Accuracy-enhanced solar resource maps of South Africa

Paper presented to the 3rd Southern African Solar Energy Conference, South Africa, 11-13 May, 2015.SolarGIS is a global database of solar resource and meteorological parameters, developed and operated by GeoModel Solar. This database is updated daily by real-time satellite, atmospheric and meteorological data inputs. The aim of presented work was accuracy enhancement of solar resource data for South Africa, Lesotho and Swaziland. This was achieved by regional adaptation of SolarGIS solar model with data measured at fourteen high-standard solar measuring stations sourced by Eskom, GeoSUN Africa, SAURAN, STERG and Ripasso Energy. The accuracy-enhancement procedure is based on correlation of the ground measurements with the satellite-based SolarGIS model and determination of correction coefficients for model inputs. Use of these coefficients reduced systematic deviation of the input aerosol data, which is key factor determining the model accuracy in Southern Africa. The user uncertainty of the longterm estimate based on adapted data is in the range of ±5% to ±7.5% for DNI, and ±3% to ±4% for GHI. The model now delivers more accurate high-resolution solar resource time series, which helps reducing financial risk and improving engineering quality of the solar power plants. The presented maps show longterm yearly averages of Direct Normal Irradiation (DNI) and Global Horizontal Irradiation (GHI) with 1-km spatial resolution. They are calculated by aggregation of sub-hourly modeled time series, representing a period 1994 to 2013. The maps are accessible from http://www.sauran.net/. High resolution data can be accessed from http://solargis.info.cf201

There is no simple model of the plasma membrane organizationyy

Ever since technologies enabled the characterization of eukaryotic plasma membranes, heterogeneities in the distributions of its constituents were observed. Over the years this led to the proposal of various models describing the plasma membrane organization such as lipid shells, picket-and-fences, lipid rafts, or protein islands, as addressed in numerous publications and reviews. Instead of emphasizing on one model we in this review give a brief overview over current models and highlight how current experimental work in one or the other way do not support the existence of a single overarching model. Instead, we highlight the vast variety of membrane properties and components, their influences and impacts. We believe that highlighting such controversial discoveries will stimulate unbiased research on plasma membrane organization and functionality, leading to a better understanding of this essential cellular structure

Arginine-rich cell-penetrating peptides induce membrane multilamellarity and subsequently enter via formation of a fusion pore

Arginine-rich cell-penetrating peptides do not enter cells by directly passing through a lipid membrane; they instead passively enter vesicles and live cells by inducing membrane multilamellarity and fusion. The molecular picture of this penetration mode, which differs qualitatively from the previously proposed direct mechanism, is provided by molecular dynamics simulations. The kinetics of vesicle agglomeration and fusion by an iconic cell-penetrating peptide-nonaarginine-are documented via real-time fluorescence techniques, while the induction of multilamellar phases in vesicles and live cells is demonstrated by a combination of electron and fluorescence microscopies. This concert of experiments and simulations reveals that the identified passive cell penetration mechanism bears analogy to vesicle fusion induced by calcium ions, indicating that the two processes may share a common mechanistic origin.Peer reviewe

Soluble MHC-peptide complexes induce rapid death of CD8+ CTL.

Soluble MHC-peptide (pMHC) complexes, commonly referred to as tetramers, are widely used to enumerate and to isolate Ag-specific CD8(+) CTL. It has been noted that such complexes, as well as microsphere- or cell-associated pMHC molecules compromise the functional integrity of CTL, e.g., by inducing apoptosis of CTL, which limits their usefulness for T cell sorting or cloning. By testing well-defined soluble pMHC complexes containing linkers of different length and valence, we find that complexes comprising short linkers (i.e., short pMHC-pMHC distances), but not those containing long linkers, induce rapid death of CTL. This cell death relies on CTL activation, the coreceptor CD8 and cytoskeleton integrity, but is not dependent on death receptors (i.e., Fas, TNFR1, and TRAILR2) or caspases. Within minutes of CTL exposure to pMHC complexes, reactive oxygen species emerged and mitochondrial membrane depolarized, which is reminiscent of caspase-independent T cell death. The morphological changes induced during this rapid CTL death are characteristic of programmed necrosis and not apoptosis. Thus, soluble pMHC complexes containing long linkers are recommended to prevent T cell death, whereas those containing short linkers can be used to eliminate Ag-specific CTL

Typical Meteorological Year Data: SolarGIS Approach

AbstractWe analyze factors to be considered when Typical Meteorological Year (TMY) is constructed from a time series data. We discuss characteristics of the input data (time period, time frequency, quality), calculation methods (weighting of parameters, coherence of parameters, selection criteria) and requirements of the resulting TMY to characterize average solar climate (P50 case) or a year with less-favorable solar resource (P90 or Pxx cases). Overview of the existing methods is presented, with summary of their features, limitations and associated risks. SolarGIS method is presented, which overcomes limitations of the older methods. We explain the underlying concept of uncertainty that is used for calculation of annual P90 or Pxx values for Direct Normal Irradiation (DNI) and Global Horizontal Irradiation (GHI). SolarGIS method fulfills the criteria required in solar industry, such as geographical representativeness, consistency of solar radiation and meteorological parameters, and yields a good representation of the P50, P90 or any other Pxx cases

Monoubiquitination and Activity of the Paracaspase MALT1 Requires Glutamate 549 in the Dimerization Interface.

The mucosa-associated lymphoid tissue protein-1 (MALT1, also known as paracaspase) is a protease whose activity is essential for the activation of lymphocytes and the growth of cells derived from human diffuse large B-cell lymphomas of the activated B-cell subtype (ABC DLBCL). Crystallographic approaches have shown that MALT1 can form dimers via its protease domain, but why dimerization is relevant for the biological activity of MALT1 remains largely unknown. Using a molecular modeling approach, we predicted Glu 549 (E549) to be localized within the MALT1 dimer interface and thus potentially relevant. Experimental mutation of this residue into alanine (E549A) led to a complete impairment of MALT1 proteolytic activity. This correlated with an impaired capacity of the mutant to form dimers of the protease domain in vitro, and a reduced capacity to promote NF-κB activation and transcription of the growth-promoting cytokine interleukin-2 in antigen receptor-stimulated lymphocytes. Moreover, this mutant could not rescue the growth of ABC DLBCL cell lines upon MALT1 silencing. Interestingly, the MALT1 mutant E549A was unable to undergo monoubiquitination, which we identified previously as a critical step in MALT1 activation. Collectively, these findings suggest a model in which E549 at the dimerization interface is required for the formation of the enzymatically active, monoubiquitinated form of MALT1

SIRPα polymorphisms, but not the prion protein, control phagocytosis of apoptotic cells

Prnp(-/-) mice lack the prion protein PrP(C) and are resistant to prion infections, but variable phenotypes have been reported in Prnp(-/-) mice and the physiological function of PrP(C) remains poorly understood. Here we examined a cell-autonomous phenotype, inhibition of macrophage phagocytosis of apoptotic cells, previously reported in Prnp(-/-) mice. Using formal genetic, genomic, and immunological analyses, we found that the regulation of phagocytosis previously ascribed to PrP(C) is instead controlled by a linked locus encoding the signal regulatory protein α (Sirpa). These findings indicate that control of phagocytosis was previously misattributed to the prion protein and illustrate the requirement for stringent approaches to eliminate confounding effects of flanking genes in studies modeling human disease in gene-targeted mice. The plethora of seemingly unrelated functions attributed to PrP(C) suggests that additional phenotypes reported in Prnp(-/-) mice may actually relate to Sirpa or other genetic confounders