Energy yield analysis of textured perovskite silicon tandem solar cells and modules.

Perovskite silicon tandem solar cells combine potentially low production costs with the ability to surpass the efficiency limit of silicon single junction solar cells. Optical modeling and optimization are crucial to achieve this ambitious goal in the near future. The optimization should seek to maximize the energy yield based on realistic environmental conditions. This work analyzes the energy yield of perovskite silicon tandem solar cells and modules based on realistic experimental data, with a special focus on the investigation of surface textures at the front and rear side of the solar cell and its implication for reflection as well as parasitic absorption properties. The investigation reveals a 7.3%rel higher energy yield for an encapsulated tandem cell with a textured front side compared with an encapsulated high efficiency single junction solar cell with 24.3% harvesting efficiency for irradiance data of the year 2014 in Freiburg/Germany.

Evaluation of the appropriateness of dosing, indication and safety of rivaroxaban in a community hospital.

WHAT IS KNOWN AND OBJECTIVE: For over 50 years, warfarin was the only oral anticoagulant approved in the United States. In 2011, the Food and Drug Administration (FDA) approved rivaroxaban. Since its introduction, rivaroxaban has served as an alternative to warfarin to minimize drug interactions and avoid drug monitoring. The objective of this study was to evaluate the appropriateness of rivaroxaban dosing, indication and safety in a community hospital and to identify areas for improvement in its use. METHODS: This single-centre, retrospective review evaluated patients who received at least one dose of rivaroxaban between November 2011 and July 2013. The primary outcome included appropriateness of the first day of therapy based on indication and renal function per FDA-approved dosing recommendations for the prevention of stroke and systemic embolism in non-valvular atrial fibrillation (NVAF) and for the treatment or prevention of venous thromboembolism (VTE). The secondary outcome included incidence of major bleeding or non-major clinically relevant bleeding. RESULTS AND DISCUSSION: Of the 445 patients evaluated, 36·9% of patients treated for NVAF and 12·4% treated for VTE were on an inappropriate regimen. Major bleeding within 12 months occurred in 3·5% of patients treated for NVAF, 1·2% for VTE and 0% for off-label indications with a similar trend for non-major clinically relevant bleeding (3·8%, 1·8% and 0%, respectively). WHAT IS NEW AND CONCLUSION: Though offering potential advantages over warfarin, the use of rivaroxaban should be monitored to increase appropriateness of therapy and improve patient safety. Therapeutic interchanges, pharmacist-directed interventions and other initiatives can be implemented to ensure appropriate use.

GlyT1 encephalopathy: Characterization of presumably disease causing GlyT1 mutations.

Glycine constitutes a major inhibitory neurotransmitter predominantly in caudal regions of the CNS. The extracellular glycine concentration is regulated synergistically by two high affinity, large capacity transporters GlyT1 and GlyT2. Both proteins are encoded by single genes SLC6A9 and SLC6A5, respectively. Mutations within the SLC6A5 gene encoding for GlyT2 have been demonstrated to be causative for hyperekplexia (OMIM #614618), a complex neuromuscular disease, in humans. In contrast, mutations within the SLC6A9 gene encoding for GlyT1 have been associated with GlyT1 encephalopathy (OMIM #601019), a disease causing severe postnatal respiratory deficiency, muscular hypotonia and arthrogryposis. The consequences of the respective GlyT1 mutations on the function of the transporter protein, however, have not yet been analysed. In this study we present the functional characterisation of three previously published GlyT1 mutations, two mutations predicted to cause truncation of GlyT1 (GlyT1Q573* and GlyT1K310F+fs*31) and one predicted to cause an amino acid exchange within transmembrane domain 7 of the transporter (GlyT1S407G), that are associated with GlyT1 encephalopathy. Additionally, the characterization of a novel mutation predicted to cause an amino acid exchange within transmembrane domain 1 (GlyT1V118M) identified in two fetuses showing increased nuchal translucency and arthrogryposis in routine ultrasound scans is demonstrated. We show that in recombinant systems the two presumably truncating mutations resulted in an intracellular retained GlyT1 protein lacking the intracellular C-terminal domain. In both cases this truncated protein did not show any residual transport activity. The point mutations, hGlyT1S407G and hGlyT1V118M, were processed correctly, but showed severely diminished activity, thus constituting a functional knock-out in-vivo. Taken together our data demonstrate that all analysed mutations of GlyT1 that have been identified in GlyT1 encephalopathy patients cause severe impairment of transporter function. This is consistent with the idea that loss of GlyT1 function is indeed causal for the disease phenotype.

Failure to confirm specificity of samples containing a very high titer of hepatitis B surface antigen (HBsAg).

Two samples repeatedly positive for HBsAg by the AusRIA II screening procedure failed to be confirmed by neutralization with anti-HBs serum. Both samples could be effectively neutralized by the same anti-HBs sera if diluted 1:10, 1:50 and 1:100 prior to testing. It is suggested that the inability to neutralize was due to a very high concentration of HBsAg in these samples.