Designing III-V Multijunction Solar Cells on Silicon

Single junction Si solar cells dominate photovoltaics but are close to their efficiency limits. This paper presents ideal limiting efficiencies for tandem and triple junction multijunction solar cells subject only to the constraint of the Si bandgap and therefore recommending optimum cell structures departing from the single junction ideal. The use of III-V materials is considered, using a novel growth method capable of yielding low defect density III-V layers on Si. In order to evaluate the real potential of these proposed multijunction designs, a quantitative model is presented, the strength of which is the joint modelling of external quantum efficiency and current-voltage characteristics using the same parameters. The method yields a single parameter fit in terms of the Shockley-Read-Hall lifetime. This model is validated by fitting experimental data of external quantum efficiency, dark current, and conversion efficiency of world record tandem and triple junction cells under terrestrial solar spectra without concentration. We apply this quantitative model to the design of tandem and triple junction solar cells, yielding cell designs capable of reaching efficiencies without concentration of 32% for the best tandem cell and 36% for the best triple junction cell. This demonstrates that efficiencies within a few percent of world records are realistically achievable without the use of concentrating optics, with growth methods being developed for multijunction cells combining III-V and Si materials.Comment: Preprint of the paper submitted to the journal Progress in Photovoltaics, selected by the Executive Committee of the 28th EU PVSEC 2013 for submission to Progress in Photovoltaics. 10 pages, 7 figure

A Reduction in Serum Cytokine Levels Parallels Healing of Venous Ulcers in Patients Undergoing Compression Therapy

AbstractIntroduction vascular endothelial growth factor (VEGF) and tumour necrosis factor alpha (TNFα) have been specifically implicated in the tissue damage associated with chronic venous disease (CVD). Furthermore, production of both factors is known to be upregulated in vessel wall cells subject to hypertension. The aim of this study was to determine the local venous levels of VEGF and TNFα in limbs with venous ulcers before and after treatment with graduated compression. Patients and methods eight patients with venous ulcers and 8 patients with varicose veins only were included in the study. For ulcer patients, serum samples were taken from the superficial veins in lower limbs and repeated after 4 weeks of treatment with 4-layered graduated compression. Serum from the arms of the same patients served as controls. Determination of the concentrations of VEGF and TNFα proteins were performed with sandwich enzyme-linked immunosorbent assays. Results both groups of patients had elevated levels of VEGF and TNFα. In patients with venous ulcers there was a reduction in the levels of both cytokines to below control values with treatment. These changes correlated with healing of the ulcers as determined by reduction in ulcer size. Conclusion these data, for the first time, suggest a central role for both TNFα and VEGF in the pathogenesis of venous ulceration which may constitute a causative link between venous hypertension and tissue pathology

Factors essential for L,D-transpeptidase-mediated peptidoglycan cross-linking and β-lactam resistance in <em>Escherichia coli</em>

International audienceThe target of β-lactam antibiotics is the D,D-transpeptidase activity of penicillin-binding proteins (PBPs) for synthesis of 4→3 cross-links in the peptidoglycan of bacterial cell walls. Unusual 3→3 cross-links formed by L,D-transpeptidases were first detected in Escherichia coli more than four decades ago, however no phenotype has previously been associated with their synthesis. Here we show that production of the L,D-transpeptidase YcbB in combination with elevated synthesis of the (p)ppGpp alarmone by RelA lead to full bypass of the D,D-transpeptidase activity of PBPs and to broad-spectrum β-lactam resistance. Production of YcbB was therefore sufficient to switch the role of (p)ppGpp from antibiotic tolerance to high-level β-lactam resistance. This observation identifies a new mode of peptidoglycan polymerization in E. coli that relies on an unexpectedly small number of enzyme activities comprising the glycosyltransferase activity of class A PBP1b and the D,D-carboxypeptidase activity of DacA in addition to the L,D-transpeptidase activity of YcbB

Application of Probiotic Bacteria to Functional Foods

End of Project ReportProbiotic cultures are described as live microbial feed supplements that improve intestinal microbial balance and are intended for maintenance of health or prevention, rather than the curing of disease. The demand for probiotic foods is increasing in Europe, Japan and the U.S. reflecting the heightened awareness among the public of the relationship between diet and health. Traditionally, the most popular food delivery systems for these cultures have been freshly fermented dairy foods, such as yogurts and fermented milks, as well as unfermented milks with cultures added. However, in the development of functional foods, the technological suitability of probiotic strains poses a serious challenge since their survival and viability may be adversely affected by processing conditions as well as by the product environment and storage conditions. This is a particular concern, given that high levels (at least 107 per gram or ml) of live micro-organisms are recommended for probiotic products. In previous studies (see DPRC No. 29) the successful manufacture of probiotic Cheddar cheese harbouring high levels (>108 cfu/g) of the probiotic Lactobacillus paracasei NFBC 338 strain was reported. Hence, the overall objective of these studies was to continue the development and evaluation of Functional Foods containing high levels of viable probiotic bacteria, with particular emphasis on overcoming the technological barriers and the identification of strains suited to particular applications, such as incorporation into Cheddar cheese and spray-dried powders.Department of Agriculture, Food and the Marin

Megasatellites: a peculiar class of giant minisatellites in genes involved in cell adhesion and pathogenicity in Candida glabrata

Minisatellites are DNA tandem repeats that are found in all sequenced genomes. In the yeast Saccharomyces cerevisiae, they are frequently encountered in genes encoding cell wall proteins. Minisatellites present in the completely sequenced genome of the pathogenic yeast Candida glabrata were similarly analyzed, and two new types of minisatellites were discovered: minisatellites that are composed of two different intermingled repeats (called compound minisatellites), and minisatellites containing unusually long repeated motifs (126–429 bp). These long repeat minisatellites may reach unusual length for such elements (up to 10 kb). Due to these peculiar properties, they have been named ‘megasatellites’. They are found essentially in genes involved in cell–cell adhesion, and could therefore be involved in the ability of this opportunistic pathogen to colonize the human host. In addition to megasatellites, found in large paralogous gene families, there are 93 minisatellites with simple shorter motifs, comparable to those found in S. cerevisiae. Most of the time, these minisatellites are not conserved between C. glabrata and S. cerevisiae, although their host genes are well conserved, raising the question of an active mechanism creating minisatellites de novo in hemiascomycetes

Genome Sequence of the Saprophyte Leptospira biflexa Provides Insights into the Evolution of Leptospira and the Pathogenesis of Leptospirosis

Leptospira biflexa is a free-living saprophytic spirochete present in aquatic environments. We determined the genome sequence of L. biflexa, making it the first saprophytic Leptospira to be sequenced. The L. biflexa genome has 3,590 protein-coding genes distributed across three circular replicons: the major 3,604 chromosome, a smaller 278-kb replicon that also carries essential genes, and a third 74-kb replicon. Comparative sequence analysis provides evidence that L. biflexa is an excellent model for the study of Leptospira evolution; we conclude that 2052 genes (61%) represent a progenitor genome that existed before divergence of pathogenic and saprophytic Leptospira species. Comparisons of the L. biflexa genome with two pathogenic Leptospira species reveal several major findings. Nearly one-third of the L. biflexa genes are absent in pathogenic Leptospira. We suggest that once incorporated into the L. biflexa genome, laterally transferred DNA undergoes minimal rearrangement due to physical restrictions imposed by high gene density and limited presence of transposable elements. In contrast, the genomes of pathogenic Leptospira species undergo frequent rearrangements, often involving recombination between insertion sequences. Identification of genes common to the two pathogenic species, L. borgpetersenii and L. interrogans, but absent in L. biflexa, is consistent with a role for these genes in pathogenesis. Differences in environmental sensing capacities of L. biflexa, L. borgpetersenii, and L. interrogans suggest a model which postulates that loss of signal transduction functions in L. borgpetersenii has impaired its survival outside a mammalian host, whereas L. interrogans has retained environmental sensory functions that facilitate disease transmission through water

Ubiquinone Analogs: A Mitochondrial Permeability Transition Pore-Dependent Pathway to Selective Cell Death

International audienceBACKGROUND: Prolonged opening of the mitochondrial permeability transition pore (PTP) leads to cell death. Various ubiquinone analogs have been shown to regulate PTP opening but the outcome of PTP regulation by ubiquinone analogs on cell fate has not been studied yet. METHODOLOGY/PRINCIPAL FINDINGS: The effects of ubiquinone 0 (Ub(0)), ubiquinone 5 (Ub(5)), ubiquinone 10 (Ub(10)) and decyl-ubiquinone (DUb) were studied in freshly isolated rat hepatocytes, cultured rat liver Clone-9 cells and cancerous rat liver MH1C1 cells. PTP regulation by ubiquinones differed significantly in permeabilized Clone-9 and MH1C1 cells from that previously reported in liver mitochondria. Ub(0) inhibited PTP opening in isolated hepatocytes and Clone-9 cells, whereas it induced PTP opening in MH1C1 cells. Ub(5) did not affect PTP opening in isolated hepatocytes and MH1C1 cells, but it induced PTP opening in Clone-9 cells. Ub(10) regulated PTP in isolated hepatocytes, whereas it did not affect PTP opening in Clone-9 and MH1C1 cells. Only DUb displayed the same effect on PTP regulation in the three hepatocyte lines tested. Despite such modifications in PTP regulation, competition between ubiquinones still occurred in Clone-9 and MH1C1 cells. As expected, Ub(5) induced a PTP-dependent cell death in Clone-9, while it did not affect MH1C1 cell viability. Ub(0) induced a PTP-dependent cell death in MH1C1 cells, but was also slightly cytotoxic in Clone-9 by an oxidative stress-dependent mechanism. CONCLUSIONS/SIGNIFICANCE: We found that various ubiquinone analogs regulate PTP in different ways depending on the cell studied. We took advantage of this unique property to develop a PTP opening-targeted strategy that leads to cell death specifically in cells where the ubiquinone analog used induces PTP opening, while sparing the cells in which it does not induce PTP opening

Running With the Ball? Making a Play for Sport Heritage Archives in Higher Education Contexts

For considerable time, academia (in particular, the Humanities) has been in an intellectual, economic and pragmatic par des deux with the culture and arts sector (in this case, heritage, museums and archives). In many ways, given their respective pursuits of scientific enquiry and learning, valuable contribution to a knowledge economy, commitment to public enlightenment, and exploration of critical and creative endeavour, a relationship between the sectors makes sense. Unity notwithstanding, the relationships have become increasingly now influenced by (en)forced contextual constraints (e.g., government policy development and intervention, neoliberal market forces, structural and ideological shifts in funding acquisition and allocation, patronage changes and demands, and/or individual political priorities) (Dubuc 2011; McCall and Gray 2014; Watson 2002). Drawing on education and heritage scholarship, and theoretical frameworks of sport culture spaces (Hardy, Loy and Booth 2009; Phillips 2012; Pinson 2017), this paper examines efforts undertaken at one specific Higher Education establishment in the United Kingdom in which institutional agendas (vis-à-vis historical and cultural foci, encouraging ‘impactful’ academic activity, brand exposure, economic efficiency, and community engagement) have contoured, and become entwined with, an embryonic sport heritage and archive project. Recalling similar arrangements elsewhere (Krüger 2014; Reilly, Clayton and Hughson 2014; Reilly 2015), the aim of this case study is to explore how the wider education and cultural policy context have precipitated an increasingly symbiotic and dependent relationship between university and cultural/arts initiatives. The paper considers how the impetus to develop a sports-based (basketball) heritage archive and study centre reflects the current fragilities of the two sectors, yet, concomitantly, reveals the potentials that might be developed from fostering greater intellectual and pragmatic alliances. The paper concludes by advocating the practical, political and ideological usefulness of network formation, sustainability measures and continued cross-sector dialogue

Caspase-2-mediated cell death is required for deleting aneuploid cells

Caspase-2, one of the most evolutionarily conserved of the caspase family, has been implicated in maintenance of chromosomal stability and tumour suppression. Caspase-2 deficient (Casp2-/-) mice develop normally but show premature ageing-related traits and when challenged by certain stressors, succumb to enhanced tumour development and aneuploidy. To test how caspase-2 protects against chromosomal instability, we utilized an ex vivo system for aneuploidy where primary splenocytes from Casp2-/- mice were exposed to anti-mitotic drugs and followed up by live cell imaging. Our data show that caspase-2 is required for deleting mitotically aberrant cells. Acute silencing of caspase-2 in cultured human cells recapitulated these results. We further generated Casp2C320S mutant mice to demonstrate that caspase-2 catalytic activity is essential for its function in limiting aneuploidy. Our results provide direct evidence that the apoptotic activity of caspase-2 is necessary for deleting cells with mitotic aberrations to limit aneuploidy.S Dawar, Y Lim, J Puccini, M White, P Thomas, L Bouchier-Hayes, D R Green, L Dorstyn and S Kuma