Industrial PVD metallization for high efficiency crystalline silicon solar cells

In this paper we present first results concerning different thermal evaporation processes for thin aluminum layers, which are carried out on a pilot system with a throughput of up to 540 wafers/h (156x156 mm2). To qualify the processes the deposited aluminum layers were evaluated with respect to homogeneity and conductivity. Additionally the effect of the different processes on the passivation quality of a thermally grown 100 nm thick SiO 2 was analyzed by means of lifetime measurements, indicating a negligible effect of the conducted process variations on the passivation quality. Finally high-efficiency silicon solar cells were prepared to determine the overall potential and to compare it with an electron beam (e-gun) evaporation process, which is used as a standard process in our laboratory. An efficiency of up to 21% was achieved by the high deposition rate technique performing at least as well as our standard high efficiency process

KRAS signaling in malignant pleural mesothelioma.

Malignant pleural mesothelioma (MPM) arises from mesothelial cells lining the pleural cavity of asbestos-exposed individuals and rapidly leads to death. MPM harbors loss-of-function mutations in BAP1, NF2, CDKN2A, and TP53, but isolated deletion of these genes alone in mice does not cause MPM and mouse models of the disease are sparse. Here, we show that a proportion of human MPM harbor point mutations, copy number alterations, and overexpression of KRAS with or without TP53 changes. These are likely pathogenic, since ectopic expression of mutant KRASG12D in the pleural mesothelium of conditional mice causes epithelioid MPM and cooperates with TP53 deletion to drive a more aggressive disease form with biphasic features and pleural effusions. Murine MPM cell lines derived from these tumors carry the initiating KRASG12D lesions, secondary Bap1 alterations, and human MPM-like gene expression profiles. Moreover, they are transplantable and actionable by KRAS inhibition. Our results indicate that KRAS alterations alone or in accomplice with TP53 alterations likely play an important and underestimated role in a proportion of patients with MPM, which warrants further exploration