Atomic oxygen effects on LDEF experiment AO171

The Solar Array Materials Passive Long Duration Exposure Facility (LDEF) Experiment (SAMPLE), AO171, contained in total approximately 100 materials and materials processes with a 300 specimen complement. With the exception of experiment solar cell and solar cell modules, all test specimens were weighed before flight, thus allowing an accurate determination of mass loss as a result of space exposure. Since almost all of the test specimens were thermal vacuum baked before flight, the mass loss sustained can be attributed principally to atomic oxygen attack. The atomic oxygen effects observed and measured in five classes of materials is documented. The atomic oxygen reactivity values generated for these materials are compared to those values derived for the same materials from exposures on short term shuttle flights. An assessment of the utility of predicting long term atomic oxygen effects from short term exposures is given. This experiment was located on Row 8 position A which allowed all experiment materials to be exposed to an atomic oxygen fluence of 6.93 x 10(exp 21) atoms/cm(sup 2) as a result of being positioned 38 degrees off the RAM direction

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension

Maternal Obesity Alters Fetal Development Due to Impaired Placental Function and has Lasting Effects on Adult Offspring

Obesity is an epidemic in many developed nations and maternal obesity can result in developmental alterations in offspring that have long-lasting effects. Two experiments were conducted to determine the impact of maternal obesity on placental development and early embryonic growth and muscle development. Experiment one utilized obese Lethal Yellow (LY) and normal weight C57BL/6 (B6) dams to assess how maternal obesity alters skeletal muscle development in mid-gestational embryos. Embryos from LY dams exhibited decreased embryo and placental weights as well as an increase in the myogenic marker desmin. Furthermore, the adipogenic marker PPARG expression was predominately localized to the neural tube and was significantly decreased in LY-derived embryos. The objective of experiment 2 was to identify how maternal obesity alters placenta development and function and may be associated with altered development of the fetus. The same mid-gestation embryos and corresponding placenta from LY and B6 dams were used. Placenta from LY dams were smaller than when developed in a B6 dam and exhibited a phenotype of reduced function. The placenta also displayed increased hypoxia markers and decreased gene expression of enzymes which regulate the transfer of active glucocorticoids from the mother to developing embryo. Interestingly, the embryos reared in an obese dam possessed decreased expression of vasculature markers. In summary, these experiments support the following findings: (1) maternal obesity decreases embryonic and placental weight and results in altered temporal regulation of myogenesis; (2) PPARG expression is localized to the neural tube and decreased in LY-derived embryos indicating a function for this transcription factor in neural tube development and suggesting that obesity alters this function; (3) placenta from an obese dam display increased hypoxemia and altered glucocorticoid metabolism resulting in altered embryonic vasculature and potentially differences in the function of various organ systems. These data represent an important shift in understanding how maternal obesity reduces skeletal muscle density during development and its long-term effects on the metabolic health of their children. Advisor: Jennifer R. Woo