Designing CIGS solar cells with front-side point contacts

In this work we show how 2D numerical simulations can be used to design and optimize front-side point contacts in surface-passivated CIGS cells. Detailed analysis of the combinations of passivation thickness, point contact size and pitch can help identifying solutions able to boost the performance of otherwise surface-limited cells: efficiencies close to those of cells with ideal (i.e., trap-free) CdS/CIGS interface can be achieved by the optimization of point contact features in the low nm range. The effect of varying the CIGS and CdS doping densities on the cell performance has also been analyzed

Corruption in migration management: a network perspective

This paper explores the relation between networks as an emerging mode of public governance and corruption. Adopting the theoretical lens of actor-network theory (ANT), the paper investigates an Italian episode of corruption related to the awarding of government contracts for the management of the Mineo’s CARA, the Europe's largest reception centre for migrants. The analysis shows that a governance network may turn corruption itself into a network where abuse of power can proliferate thanks to the opacity resulting from the multiplicity of actors, interactions, and fragmentation characterizing the governance system

Band gap widening at random CIGS grain boundary detected by valence electron energy loss spectroscopy

Cu(In,Ga) Se₂ (CIGS) thin film solar cells have demonstrated very high efficiencies, but still the role of nanoscale inhomogeneities in CIGS and their impact on the solar cell performance are not yet clearly understood. Due to the polycrystalline structure of CIGS, grain boundaries are very common structural defects that are also accompanied by compositional variations. In this work, we apply valence electron energy loss spectroscopy in scanning transmission electron microscopy to study the local band gap energy at a grain boundary in the CIGS absorber layer. Based on this example, we demonstrate the capabilities of a 2nd generation monochromator that provides a very high energy resolution and allows for directly relating the chemical composition and the band gap energy across the grain boundary. A band gap widening of about 20 meV is observed at the grain boundary. Furthermore, the compositional analysis by core-loss EELS reveals an enrichment of In together with a Cu, Ga and Se depletion at the same area. The experimentally obtained results can therefore be well explained by the presence of a valence band barrier at the grain boundary

Réponse des fibroblastes humains dermiques normaux en culture à de très faibles débits de dose d'irradiation chronique

Des fibroblastes dermiques humains en culture ont été irradiés par une source de 60Co (débit de dose 6,25 mGy / jour) et exposés pendant 8 jours (dose absorbée totale 50 mGy). La prolifération, les teneurs en protéines et ADN n'ont pas été modifiées sous irradiation. Le potentiel transmembranaire de 200 cellules était comparable dans les cellules irradiées (9,4 ± 4,9 eV) et les cellules témoins (10,2 ± 2,0 eV). Les dosages de l'activité de la glucose-6-phosphate deshydrogénase (G6P-DH, enzyme-clé de la voie des pentoses phosphates) de la glycéraldéhyde-3-phosphate deshydrogénase (GAP-DH) et de la pyruvate kinase (enzyme-clé de la glycolyse), ont montré que cette irradiation chronique n'induisait pas de changement de l'activité de la G6P-DH. Au contraire, les activités de la GAP-DH et de la pyruvate kinase étaient significativement - mais transitoirement - inhibées (jusqu'à 25 %) au début de la phase exponentielle de croissance (4e, 5e jour). L'activité catalasique (enzyme de destruction de l'H2O2) ne fut pas significativement modifiée sous irradiation. Une corrélation a été observée entre l'augmentation de l'activité catalasique globale dans les cultures et la restauration d'une activité normale de la GAP-DH, probablement en rapport avec une diminution de l'oxydation des groupements SH

Impact of sleep restriction on metabolic outcomes induced by overfeeding: a randomized controlled trial in healthy individuals.

Overconsumption of energy-dense foods and sleep restriction are both associated with the development of metabolic and cardiovascular diseases, but their combined effects remain poorly evaluated. The aim of this study was to assess whether sleep restriction potentiates the effects of a short-term overfeeding on intrahepatocellular lipid (IHCL) concentrations and on glucose homeostasis. Ten healthy subjects were exposed to a 6-d overfeeding period (130% daily energy needs, with 15% extra energy as sucrose and 15% as fat), with normal sleep (8 h sleep opportunity time) or sleep restriction (4 h sleep opportunity time), according to a randomized, crossover design. At baseline and after intervention, IHCL concentrations were measured by proton magnetic resonance spectroscopy, and a dual intravenous [6,6-2H2]-, oral 13C-labeled glucose tolerance test and a polysomnographic recording were performed. Overfeeding significantly increased IHCL concentrations (Poverfeeding < 0.001; overfeeding + normal sleep: +53% ± 16%). During the oral glucose tolerance test, overfeeding significantly increased endogenous glucose production (Poverfeeding = 0.034) and the oxidation of 13C-labeled glucose load (Poverfeeding = 0.038). Sleep restriction significantly decreased total sleep time, and the duration of stages 1 and 2 and rapid eye movement sleep (all P < 0.001), whereas slow-wave sleep duration was preserved (Poverfeeding × sleep = 0.809). Compared with overfeeding, overfeeding + sleep restriction did not change IHCL concentrations (Poverfeeding × sleep = 0.541; +83% ± 33%), endogenous glucose production (Poverfeeding × sleep = 0.567), or exogenous glucose oxidation (Poverfeeding × sleep = 0.118). Sleep restriction did not significantly alter blood pressure, heart rate, or plasma cortisol concentrations (all Poverfeeding × sleep = NS). Six days of a high-sucrose, high-fat overfeeding diet significantly increased IHCL concentrations and increased endogenous glucose production, suggesting hepatic insulin resistance. These effects of overfeeding were not altered by sleep restriction. This trial was registered at clinicaltrials.gov as NCT02075723. Other study ID numbers: SleepDep 02/14