Small PV Systems Performance Evaluation at NREL's Outdoor Test Facility Using the PVUSA Power Rating Method

The PV Systems Performance and Reliability R & D group currently has seven grid-tied 1-2 kilowatt PV systems deployed at NREL's Outdoor Test Facility (OTF) and two 6 kilowatt systems mounted on the roof of NREL's Solar Energy Research Facility (SERF). The systems, which employ several PV module technologies including crystalline silicon (c-Si), amorphous silicon (a-Si), cadmium telluride (CdTe), and copper indium diselenide (CIS), are being monitored to determine the long-term performance and reliability of the modules and arrays under actual field conditions. The length of observation ranges from 2 months for our newest system to 11 years for our oldest systems. The annual degradation and seasonal fluctuation of the systems' power output are calculated using the PV for Utility-Scale Applications (PVUSA) power rating regression model

Performance Evaluation of a 1.5-kWdc a-Si PV Array Using the PVUSA Power Rating Method at NREL's Outdoor Test Facility

As part of the work conducted in the PV Systems Reliability and Performance R&D Task, a 1.5-kWdc photovoltaic (PV) array consisting of 36 Solarex MST-43MV dual-junction a-Si modules was installed and its performance monitored for almost six years (September 1999 through May 2005) at the National Renewable Energy Laboratory (NREL) Outdoor Test Facility (OTF). This paper describes the system and its performance based on the PV for Utility-Scale Applications (PVUSA) power rating method

Capabilities of the High Voltage Stress Test System at the Outdoor Test Facility

We illustrate the capabilities of the High Voltage Stress Test (HVST) which operates continuously in the array field east of the Outdoor Test Facility at the National Renewable Energy Laboratory. Because we know that photovoltaic (PV) modules generating electrical power in both residential and utility-scale array installations will develop high-voltage biases approaching 600 VDC and 1,000 VDC, respectively, we expect such high voltages will result in current leakage between cells and ground, typically through the frames or mounts. We know that inevitably such leakage currents are capable of producing electrochemical corrosion that adversely impacts long-term module performance. With the HVST, we stress or operate PV modules under high-voltage bias, to characterize their leakage currents under all prevailing ambient conditions and assess performance changes emanating from high-voltage stress. We perform this test both on single modules and an active array

Sexual dimorphism in postcranial skeletal shape suggests male‐biased specialization for physical competition in anthropoid primates

Sexual dimorphism often arises as a response to selection on traits that improve a male's ability to physically compete for access to mates. In primates, sexual dimorphism in body mass and canine size is more common in species with intense male–male competition. However, in addition to these traits, other musculoskeletal adaptations may improve male fighting performance. Postcranial traits that increase strength, agility, and maneuverability may also be under selection. To test the hypothesis that males, as compared to females, are more specialized for physical competition in their postcranial anatomy, we compared sex‐specific skeletal shape using a set of functional indices predicted to improve fighting performance. Across species, we found significant sexual dimorphism in a subset of these indices, indicating the presence of skeletal shape sexual dimorphism in our sample of anthropoid primates. Mean skeletal shape sexual dimorphism was positively correlated with sexual dimorphism in body size, an indicator of the intensity of male–male competition, even when controlling for both body mass and phylogenetic relatedness. These results suggest that selection on male fighting ability has played a role in the evolution of postcranial sexual dimorphism in primates

Human PAPS Synthase Isoforms Are Dynamically Regulated Enzymes with Access to Nucleus and Cytoplasm

In higher eukaryotes, PAPS synthases are the only enzymes producing the essential sulphate-donor 3′-phospho-adenosine-5′-phosphosulphate (PAPS). Recently, PAPS synthases have been associated with several genetic diseases and retroviral infection. To improve our understanding of their pathobiological functions, we analysed the intracellular localisation of the two human PAPS synthases, PAPSS1 and PAPSS2. For both enzymes, we observed pronounced heterogeneity in their subcellular localisation. PAPSS1 was predominantly nuclear, whereas PAPSS2 localised mainly within the cytoplasm. Treatment with the nuclear export inhibitor leptomycin B had little effect on their localisation. However, a mutagenesis screen revealed an Arg-Arg motif at the kinase interface exhibiting export activity. Notably, both isoforms contain a conserved N-terminal basic Lys-Lys-Xaa-Lys motif indispensable for their nuclear localisation. This nuclear localisation signal was more efficient in PAPSS1 than in PAPSS2. The activities of the identified localisation signals were confirmed by microinjection studies. Collectively, we describe unusual localisation signals of both PAPS synthase isoforms, mobile enzymes capable of executing their function in the cytoplasm as well as in the nucleus

Type I insulin-like growth factor receptor over-expression induces proliferation and anti-apoptotic signaling in a three-dimensional culture model of breast epithelial cells

INTRODUCTION: Activation of the type I insulin-like growth factor receptor (IGFIR) promotes proliferation and inhibits apoptosis in a variety of cell types. Transgenic mice expressing a constitutively active IGFIR or IGF-I develop mammary tumors and increased levels of IGFIR have been detected in primary breast cancers. However, the contribution of IGFIR activation in promoting breast cancer progression remains unknown. Mammary epithelial cell lines grown in three-dimensional cultures form acinar structures that mimic the round, polarized, hollow and growth-arrested features of mammary alveoli. We used this system to determine how proliferation and survival signaling by IGFIR activation affects breast epithelial cell biology and contributes to breast cancer progression. METHODS: Pooled, stable MCF-10A breast epithelial cells expressing wild-type IGFIR or kinase-dead IGFIR (K1003A) were generated using retroviral-mediated gene transfer. The effects of over-expression of wild-type or kinase-dead IGFIR on breast epithelial cell biology were analyzed by confocal microscopy of three-dimensional cultures. The contribution of signaling pathways downstream of IGFIR activation to proliferation and apoptosis were determined by pharmacological inhibition of phosphatidylinositol 3' kinase (PI3K) with LY294002, MAP kinase kinase (MEK) with UO126 and mammalian target of rapamycin (mTOR) with rapamycin. RESULTS: We found that MCF-10A cells over-expressing the IGFIR formed large, misshapen acinar structures with filled lumina and disrupted apico-basal polarization. This phenotype was ligand-dependent, occurring with IGF-I or supraphysiological doses of insulin, and did not occur in cells over-expressing the kinase-dead receptor. We observed increased proliferation, decreased apoptosis and increased phosphorylation of Ser(473 )of Akt and Ser(2448 )of mTOR throughout IGFIR structures. Inhibition of PI3K with LY294002 or MEK with UO126 prevented the development of acinar structures from IGFIR-expressing but not control cells. The mTOR inhibitor rapamycin failed to prevent IGFIR-induced hyperproliferation and survival signaling. CONCLUSION: Increased proliferation and survival signaling as well as loss of apico-basal polarity by IGFIR activation in mammary epithelial cells may promote early lesions of breast cancer. Three-dimensional cultures of MCF-10A cells over-expressing the IGFIR are a useful model with which to study the role of IGFIR signaling in breast cancer progression and for characterizing the effects of chemotherapeutics targeted to IGFIR signaling