The Effect of fuel and poison management on nuclear power systems

Statement of responsibility on title page reads: N.B. McLeod, M. Benedict, K. Uematsu, H.L. Witting, and K.S. Ram"September 15, 1961."Submitted by the first author as a Ph. D. thesis, Massachusetts Institute of Technology, Dept. of Nuclear Engineering, 1962"NYO-9715, TID 4500 Category, UC-80 Reactor Technology.""This work was done in part at the MIT Computation Center."Includes bibliographical references (p. 492-496)Report; June, 1959 - September, 1961Contract no. AT(30-1)-207

Evidence and patterns of tuna spawning inside a large no-take marine protected area

© The Author(s), 2019. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Hernandez, C. M., Witting, J., Willis, C., Thorrold, S. R., Llopiz, J. K., & Rotjan, R. D. Evidence and patterns of tuna spawning inside a large no-take marine protected area. Scientific Reports, 9(1), (2019): 10772, doi:10.1038/s41598-019-47161-0.The Phoenix Islands Protected Area (PIPA), one of the world’s largest marine protected areas, represents 11% of the exclusive economic zone of the Republic of Kiribati, which earns much of its GDP by selling tuna fishing licenses to foreign nations. We have determined that PIPA is a spawning area for skipjack (Katsuwonus pelamis), bigeye (Thunnus obesus), and yellowfin (Thunnus albacares) tunas. Our approach included sampling larvae on cruises in 2015–2017 and using a biological-physical model to estimate spawning locations for collected larvae. Temperature and chlorophyll conditions varied markedly due to observed ENSO states: El Niño (2015) and neutral (2016–2017). However, larval tuna distributions were similar amongst years. Generally, skipjack larvae were patchy and more abundant near PIPA’s northeast corner, while Thunnus larvae exhibited lower and more even abundances. Genetic barcoding confirmed the presence of bigeye (Thunnus obesus) and yellowfin (Thunnus albacares) tuna larvae. Model simulations indicated that most of the larvae collected inside PIPA in 2015 were spawned inside, while stronger currents in 2016 moved more larvae across PIPA’s boundaries. Larval distributions and relative spawning output simulations indicated that both focal taxa spawned inside PIPA in all 3 study years, demonstrating that PIPA is protecting viable tuna spawning habitat.Funding and support was provided by the PIPA Trust, Waitt and Oceans5 Foundations, Sea Education Association, the Prince Albert of Monaco Foundation II, New England Aquarium, and Boston University to R.R. and J.W. C.H. was additionally supported by a National Science Foundation Graduate Research Fellowship. J.L. was additionally supported by NOAA through the Cooperative Institute for the North Atlantic Region (CINAR) under Cooperative Agreement NA14OAR4320158 in the form a CINAR Fellow Award, as well as by the WHOI Academic Programs Office. We thank A. Breef-Pilz for onboard sampling assistance, as well as S. Glancy, J. Pringle, E. Martin, J. Fisher, H. Goss, J. Jaskiel, S. Sheehan, and C. Moller for lab assistance. We thank the PIPA Trust and the PIPA Implementation Office for their support, as well as on-ship Kiribati Observers for their support and assistance: Tekeua Auatabu, Iannang Teaioro, Toaea Beiateuea, Taremon Korere, Kareati Waysang, and Moamoa Kabuati. We thank Q. Hanich for reading sections of this paper in advance. This research was conducted under Kiribati and PIPA permits PRP #s 3/17, 1/16, and 2/15 to JW

Effects of 8 weeks of CPAP on lipid-based oxidative markers in obstructive sleep apnea: a randomized trial

Dyslipidaemia and increased oxidative stress have been reported in severe obstructive sleep apnea, and both may be related to the development of cardiovascular disease. We have previously shown in a randomized crossover study in patients with moderate to severe obstructive sleep apnea that therapeutic continuous positive airway pressure treatment for 8 weeks improved postprandial triglycerides and total cholesterol when compared with sham continuous positive airway pressure. From this study we have now compared the effect of 8 weeks of therapeutic continuous positive airway pressure and sham continuous positive airway pressure on oxidative lipid damage and plasma lipophilic antioxidant levels. Unesterified cholesterol, esterified unsaturated fatty acids (cholesteryl linoleate: C18:2; and cholesteryl arachidonate: C20:4; the major unsaturated and oxidizable lipids in low-density lipoproteins), their corresponding oxidized products [cholesteryl ester-derived lipid hydroperoxides and hydroxides (CE-O(O)H)] and antioxidant vitamin E were assessed at 20:30 hours before sleep, and at 06:00 and 08:30 hours after sleep. Amongst the 29 patients completing the study, three had incomplete or missing [CE-O(O)H] data. The mean apnea -hypopnoea index, age and body mass index were 38 per hour, 49 years and 32 kg m(-2) , respectively. No differences in lipid-based oxidative markers or lipophilic antioxidant levels were observed between the continuous positive airway pressure and sham continuous positive airway pressure arms at any of the three time-points [unesterified cholesterol 0.01 mm, P > 0.05; cholesteryl linoleate: C18:2 0.05 mm, P > 0.05; cholesteryl arachidonate: C20:4 0.02 mm, P = 0.05; CE-O(O)H 2.5 nm, P > 0.05; and lipid-soluble antioxidant vitamin E 0.03 μm, P > 0.05]. In this study, accumulating CE-O(O)H, a marker of lipid oxidation, does not appear to play a role in oxidative stress in obstructive sleep apnea.National Health and Medical Research Council project grant 30193

Dietary fatty acids and mortality risk from heart disease in US adults: an analysis based on NHANES

We investigated the association of dietary intake of major types of fatty acids with heart disease mortality in a general adult cohort with or without a prior diagnosis of myocardial infarction (MI). This cohort study included US adults who attended the National Health and Nutrition Examination Surveys from 1988 to 2014. Heart disease mortality was ascertained by linkage to the National Death Index records through 31 December 2015. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of fatty acid intake for heart disease mortality. This cohort included 45,820 adults among which 1,541 had a prior diagnosis of MI. Participants were followed up for 532,722 person-years (mean follow-up, 11.6 years), with 2,313 deaths recorded from heart disease being recorded. Intake of saturated (SFAs) and monounsaturated fatty acids (MUFAs) was associated with heart disease mortality after adjustment for all the tested confounders. In contrast, a 5% higher calorie intake from polyunsaturated fatty acids (PUFAs) was associated with a 9% (HR, 0.91; 95% CI 0.83–1.00; P = 0.048) lower multivariate-adjusted risk of heart disease mortality. Sub-analyses showed that this inverse association was present in those without a prior diagnosis of MI (HR,0.89; 95% CI 0.80–0.99) but not in those with the condition (HR, 0.94; 95% CI 0.75–1.16). The lack of association in the MI group could be due to a small sample size or severity and procedural complications (e.g., stenting and medication adherence) of the disease. Higher PUFA intake was associated with a favourable lipid profile. However, further adjustment for plasma lipids did not materially change the inverse association between PUFAs and heart disease mortality. Higher intake of PUFAs, but not SFAs and MUFAs, was associated with a lower adjusted risk of heart disease mortality in a large population of US adults supporting the need to increase dietary PUFA intake in the general public

Physical Acoustics

Contains reports on four research projects.U. S. Navy (Office of Naval Research) under Contract Nonr- 1841(42

Release of Enzymatically Active Deubiquitinating Enzymes upon Reversible Capture by Disulfide Ubiquitin Reagents

Chemical Immunolog

CAR-T cell. the long and winding road to solid tumors

Adoptive cell therapy of solid tumors with reprogrammed T cells can be considered the "next generation" of cancer hallmarks. CAR-T cells fail to be as effective as in liquid tumors for the inability to reach and survive in the microenvironment surrounding the neoplastic foci. The intricate net of cross-interactions occurring between tumor components, stromal and immune cells leads to an ineffective anergic status favoring the evasion from the host's defenses. Our goal is hereby to trace the road imposed by solid tumors to CAR-T cells, highlighting pitfalls and strategies to be developed and refined to possibly overcome these hurdles