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Atomic‐Layer‐Deposited Aluminum and Zirconium Oxides for Surface Passivation of TiO2 in High‐Efficiency Organic Photovoltaics
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Maria Vasilopoulou Dimitra G. Georgiadou Anastasia Soultati Nikos Boukos Spyros Gardelis Leonidas C. Palilis Mihalis Fakis Georgios Skoulatakis Stella Kennou Martha Botzakaki Stavroula Georga Christoforos A. Krontiras Florian Auras Dina Fattakhova‐Rohlfing Thomas Bein Theodoros A. Papadopoulos Dimitrios Davazoglou Panagiotis Argitis 《Liver Transplantation》2014,4(15)
The reduction in electronic recombination losses by the passivation of surfaces is a key factor enabling high‐efficiency solar cells. Here a strategy to passivate surface trap states of TiO2 films used as cathode interlayers in organic photovoltaics (OPVs) through applying alumina (Al2O3) or zirconia (ZrO2) insulating nanolayers by thermal atomic layer deposition (ALD) is investigated. The results suggest that the surface traps in TiO2 are oxygen vacancies, which cause undesirable recombination and high electron extraction barrier, reducing the open‐circuit voltage and the short‐circuit current of the complete OPV device. It is found that the ALD metal oxides enable excellent passivation of the TiO2 surface followed by a downward shift of the conduction band minimum. OPV devices based on different photoactive layers and using the passivated TiO2 electron extraction layers exhibit a significant enhancement of more than 30% in their power conversion efficiencies compared to their reference devices without the insulating metal oxide nanolayers. This is a result of significant suppression of charge recombination and enhanced electron extraction rates at the TiO2/ALD metal oxide/organic interface. 相似文献
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Mrkonjic M Roslin NM Greenwood CM Raptis S Pollett A Laird PW Pethe VV Chiang T Daftary D Dicks E Thibodeau SN Gallinger S Parfrey PS Younghusband HB Potter JD Hudson TJ McLaughlin JR Green RC Zanke BW Newcomb PA Paterson AD Bapat B 《PloS one》2010,5(10):e13314
Background
We previously identified an association between a mismatch repair gene, MLH1, promoter SNP (rs1800734) and microsatellite unstable (MSI-H) colorectal cancers (CRCs) in two samples. The current study expanded on this finding as we explored the genetic basis of DNA methylation in this region of chromosome 3. We hypothesized that specific polymorphisms in the MLH1 gene region predispose it to DNA methylation, resulting in the loss of MLH1 gene expression, mismatch-repair function, and consequently to genome-wide microsatellite instability.Methodology/Principal Findings
We first tested our hypothesis in one sample from Ontario (901 cases, 1,097 controls) and replicated major findings in two additional samples from Newfoundland and Labrador (479 cases, 336 controls) and from Seattle (591 cases, 629 controls). Logistic regression was used to test for association between SNPs in the region of MLH1 and CRC, MSI-H CRC, MLH1 gene expression in CRC, and DNA methylation in CRC. The association between rs1800734 and MSI-H CRCs, previously reported in Ontario and Newfoundland, was replicated in the Seattle sample. Two additional SNPs, in strong linkage disequilibrium with rs1800734, showed strong associations with MLH1 promoter methylation, loss of MLH1 protein, and MSI-H CRC in all three samples. The logistic regression model of MSI-H CRC that included MLH1-promoter-methylation status and MLH1 immunohisotchemistry status fit most parsimoniously in all three samples combined. When rs1800734 was added to this model, its effect was not statistically significant (P-value = 0.72 vs. 2.3×10−4 when the SNP was examined alone).Conclusions/Significance
The observed association of rs1800734 with MSI-H CRC occurs through its effect on the MLH1 promoter methylation, MLH1 IHC deficiency, or both. 相似文献54.
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Cajal-Retzius (CR) cells, the predominant source of reelin in developing neocortex, are thought to be essential for the inside out formation of neocortical layers. Fate mapping revealed that a large population of neocortical CR cells arises from the cortical hem. To investigate the function of CR cells, we therefore genetically ablated the hem. Neocortical CR cells were distributed beneath the pial surface in control mice, but were virtually absent in hem-ablated mice from embryonic day (E) 10.5 until birth. CR cells derived from other sources did not invade the neocortical primordium to compensate for hem loss. We predicted that neocortical layers would be inverted in hem-ablated animals, as in reeler mice, deficient in reelin signaling. Against expectation, layers showed the standard order. Low levels of reelin in the cortical primordium, or diffusion of reelin from other sites, may have allowed lamination to proceed. Our findings indicate, however, that the sheet of reelin-rich CR cells that covers the neocortical primordium is not required to direct layer order. 相似文献
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Stavroula K. Hatzios Michael W. Schelle Cynthia M. Holsclaw Christopher R. Behrens Zsofia Botyanszki Fiona L. Lin Brian L. Carlson Pawan Kumar Julie A. Leary Carolyn R. Bertozzi 《The Journal of biological chemistry》2009,284(19):12745-12751
Mycobacterium tuberculosis possesses an unusual cell wall that is
replete with virulence-enhancing lipids. One cell wall molecule unique to
pathogenic M. tuberculosis is polyacyltrehalose (PAT), a
pentaacylated, trehalose-based glycolipid. Little is known about the
biosynthesis of PAT, although its biosynthetic gene cluster has been
identified and found to resemble that of the better studied M.
tuberculosis cell wall component sulfolipid-1. In this study, we sought
to elucidate the function of papA3, a gene from the PAT locus
encoding a putative acyltransferase. To determine whether PapA3 participates
in PAT assembly, we expressed the protein heterologously and evaluated its
acyltransferase activity in vitro. The purified enzyme catalyzed the
sequential esterification of trehalose with two palmitoyl groups, generating a
diacylated product similar to the 2,3-diacyltrehalose glycolipids of M.
tuberculosis. Notably, PapA3 was selective for trehalose; no activity was
observed with other structurally related disaccharides. Disruption of the
papA3 gene from M. tuberculosis resulted in the loss of PAT
from bacterial lipid extracts. Complementation of the mutant strain restored
PAT production, demonstrating that PapA3 is essential for the biosynthesis of
this glycolipid in vivo. Furthermore, we determined that the PAT
biosynthetic machinery has no cross-talk with that for sulfolipid-1 despite
their related structures.Mycobacterium tuberculosis, the bacterium that causes tuberculosis
in humans, has a complex cell wall that contains a number of unique
glycolipids intimately linked to mycobacterial pathogenesis
(1,
2). The biosynthesis of many of
these virulence factors, including the trehalose mycolates, phenolic
glycolipids, and sulfolipid-1
(SL-1),3 is largely
understood
(3–5).
In contrast, relatively little is known about the biosynthesis of other
prominent M. tuberculosis glycolipids, such as di-, tri-, and
polyacyltrehaloses. These acyltrehaloses are located in the outer surface of
the cell wall and contain di- and tri-methyl branched fatty acids that are
only found in pathogenic species of mycobacteria
(6,
7). Previous studies suggest a
role for these glycolipids in anchoring the bacterial capsule, which impedes
phagocytosis by host cells
(6).The major polyacyltrehalose (PAT) of M. tuberculosis, also
referred to as pentaacyl or polyphthienoyl trehalose, consists of five acyl
chains, four mycolipenic (phthienoic) acids and one fully saturated fatty
acid, linked to trehalose (Fig.
1A) (8).
The mycolipenic acid side chains of PAT are products of the polyketide
synthase gene pks3/4
(7). Disruption of
pks3/4 (also referred to as msl3
(7)) abolishes PAT biosynthesis
and causes cell aggregation. At present, the remaining proteins required for
PAT assembly have not been characterized.Open in a separate windowFIGURE 1.PAT and SL-1 share related structures and biosynthetic gene
clusters. A, structure of PAT. B, structure of SL-1.
C, genomic arrangement of the PAT and SL-1 biosynthetic gene
clusters.Interestingly, the PAT biosynthetic gene cluster strongly resembles that of
SL-1, which is a structurally similar trehalose-based glycolipid unique to
pathogenic mycobacteria (Fig.
1B) (9).
Both gene clusters contain polyketide synthase (pks), acyltransferase
(pap), and lipid transport (mmpL) genes in a similar genomic
arrangement (Fig. 1C).
The SL-1 locus encodes two acyltransferase genes, papA1 and
papA2, which are required for SL-1 biosynthesis
(5,
10). These proteins belong to
the mycobacterium-specific polyketide-associated protein (Pap) family of
acyltransferases, which share a conserved
HX3DX14Y motif that is required for
activity (11). The PapA2
enzyme catalyzes the esterification of the 2′-position of trehalose
2-sulfate with a saturated fatty acid. PapA1 mediates the subsequent
esterification of this intermediate with a hydroxyphthioceranoyl group
produced by Pks2 (5).
Interestingly, the PAT locus contains a gene, Rv1182, that is
homologous to both papA1 and papA2 (55 and 53% amino acid
identity, respectively). This gene is annotated as papA3 in the
genome and was previously shown to encode a protein bearing the signature Pap
motif (11).Here we demonstrate that papA3 encodes an acyltransferase
essential for the biosynthesis of PAT. Deletion of the papA3 gene
resulted in loss of the glycolipid from M. tuberculosis lipid
extracts, as determined by high resolution mass spectrometry. Moreover, the
purified enzyme was shown to selectively and sequentially acylate trehalose
in vitro, generating a diacylated product similar to the
2,3-diacyltrehaloses of M. tuberculosis. Together, these data confirm
that PapA3 plays a crucial role in PAT biosynthesis and highlight its
potential involvement in the biosynthesis of related M. tuberculosis
acyltrehaloses. 相似文献
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Dominique Ziech Rodrigo Franco Alexandros G. Georgakilas Stavroula Georgakila Vasiliki Malamou-Mitsi Onard Schoneveld Aglaia Pappa Mihalis I. Panayiotidis 《Chemico-biological interactions》2010,188(2):334-339
Although we have greatly benefited from the use of traditional epidemiological approaches in linking environmental exposure to human disease, we are still lacking knowledge in to how such exposure participates in disease development. However, molecular epidemiological studies have provided us with evidence linking oxidative stress with the pathogenesis of human disease and in particular carcinogenesis. To this end, oxidative stress-based biomarkers have proved to be essential in revealing how oxidative stress may be mediating toxicity induced by many known carcinogenic environmental agents. Therefore, throughout this review article, we aim to address the current state of oxidative stress-based biomarker development with major emphasis pertaining to biomarkers of DNA, lipid and protein oxidation. 相似文献
59.
Aristeidis Parmakelis Panayiota Kotsakiozi Iasmi Stathi Stavroula Poulikarakou Victor Fet 《Biological journal of the Linnean Society. Linnean Society of London》2013,110(4):728-748
Phylogenetic analysis of the genus Euscorpius (Scorpiones: Euscorpiidae) across the Mediterranean region (86 specimens, 77 localities, four DNA markers: 16S rDNA, COI, COII, and ITS1), focusing on Greek fauna, revealed high variation, deep clade divergences, many cryptic lineages, paraphyly at subgenus level, and sympatry of several new and formerly known lineages. Numerous specimens from mainland and insular Greece, undoubtedly the least studied region of the genus' distribution, have been included. The reconstructed phylogeny covers representative taxa and populations across the entire genus of Euscorpius. The deepest clades detected within Euscorpius correspond (partially) to its current subgeneric division, outlining subgenera Tetratrichobothrius and Alpiscorpius. The rest of the genus falls into several clades, including subgenus Polytrichobothrius and a paraphyletic subgenus Euscorpius s.s. Several cryptic lineages are recovered, especially on the islands. The inadequacy of the morphological characters used in the taxonomy of the genus to delineate species is discussed. Finally, the time frame of differentiation of Euscorpius in the study region is estimated and the distributional patterns of the lineages are contrasted with those of other highly diversified invertebrate genera occurring in the study region. © 2013 The Linnean Society of London, Biological Journal of the Linnean Society, 2013, 110 , 728–748. 相似文献
60.
Stavroula Balomenou Agnes Fouet Mary Tzanodaskalaki Evelyne Couture‐Tosi Ivo G. Boneca 《Molecular microbiology》2013,87(4):867-883
Peptidoglycan deacetylases (PGNG‐dacs) belong to the Carbohydrate Esterase Family 4 (CE4) and have been described as required for bacterial evasion to lysozyme and innate immune responses. Interestingly, there is an unusual occurrence of 10 putative polysaccharide deacetylases, including five PGNG‐dacs, in the Bacillus sp. genomes, especially B. cereus and B. anthracis. To elucidate the physiological role of these multiple deacetylases, we employed genetic analysis and protein localization studies of five putative PGNG‐dacs from B. anthracis as well as biochemical analysis of their corresponding homologues from B. cereus. Our data confirm that three enzymes are PGNG‐dacs. While BA1977, associated with lateral peptidoglycan synthesis, is a bona fide peptidoglycan deacetylase involved in resistance to host lysozyme and required for full virulence, BA1961 and BA3679 participate in the biogenesis of the peptidoglycan during both elongation and cell division. Furthermore, two enzymes are important for neutral polysaccharide attachment to PG and consequently anchoring of S‐layer proteins (BA5436) and for polysaccharide modification (BA2944). Our results provide novel and fundamental insights into the function of polysaccharide deacetylases in a major bioterrorism agent. 相似文献