The effect of dielectric spacer thickness on surface plasmon enhanced solar cells for front and rear side depositions

The excitation of surface plasmons on metallic nanoparticles has the potential to significantly improve the performance of solar cells, in particular thin-film structures. In this article, we investigate the effect of the dielectric spacer layer thickness on the photocurrent enhancement of 2 μm thick, thin-film poly-Si on glass solar cells, due to random arrays of self-assembled Ag nanoparticlesdeposited on the front or the rear of the cells. We report a strong asymmetry in the external quantum efficiency (EQE) of the cell for front and rear located particles for different spacer thicknesses, which is attributed to differences in the scattering behavior of the nanoparticles. We find that for random arrays, with spectrally broad scattering resonances, the strength of the driving field and the coupling efficiency are more important for light trapping than the resonance wavelength. For particles located on the front of the cells it is desirable to have a thin dielectric spacer layer to enhance the scattering from the Ag nanoparticles. Additionally, light trapping provided by the random sized particles on the front can overcome suppression of light transmitted in the visible wavelength regions for thin layers of Si, to result in overall EQE enhancements. However, for particles deposited on the rear it is more beneficial to have the particles as close to the Si substrate as possible to increase both the scattering and the coupling efficiency.K.R.C. acknowledges the support of an Australian Research Council fellowship and the EU FP7 PRIMA project

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

Most of diabetic cardiovascular complications are attributed to endothelial dysfunction and impaired angiogenesis. Endoplasmic Reticulum (ER) and oxidative stresses were shown to play a pivotal role in the development of endothelial dysfunction in diabetes. Hemeoxygenase-1 (HO-1) was shown to protect against oxidative stress in diabetes; however, its role in alleviating ER stress-induced endothelial dysfunction remains not fully elucidated. We aim here to test the protective role of HO-1 against high glucose-mediated ER stress and endothelial dysfunction and understand the underlying mechanisms with special emphasis on oxidative stress, inflammation and cell death.Human Umbilical Vein Endothelial Cells (HUVECs) were grown in either physiological or intermittent high concentrations of glucose for 5days in the presence or absence of Cobalt (III) Protoporphyrin IX chloride (CoPP, HO-1 inducer) or 4-Phenyl Butyric Acid (PBA, ER stress inhibitor). Using an integrated cellular and molecular approach, we then assessed ER stress and inflammatory responses, in addition to apoptosis and angiogenic capacity in these cells.Our results show that HO-1 induction prevented high glucose-mediated increase of mRNA and protein expression of key ER stress markers. Cells incubated with high glucose exhibited high levels of oxidative stress, activation of major inflammatory and apoptotic responses [nuclear factor (NF)-κB and c-Jun N-terminal kinase (JNK)] and increased rate of apoptosis; however, cells pre-treated with CoPP or PBA were fully protected. In addition, high glucose enhanced caspases 3 and 7 cleavage and activity and augmented cleaved poly ADP ribose polymerase (PARP) expression whereas HO-1 induction prevented these effects. Finally, HO-1 induction and ER stress inhibition prevented high glucose-induced reduction in NO release and impaired the angiogenic capacity of HUVECs, and enhanced vascular endothelial growth factor (VEGF)-A expression.Altogether, we show here the critical role of ER stress-mediated cell death in diabetes-induced endothelial dysfunction and impaired angiogenesis and underscore the role of HO-1 induction as a key therapeutic modulator for ER stress response in ischemic disorders and diabetes. Our results also highlight the complex interplay between ER stress response and oxidative stress.This work was supported with grants to Dr Abdelali Agouni from the Royal Society, the Physiological Society, and Qatar University (grant QUUG-CPH-CPH-15/16-6). Mr Maamoun and Ms. Zachariah are supported by doctoral scholarships from Egyptian cultural bureau and Government of Botswana, respectively

Boosting and lassoing new prostate cancer SNP risk factors and their connection to selenium

We begin by arguing that the often used algorithm for the discovery and use of disease risk factors, stepwise logistic regression, is unstable. We then argue that there are other algorithms available that are much more stable and reliable (e.g. the lasso and gradient boosting). We then propose a protocol for the discovery and use of risk factors using lasso or boosting variable selection. We then illustrate the use of the protocol with a set of prostate cancer data and show that it recovers known risk factors. Finally, we use the protocol to identify new and important SNP based risk factors for prostate cancer and further seek evidence for or against the hypothesis of an anticancer function for Selenium in prostate cancer. We find that the anticancer effect may depend on the SNP-SNP interaction and, in particular, which alleles are present

Effective light trapping in polycrystalline silicon thin-film solar cells by means of rear localized surface plasmons

Significant photocurrent enhancement has been achieved for evaporated solid-phase-crystallized polycrystalline siliconthin-filmsolar cells on glass, due to light trapping provided by Agnanoparticles located on the rear siliconsurface of the cells. This configuration takes advantage of the high scattering cross-section and coupling efficiency of rear-located particles formed directly on the optically dense silicon layer. We report short-circuit current enhancement of 29% due to Agnanoparticles, increasing to 38% when combined with a detached back surface reflector. Compared to conventional light trapping schemes for these cells, this method achieves 1/3 higher short-circuit current

Is late-life dependency increasing or not? A comparison of the Cognitive Function and Ageing Studies (CFAS)

Background: Little is known about how dependency levels have changed between generational cohorts of older people. We estimated years lived in different care states at age 65 in 1991 and 2011 and new projections of future demand for care. Methods: Two population-based studies of older people in defined geographical areas conducted two decades apart (the Cognitive Function and Ageing Studies) provided prevalence estimates of dependency in four states: high (24-hour care); medium (daily care); low (less than daily); independent. Years in each dependency state were calculated by Sullivan’s method. To project future demand, the proportions in each dependency state (by age group and sex) were applied to the 2014 England population projections. Findings: Between 1991 and 2011 there were significant increases in years lived from age 65 with low (men:1·7 years, 95%CI 1·0-2·4; women:2·4 years, 95%CI 1·8-3·1) and high dependency (men:0·9 years, 95%CI 0·2-1·7; women:1·3 years, 95%CI 0·5-2·1). The majority of men’s extra years of life were independent (36%) or with low dependency (36%) whilst for women the majority were spent with low dependency (58%), only 5% being independent. There were substantial reductions in the proportions with medium and high dependency who lived in care homes, although, if these dependency and care home proportions remain constant in the future, further population ageing will require an extra 71,000 care home places by 2025. Interpretation: On average older men now spend 2.4 years and women 3.0 years with substantial care needs (medium or high dependency), and most will live in the community. These findings have considerable implications for older people’s families who provide the majority of unpaid care, but the findings also supply valuable new information for governments and care providers planning the resources and funding required for the care of their future ageing populations

Boosting and lassoing new prostate cancer SNP risk factors and their connection to selenium

We begin by arguing that the often used algorithm for the discovery and use of disease risk factors, stepwise logistic regression, is unstable. We then argue that there are other algorithms available that are much more stable and reliable (e.g. the lasso and gradient boosting). We then propose a protocol for the discovery and use of risk factors using lasso or boosting variable selection. We then illustrate the use of the protocol with a set of prostate cancer data and show that it recovers known risk factors. Finally, we use the protocol to identify new and important SNP based risk factors for prostate cancer and further seek evidence for or against the hypothesis of an anticancer function for Selenium in prostate cancer. We find that the anticancer effect may depend on the SNP-SNP interaction and, in particular, which alleles are present

Measuring psychological health in the perinatal period: workshop consensus statement, 19 March 2013

This consensus statement is the result of an invited workshop funded by the society for Reproductive and Infant Psychology on Measuring Psychological Health in the Perinatal Period which was held in Oxford on the 19th March 2013. The details of those who participated in the workshop can be found at the end of the consensus statement. The workshop evolved out of recognition that a major limitation to research and practice in the perinatal period is identifying valid, reliable and clinically relevant measures of psychological health

Human Adaptation to Coastal Evolution: Late Quaternary evidence from Southeast Asia (SUNDASIA) – A report on the second year of the project.

The 3.5 year SUNDASIA projectis a collaborative venture between Vietnamese and UK institutions that is reconstructing a detailed picture of the impact changing sea levels and environmental conditions had on prehistoric socioeconomic systems in the Song Hong River delta area of northern Vietnam. The project is centred in the Tràng An World Heritage Site (WHS) of Ninh Binh province and is co-funded through the UK Arts and Humanities Research Council portion of the British Government’s ‘Global Challenges Research Fund’, and the Xuan Truong Construction Enterprise. At the end of the project’s second year, field data-collection is now largely complete. Data collection locales have been catalogued across the WHS, with highest resolution recovery within a 2 km wide corridor extending (west-east) through the centre of the massif: an area of c. 1500 ha (or 25% of the core zone of WHS). In order to integrate different lines of evidence within a searchable Geographic Information Science (GIS) data base, and to aid future natural and cultural heritage management, site-specific information is referenced within a 4 x 4 km alpha-numeric grid covering the core and buffer zones of the property. While not exhaustive, data obtained will provide an authoritative picture of human responses to changing conditions from c. 37,000 years ago to the present; incorporating archaeological and palaeoecological reconstruction with heritage management and landscape conservation priorities. This report draws on published and grey literature to detail the work being undertaken and is presented in the context of the project’s three central research questions

Selenoprotein gene nomenclature

The human genome contains 25 genes coding for selenocysteine-containing proteins (selenoproteins). These proteins are involved in a variety of functions, most notably redox homeostasis. Selenoprotein enzymes with known functions are designated according to these functions: TXNRD1, TXNRD2, and TXNRD3 (thioredoxin reductases), GPX1, GPX2, GPX3, GPX4 and GPX6 (glutathione peroxidases), DIO1, DIO2, and DIO3 (iodothyronine deiodinases), MSRB1 (methionine-R-sulfoxide reductase 1) and SEPHS2 (selenophosphate synthetase 2). Selenoproteins without known functions have traditionally been denoted by SEL or SEP symbols. However, these symbols are sometimes ambiguous and conflict with the approved nomenclature for several other genes. Therefore, there is a need to implement a rational and coherent nomenclature system for selenoprotein-encoding genes. Our solution is to use the root symbol SELENO followed by a letter. This nomenclature applies to SELENOF (selenoprotein F, the 15 kDa selenoprotein, SEP15), SELENOH (selenoprotein H, SELH, C11orf31), SELENOI (selenoprotein I, SELI, EPT1), SELENOK (selenoprotein K, SELK), SELENOM (selenoprotein M, SELM), SELENON (selenoprotein N, SEPN1, SELN), SELENOO (selenoprotein O, SELO), SELENOP (selenoprotein P, SeP, SEPP1, SELP), SELENOS (selenoprotein S, SELS, SEPS1, VIMP), SELENOT (selenoprotein T, SELT), SELENOV (selenoprotein V, SELV) and SELENOW (selenoprotein W, SELW, SEPW1). This system, approved by the HUGO Gene Nomenclature Committee, also resolves conflicting, missing and ambiguous designations for selenoprotein genes and is applicable to selenoproteins across vertebrates