147 research outputs found
Paper Session II-C - Decreasing the cost of Spacecraft Processing
This paper focuses on spacecraft and payload design for efficient and low-cost launch site processing. An important assumption here is the use of a modern processing facility, one that is optimized for satellites designed for low-cost operations at the launch site. A typical spacecraft processing flow includes operations in three different areas: non-hazardous, hazardous, and on-pad checkout activities. Smart design practices in each of these areas can reduce the time span for payload processing and thus lower costs throughout the operation. A state-ofthe- art processing facility requires a large expenditure of funds up front, but will recoup those dollars over the useful life of the facility and the satellites processing through it. It is the purpose of this paper to propose a series of design requirements for any satellite application, be it a series intended as part of a constellation (e.g. GPS) or a one-time mission (e.g. Cassini). New spacecraft designers must be able to think past the boundaries of the satellite bus and its payload and determine how the system will be readied for launch at the launch base. This requires a systems approach to design, one based on a rigorous requirements definition process and regular interaction with the engineers who will perform the processing operations prior to launch. Most engineers are not schooled in designing for ease of processing - they are taught how to create a satellite to perform a certain mission. This paper aims to highlight efficient and simple launch site processing activities. While not serving as an all-inclusive checklist for smart processing, this paper tries to get the new spacecraft engineer to start thinking about streamlining launch base activities
Design optimization and construction of the thyratron / PFN based cost model modulator for NLC
Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16.
Keratin 16 (K16) is a cytoskeletal scaffolding protein highly expressed at pressure-bearing sites of the mammalian footpad. It can be induced in hyperproliferative states such as wound healing, inflammation and cancer. Here we show that the inactive rhomboid protease RHBDF2 (iRHOM2) regulates thickening of the footpad epidermis through its interaction with K16. K16 expression is absent in the thinned footpads of irhom2-/- mice compared with irhom2+/+mice, due to reduced keratinocyte proliferation. Gain-of-function mutations in iRHOM2 underlie Tylosis with oesophageal cancer (TOC), characterized by palmoplantar thickening, upregulate K16 with robust downregulation of its type II keratin binding partner, K6. By orchestrating the remodelling and turnover of K16, and uncoupling it from K6, iRHOM2 regulates the epithelial response to physical stress. These findings contribute to our understanding of the molecular mechanisms underlying hyperproliferation of the palmoplantar epidermis in both physiological and disease states, and how this 'stress' keratin is regulated
Corona Health -- A Study- and Sensor-based Mobile App Platform Exploring Aspects of the COVID-19 Pandemic
Physical and mental well-being during the COVID-19 pandemic is typically
assessed via surveys, which might make it difficult to conduct longitudinal
studies and might lead to data suffering from recall bias. Ecological momentary
assessment (EMA) driven smartphone apps can help alleviate such issues,
allowing for in situ recordings. Implementing such an app is not trivial,
necessitates strict regulatory and legal requirements, and requires short
development cycles to appropriately react to abrupt changes in the pandemic.
Based on an existing app framework, we developed Corona Health, an app that
serves as a platform for deploying questionnaire-based studies in combination
with recordings of mobile sensors. In this paper, we present the technical
details of Corona Health and provide first insights into the collected data.
Through collaborative efforts from experts from public health, medicine,
psychology, and computer science, we released Corona Health publicly on Google
Play and the Apple App Store (in July, 2020) in 8 languages and attracted 7,290
installations so far. Currently, five studies related to physical and mental
well-being are deployed and 17,241 questionnaires have been filled out. Corona
Health proves to be a viable tool for conducting research related to the
COVID-19 pandemic and can serve as a blueprint for future EMA-based studies.
The data we collected will substantially improve our knowledge on mental and
physical health states, traits and trajectories as well as its risk and
protective factors over the course of the COVID-19 pandemic and its diverse
prevention measures
Summer effects on body mass index (BMI) gain and growth patterns of American Indian children from kindergarten to first grade: a prospective study
<p>Abstract</p> <p>Background</p> <p>Overweight and obesity are highly prevalent among American Indian children, especially those living on reservations. There is little scientific evidence about the effects of summer vacation on obesity development in children. The purpose of this study was to investigate the effects of summer vacation between kindergarten and first grade on growth in height, weight, and body mass index (BMI) for a sample of American Indian children.</p> <p>Methods</p> <p>Children had their height and weight measured in four rounds of data collection (yielded three intervals: kindergarten, summer vacation, and first grade) as part of a school-based obesity prevention trial (Bright Start) in a Northern Plains Indian Reservation. Demographic variables were collected at baseline from parent surveys. Growth velocities (Z-score units/year) for BMI, weight, and height were estimated and compared for each interval using generalized linear mixed models.</p> <p>Results</p> <p>The children were taller and heavier than median of same age counterparts. Height Z-scores were positively associated with increasing weight status category. The mean weight velocity during summer was significantly less than during the school year. More rapid growth velocity in height during summer than during school year was observed. Obese children gained less adjusted-BMI in the first grade after gaining more than their counterparts during the previous two intervals. No statistically significant interval effects were found for height and BMI velocities.</p> <p>Conclusions</p> <p>There was no indication of a significant summer effect on children's BMI. Rather than seasonal or school-related patterns, the predominant pattern indicated by weight-Z and BMI-Z velocities might be related to age or maturation.</p> <p>Trial registration</p> <p>Bright Start: Obesity Prevention in American Indian Children Clinical Trial Govt ID# <a href="http://www.clinicaltrials.gov/ct2/show/NCT00123032">NCT00123032</a></p
Associations between APOE Variants and Metabolic Traits and the Impact of Psychological Stress
In a previous study, we observed that associations between APOE rs439401 and metabolic traits were moderated by chronic stress. Thus, in a population of stressed and non-stressed Danish men, we examined whether associations between APOE rs439401 and a panel of metabolic quantitative traits, all metabolic traits which may lead to T2D and CVD were moderated by psychological stress.Obese young men (n = 475, BMI ≥ 31.0 kg/m(2)) and a randomly selected control group (n = 709) identified from a population of 141,800 men were re-examined in two surveys (S-46: mean age 46, S-49: mean age 49 years) where anthropometric and biochemical measures were available. Psychological stress factors were assessed by a self-administered 7-item questionnaire. Each item had the possible response categories "yes" and "no" and assessed familial problems and conflicts. Summing positive responses constituted a stress item score, which was then dichotomized into stressed and non-stressed. Logistic regression analysis, applying a recessive genetic model, was used to assess odds ratios (OR) of the associations between APOE rs439401 genotypes and adverse levels of metabolic traits.The APOE rs439401 TT-genotype associated positively with BMI (OR = 1.09 [1.01; 1.17]), waist circumference (OR = 1.09 [1.02; 1.17]) in stressed men at S-46. Positive associations were observed for fasting plasma glucose (OR = 1.42 [1.07; 1.87]), serum triglycerides (OR = 1.41 [1.05; 1.91]) and with fasting plasma insulin (OR = 1.48 [1.05; 2.08]) in stressed men at S-49. Rs439401 TT-genotype also associated positively with surrogate measures of insulin resistance (HOMA-IR; OR = 1.21 [1.03; 1.41]) and inversely with insulin sensitivity (Stumvoll index; OR = 0.90 [0.82; 0.99], BIGTT-S(I); OR = 0.60 [0.43; 0.85]) in stressed men. No significant associations were observed in non-stressed men, albeit the estimates showed similar but weaker trends as in stressed men.The present results suggest that the APOE rs439401 TT-genotype is associated with an adverse metabolic profile in a population of psychologically stressed Danish men
Heart disease is common in humans and chimpanzees, but is caused by different pathological processes
Heart disease is common in both humans and chimpanzees, manifesting typically as sudden cardiac arrest or progressive heart failure. Surprisingly, although chimpanzees are our closest evolutionary relatives, the major cause of heart disease is different in the two species. Histopathology data of affected chimpanzee hearts from two primate centers, and analysis of literature indicate that sudden death in chimpanzees (and in gorillas and orangutans) is commonly associated with diffuse interstitial myocardial fibrosis of unknown cause. In contrast, most human heart disease results from coronary artery atherosclerosis, which occludes myocardial blood supply, causing ischemic damage. The typical myocardial infarction of humans due to coronary artery thrombosis is rare in these apes, despite their human-like coronary-risk-prone blood lipid profiles. Instead, chimpanzee ‘heart attacks’ are likely due to arrythmias triggered by myocardial fibrosis. Why do humans not often suffer from the fibrotic heart disease so common in our closest evolutionary cousins? Conversely, why do chimpanzees not have the kind of heart disease so common in humans? The answers could be of value to medical care, as well as to understanding human evolution. A preliminary attempt is made to explore possibilities at the histological level, with a focus on glycosylation changes
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The effect of the apolipoprotein E genotype on response to personalized dietary advice intervention: findings from the Food4Me randomized controlled trial
Background: The apolipoprotein E (APOE) risk allele (ɛ4) is associated with higher total cholesterol (TC), amplified response to saturated fatty acid (SFA) reduction, and increased cardiovascular disease. Although knowledge of gene risk may enhance dietary change, it is unclear whether ɛ4 carriers would benefit from gene-based personalized nutrition (PN).
Objectives: The aims of this study were to 1) investigate interactions between APOE genotype and habitual dietary fat intake and modulations of fat intake on metabolic outcomes; 2) determine whether gene-based PN results in greater dietary change than do standard dietary advice (level 0) and nongene-based PN (levels 1–2); and 3) assess the impact of knowledge of APOE risk (risk: E4+, nonrisk: E4−) on dietary change after gene-based PN (level 3).
Design: Individuals (n = 1466) recruited into the Food4Me pan-European PN dietary intervention study were randomly assigned to 4 treatment arms and genotyped for APOE (rs429358 and rs7412). Diet and dried blood spot TC and ω-3 (n–3) index were determined at baseline and after a 6-mo intervention. Data were analyzed with the use of adjusted general linear models.
Results: Significantly higher TC concentrations were observed in E4+ participants than in E4− (P < 0.05). Although there were no significant differences in APOE response to gene-based PN (E4+ compared with E4−), both groups had a greater reduction in SFA (percentage of total energy) intake than at level 0 (mean ± SD: E4+, −0.72% ± 0.35% compared with −1.95% ± 0.45%, P = 0.035; E4−, −0.31% ± 0.20% compared with −1.68% ± 0.35%, P = 0.029). Gene-based PN was associated with a smaller reduction in SFA intake than in nongene-based PN (level 2) for E4− participants (−1.68% ± 0.35% compared with −2.56% ± 0.27%, P = 0.025).
Conclusions: The APOE ɛ4 allele was associated with higher TC. Although gene-based PN targeted to APOE was more effective in reducing SFA intake than standard dietary advice, there was no difference between APOE “risk” and “nonrisk” groups. Furthermore, disclosure of APOE nonrisk may have weakened dietary response to PN
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