Avionics for a Small Satellite

This paper discusses a small. seven and a half (7.5) inch diameter. satellite that NASA-JSC is developing as a technology demonstrator for an astronaut assistant free flyer. The Free Flyer is designed to off load flight crew work load by performing inspections of the exterior of Space Shuttle or International Space Station. The Free Flyer is designed to be operated by the flight crew thereby reducing the number of Extra Vehicle Activities (EVA) or by an astronaut on the ground further reducing crew work load. The paper focuses on the design constraint of a small satellite and the technology approach used to achieve the set of high performance requirements specified for the Free Flyer. Particular attention is paid to the processor card as it is the heart and system integration point of the Free Flyer

REPORT on Research into ‘closing the gap’ : raising achievement for disadvantaged pupils

This research was commissioned by Peterborough City Council as a work stream as part of their Closing the Gap project. There is a gap in performance between children from rich and poor backgrounds in many countries, but the gap in the UK is considered to be significant (OECD, 2014; Strand 2014). Work by the Joseph Rowntree Foundation has estimated that there will be 3.5 million UK children living in poverty by 2020 (JRF, 2014). One strategy to attempt to address the problem was the introduction of The Pupil Premium by the Coalition Government in 2011 to provide additional funding to state funded schools to close the attainment gap between disadvantaged children and their peers by raising the attainment levels of those children from disadvantaged backgrounds (Ofsted, 2012)

Abnormal infant islet morphology precedes insulin resistance in PCOS-like monkeys.

Polycystic ovary syndrome (PCOS) is prevalent in reproductive-aged women and confounded by metabolic morbidities, including insulin resistance and type 2 diabetes. Although the etiology of PCOS is undefined, contribution of prenatal androgen (PA) exposure has been proposed in a rhesus monkey model as premenopausal PA female adults have PCOS-like phenotypes in addition to insulin resistance and decreased glucose tolerance. PA female infants exhibit relative hyperinsulinemia, suggesting prenatal sequelae of androgen excess on glucose metabolism and an antecedent to future metabolic disease. We assessed consequences of PA exposure on pancreatic islet morphology to identify evidence of programming on islet development. Islet counts and size were quantified and correlated with data from intravenous glucose tolerance tests (ivGTT) obtained from dams and their offspring. Average islet size was decreased in PA female infants along with corresponding increases in islet number, while islet fractional area was preserved. Infants also demonstrated an increase in both the proliferation marker Ki67 within islets and the beta to alpha cell ratio suggestive of enhanced beta cell expansion. PA adult females have reduced proportion of small islets without changes in proliferative or apoptotic markers, or in beta to alpha cell ratios. Together, these data suggest in utero androgen excess combined with mild maternal glucose intolerance alter infant and adult islet morphology, implicating deviant islet development. Marked infant, but subtle adult, morphological differences provide evidence of islet post-natal plasticity in adapting to changing physiologic demands: from insulin sensitivity and relative hypersecretion to insulin resistance and diminished insulin response to glucose in the mature PCOS-like phenotype