explants at 32°C for up to 48h. About 90% of fibers from WldS mice remained innervated, compared with about 36% in wild-type muscles at the 24-h checkpoint. Periodic high-frequency nerve stimulation (100Hz: 1s/100s) reduced synaptic protection in WldS preparations by about 50%. This effect was abolished in reduced Ca2+ solutions. Next, we assayed FDB and DL innervation after 7days of complete tetrodotoxin (TTX)-block of sciatic nerve conduction in vivo, followed by tibial nerve axotomy. Five days later, only about 9% of motor endplates remained innervated in the paralyzed muscles, compared with about 50% in 5day-axotomized muscles from saline-control-treated WldS mice with no conditioning nerve block. Finally, we gave mice access to running wheels for up to 4weeks prior to axotomy. Surprisingly, exercising WldS mice ad libitum for 4weeks increased about twofold the amount of subsequent axotomy-induced synaptic degeneration. Together, the data suggest that vulnerability of mature neuromuscular synapses to axotomy, a potent neurodegenerative trigger, may be enhanced bimodally, either by disuse or by hyperactivity

    Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

    Get PDF
    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.

    Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease

    Get PDF
    BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. CONCLUSIONS: Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)
    corecore