Low Temperature Atomic Layer Deposited Magnesium Oxide as a Passivating Electron Contact for c Si Based Solar Cells

In this article, we explore magnesium oxide MgO as electron selective contact layer in silicon heterojunction solar cells. We report on the successful deposition of MgO layers by atomic layer deposition at low temperatures amp; 8804;200 C using bis ethylcyclopentadienyl magnesium Mg CpEt 2 and H2O as precursors. Depositions were carried out on bare crystalline silicon c Si wafers and c Si wafers with an intrinsic amorphous hydrogenated silicon i aSi H passivation layer. The resulting interfacial properties, surface passivation quality, and contact resistivity were investigated. Upon initial deposition of MgO on an i aSi H c Si stack, the c Si surface passivation degrades drastically. However, with an additional annealing step of 5 min at 200 250 C, it is possible to reverse the degradation and even to achieve charge carrier lifetimes in excess of those achieved with an i aSi H alone. Furthermore, we show that MgO forms an ohmic contact with both MgO i aSi H c Si and MgO c Si stacks, and we demonstrate solar cells using both types of stacks as electron contact layer

PO x

Thin-film stacks of phosphorus oxide (POx) and aluminium oxide (Al2O3) are shown to provide highly effective passivation of crystalline silicon (c-Si) surfaces. Surface recombination velocities as low as 1.7 cm s-1 and saturation current densities J0 s as low as 3.3 fA cm-2 are obtained on n-type (100) c-Si surfaces passivated by 6 nm/14 nm thick POx/Al2O3 stacks deposited in an atomic layer deposition system and annealed at 450 °C. This excellent passivation can be attributed in part to an unusually large positive fixed charge density of up to 4.7 × 1012 cm-2, which makes such stacks especially suitable for passivation of n-type Si surfaces

Metallothioneins as dynamic markers for brain disease in lysosomal disorders

Objective To facilitate development of novel disease-modifying therapies for lysosomal storage disorder (LSDs) characterized by nervous system involvement such as metachromatic leukodystrophy (MLD), molecular markers for monitoring disease progression and therapeutic response are needed. To this end, we sought to identify blood transcripts associated with the progression of MLD. Methods Genome-wide expression analysis was performed in primary T lymphocytes of 24 patients with MLD compared to 24 age- and sex-matched healthy controls. Genes associated with MLD were identified, confirmed on a quantitative polymerase chain reaction platform, and replicated in an independent patient cohort. mRNA and protein expression of the prioritized gene family of metallothioneins was evaluated in postmortem patient brains and in mouse models representing 6 other LSDs. Metallothionein expression during disease progression and in response to specific treatment was evaluated in 1 of the tested LSD mouse models. Finally, a set of in vitro studies was planned to dissect the biological functions exerted by this class of molecules. Results Metallothionein genes were significantly overexpressed in T lymphocytes and brain of patients with MLD and generally marked nervous tissue damage in the LSDs here evaluated. Overexpression of metallothioneins correlated with measures of disease progression in mice and patients, whereas their levels decreased in mice upon therapeutic treatment. In vitro studies indicated that metallothionein expression is regulated in response to oxidative stress and inflammation, which are biochemical hallmarks of lysosomal storage diseases. Interpretation Metallothioneins are potential markers of neurologic disease processes and treatment response in LSDs.Ann Neurol 2014;75:127-137 \ua9 2013 Child Neurology Society/American Neurological Association