Does Basic Skills Education Work? Some Evidence from the National Adult Literacy Survey

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The role of planets in shaping planetary nebulae

In 1997 Soker laid out a framework for understanding the formation and shaping of planetary nebulae (PN). Starting from the assumption that non-spherical PN cannot be formed by single stars, he linked PN morphologies to the binary mechanisms that may have formed them, basing these connections almost entirely on observational arguments. In light of the last decade of discovery in the field of PN, we revise this framework, which, although simplistic, can still serve as a benchmark against which to test theories of PN origin and shaping. Within the framework, we revisit the role of planets in shaping PN. Soker invoked a planetary role in shaping PN because there are not enough close binaries to shape the large fraction of non-spherical PN. In this paper we adopt a model whereby only ~20% of all 1-8 solar mass stars make a PN. This reduces the need for planetary shaping. Through a propagation of percentages argument, and starting from the assumption that planets can only shape mildly elliptical PN, we conclude, like in Soker, that ~20% of all PN were shaped via planetary and other substellar interactions but we add that this corresponds to only ~5% of all 1-8 solar mass stars. This may be in line with findings of planets around main sequence stars. PN shaping by planets is made plausible by the recent discovery of planets that have survived interactions with red giant branch (RGB) stars. Finally, we conclude that of the ~80% of 1-8 solar mass stars that do not make a PN, about one quarter do not even ascend the AGB due to interactions with stellar and substellar companions, while three quarters ascend the AGB but do not make a PN. Once these stars leave the AGB they evolve normally and can be confused with post-RGB, extreme horizontal branch stars. We propose tests to identify them.Comment: 23 pages, accepted by PAS

Authority and the Future of Consent in Population-Level Biomedical Research

Population-level biomedical research has become crucial to the health system’s ability to improve the health ofthe population. This form of research raises a number of well-documented ethical concerns, perhaps the mostsignificant of which is the inability of the researcher to obtain fully informed specific consent from participants.Two proposed technical solutions to this problem of consent in large-scale biomedical research that havebecome increasingly popular are meta-consent and dynamic consent. We critically examine the ethical andpractical credentials of these proposals and find them lacking. We suggest that the consent problem is notsolved by adopting a technology driven approach grounded in a notion of ‘specific’ consent but by takingseriously the role of research governance in combination with broader conceptions of consent. In our view, theseapproaches misconstrue the rightful location of authority in the way in which population-level biomedicalresearch activities are structured and organized. We conclude by showing how and why the authority fordetermining the nature and shape of choice making about participation ought not to lie with individual participants, but rather with the researchers and the research governance process, and that this necessarily leads tothe endorsement of a fully articulated broad consent approach

An occupational therapy intervention for residents with stroke related disabilities in UK care homes (OTCH): cluster randomised controlled trial

Objective To evaluate the clinical efficacy of an established programme of occupational therapy in maintaining functional activity and reducing further health risks from inactivity in care home residents living with stroke sequelae. Design Pragmatic, parallel group, cluster randomised controlled trial. Setting 228 care homes (>10 beds each), both with and without the provision of nursing care, local to 11 trial administrative centres across the United Kingdom. Participants 1042 care home residents with a history of stroke or transient ischaemic attack, including those with language and cognitive impairments, not receiving end of life care. 114 homes (n=568 residents, 64% from homes providing nursing care) were allocated to the intervention arm and 114 homes (n=474 residents, 65% from homes providing nursing care) to standard care (control arm). Participating care homes were randomised between May 2010 and March 2012. Intervention Targeted three month programme of occupational therapy, delivered by qualified occupational therapists and assistants, involving patient centred goal setting, education of care home staff, and adaptations to the environment. Main outcome measures Primary outcome at the participant level: scores on the Barthel index of activities of daily living at three months post-randomisation. Secondary outcome measures at the participant level: Barthel index scores at six and 12 months post-randomisation, and scores on the Rivermead mobility index, geriatric depression scale-15, and EuroQol EQ-5D-3L questionnaire, at all time points. Results 64% of the participants were women and 93% were white, with a mean age of 82.9 years. Baseline characteristics were similar between groups for all measures, personal characteristics, and diagnostic tests. Overall, 2538 occupational therapy visits were made to 498 participants in the intervention arm (mean 5.1 visits per participant). No adverse events attributable to the intervention were recorded. 162 (11%) died before the primary outcome time point, and 313 (30%) died over the 12 months of the trial. The primary outcome measure did not differ significantly between the treatment arms. The adjusted mean difference in Barthel index score at three months was 0.19 points higher in the intervention arm (95% confidence interval −0.33 to 0.70, P=0.48). Secondary outcome measures also showed no significant differences at all time points. Conclusions This large phase III study provided no evidence of benefit for the provision of a routine occupational therapy service, including staff training, for care home residents living with stroke related disabilities. The established three month individualised course of occupational therapy targeting stroke related disabilities did not have an impact on measures of functional activity, mobility, mood, or health related quality of life, at all observational time points. Providing and targeting ameliorative care in this clinically complex population requires alternative strategies

Mesenchyme Homeobox 2 Enhances Migration of Endothelial Colony Forming Cells Exposed to Intrauterine Diabetes Mellitus

Diabetes mellitus (DM) during pregnancy has long-lasting implications for the fetus, including cardiovascular morbidity. Previously, we showed that endothelial colony forming cells (ECFCs) from DM human pregnancies have decreased vasculogenic potential. Here, we evaluate whether the molecular mechanism responsible for this phenotype involves the transcription factor, Mesenchyme Homeobox 2 (MEOX2). In human umbilical vein endothelial cells, MEOX2 upregulates cyclin-dependent kinase inhibitor expression, resulting in increased senescence and decreased proliferation. We hypothesized that dysregulated MEOX2 expression in neonatal ECFCs from DM pregnancies decreases network formation through increased senescence and altered cell cycle progression. Our studies show that nuclear MEOX2 is increased in ECFCs from DM pregnancies. To determine if MEOX2 is sufficient and/or required to induce impaired network formation, MEOX2 was overexpressed and depleted in ECFCs from control and DM pregnancies, respectively. Surprisingly, MEOX2 overexpression in control ECFCs resulted in increased network formation, altered cell cycle progression, and increased senescence. In contrast, MEOX2 knockdown in ECFCs from DM pregnancies led to decreased network formation, while cell cycle progression and senescence were unaffected. Importantly, migration studies demonstrated that MEOX2 overexpression increased migration, while MEOX2 knockdown decreased migration. Taken together, these data suggest that altered migration may be mediating the impaired vasculogenesis of ECFCs from DM pregnancies. While initially believed to be maladaptive, these data suggest that MEOX2 may serve a protective role, enabling increased vessel formation despite exposure to a DM intrauterine environment. J. Cell. Physiol. 232: 1885-1892, 2017

Inversion in the In0.53Ga0.47As metal-oxide-semiconductor system: Impact of the In0.53Ga0.47As doping concentration

In0.53Ga0.47As metal-oxide-semiconductor (MOS) capacitors with an Al2O3 gate oxide and a range of n and p-type In0.53Ga0.47As epitaxial concentrations were examined. Multi-frequency capacitance-voltage and conductance-voltage characterization exhibited minority carrier responses consistent with surface inversion. The measured minimum capacitance at high frequency (1 MHz) was in excellent agreement with the theoretical minimum capacitance calculated assuming an inverted surface. Minority carrier generation lifetimes, sg, extracted from experimentally measured transition frequencies, xm, using physics based a.c. simulations, demonstrated a reduction in sg with increasing epitaxial doping concentration. The frequency scaled conductance, G/x, in strong inversion allowed the estimation of accurate Cox values for these MOS devices

Dune formation on the present Mars

We apply a model for sand dunes to calculate formation of dunes on Mars under the present Martian atmospheric conditions. We find that different dune shapes as those imaged by Mars Global Surveyor could have been formed by the action of sand-moving winds occuring on today's Mars. Our calculations show, however, that Martian dunes could be only formed due to the higher efficiency of Martian winds in carrying grains into saltation. The model equations are solved to study saltation transport under different atmospheric conditions valid for Mars. We obtain an estimate for the wind speed and migration velocity of barchan dunes at different places on Mars. From comparison with the shape of bimodal sand dunes, we find an estimate for the timescale of the changes in Martian wind regimes.Comment: 16 pages, 12 figure

Millimetre observations of Pleiades stars: a lack of solar-analogue planetesimal discs at 100 Myr?

Solar analogues approximately 100 Myr old may have dusty debris from collisions within evolving cometary belts, and such remnant discs might also be associated with earlier stellar-spin braking. We observed at 1.2 mm wavelength a sample of 17 fast and slow rotators, mostly single K dwarfs, in the 100 Myr Pleiades cluster. No dust was detected for individual stars or the ensemble, so there are no cold massive debris discs nor any discernible relation of such distant material to stellar spin. The net limits from these data and our earlier far-infrared results imply that the typical Pleiades G/K dwarf has a relative disc-to-star luminosity ≲ 2 × 10^(−4). Collisional evolution models have predicted greater luminosities at the 10^8 yr epoch, for debris discs evolving out of a proto-solar nebula. This suggests that substantial primordial discs such as that of the Sun are not the norm amongst young solar analogues, or that dynamical interactions with giant planets can remove much of the comet belt by as early as 100 Myr

The role of depression in the association between mobilisation timing and live discharge after hip fracture surgery: Secondary analysis of the UK National Hip Fracture Database

Purpose The aim was to compare the probability of discharge after hip fracture surgery conditional on being alive and in hospital between patients mobilised within and beyond 36-hours of surgery across groups defined by depression. Methods Data were taken from the National Hip Fracture Database and included patients 60 years of age or older who underwent hip fracture surgery in England and Wales between 2014 and 2016. The conditional probability of postsurgical live discharge was estimated for patients mobilised early and for patients mobilised late across groups with and without depression. The association between mobilisation timing and the conditional probability of live discharge were also estimated separately through adjusted generalized linear models. Results Data were analysed for 116,274 patients. A diagnosis of depression was present in 8.31% patients. In those with depression, 7,412 (76.7%) patients mobilised early. In those without depression, 84,085 (78.9%) patients mobilised early. By day 30 after surgery, the adjusted odds ratio of discharge among those who mobilised early compared to late was 1.79 (95% CI: 1.56–2.05, p<0.001) and 1.92 (95% CI: 1.84–2.00, p<0.001) for those with and without depression, respectively. Conclusion A similar proportion of patients with depression mobilised early after hip fracture surgery when compared to those without a diagnosis of depression. The association between mobilisation timing and time to live discharge was observed for patients with and without depression

Epigenetic regulation in neonatal ECFCs following intrauterine exposure to gestational diabetes

poster abstractGestational diabetes (GDM) complicates up to 10% of pregnancies. In addition to acute risks, the children of diabetic mothers have an increased risk of obesity, diabetes, and hypertension, starting in childhood. While the causes of this increased risk are unknown, previous studies in our lab have identified functional deficits in endothelial colony forming cells (ECFCs) isolated from the cord blood of GDM pregnancies. This study focused on identifying genes that have altered epigenetic modifications that result in abnormal mRNA and protein expression in ECFCs from the cord blood GDM pregnancies. The objective of this study was to identify mRNA expression and DNA methylation alterations in ECFCs that may help identify the causes of ECFC dysfunction following intrauterine exposure to GDM. ECFCs were obtained from control and GDM pregnancies. DNA, RNA, and protein samples were isolated in parallel from ECFCs. RNA microarray analysis using the Affymetrix Human 1.0 Gene Array was used to identify gene expression alterations in GDM ECFCs compared to control ECFCs. Genome-wide DNA methylation was assessed using an Infinium 450K Methylation Array for DNA samples at >450,000 CpG sites. Correlation analysis was performed to identify possible sites that have altered CpG methylation and RNA expression. RNA expression results were validated using qRT-PCR and western blotting. Bisulfite sequencing of genomic DNA from the ECFCs was performed to identify additional sites with altered methylation for regions not included in the DNA methylation array. Of the 28,000 genetic loci tested, 596 mRNAs were altered between control and GDM ECFCs (p<0.01). More stringent criteria identified 38 genes for further investigation by limiting analysis to genes that exhibited increased or decreased expression by at least 50%, with a p<0.01. PLAC8 was identified as being increased 5-fold by microarray analysis, a result which was confirmed in two cohorts by qRT-PCR and western blotting. Analysis of the methylation array and bisulfite sequencing results revealed 3 regions surrounding the transcriptional start site of PLAC8 gene whose CpG methylation negatively correlate with RNA expression in samples from control and GDM ECFCs. In contrast, a CpG island is fully unmethylated in both control and GDM ECFCs. The discovery of CpG sites whose methylation correlates with PLAC8 mRNA expression in ECFCs is consistent with the hypothesis that intrauterine exposure to GDM results in epigenetic changes. Analysis of methylation at this site could be used as a biomarker for children of mothers with GDM who may be at risk for disease later in life. Using bisulfite pyrosequencing, we are currently developing assays to quickly determine if methylation of the PLAC8 putative promoter region is altered in cord blood mononuclear cells obtained from GDM or healthy control pregnancies. We are also investigating the role of methylation in regulating PLAC8 RNA expression, determining if there is altered histone modifications and transcription factor binding in these regions, and examining other genes that may comprise a molecular signature of ECFC dysfunction