203 research outputs found
Charge density dependent nongeminate recombination in organic bulk heterojunction solar cells
Apparent recombination orders exceeding the value of two expected for
bimolecular recombination have been reported for organic solar cells in various
publications. Two prominent explanations are bimolecular losses with a carrier
concentration dependent prefactor due to a trapping limited mobility, and
protection of trapped charge carriers from recombination by a donor--acceptor
phase separation until reemission from these deep states. In order to clarify
which mechanism is dominant we performed temperature and illumination dependent
charge extraction measurements under open circuit as well as short circuit
conditions at poly(3-hexylthiophene-2,5-diyl):[6,6]-phenyl-Cbutyric acid
methyl ester (P3HT:PCBM) and PTB7:PCBM
(Poly[[4,8-bis[(2-ethylhexyl)oxy]benzo[1,2-b:4,5-b']dithiophene-2,6-diyl][3-fluoro-2-[(2-ethylhexyl)carbonyl]thieno[3,4-b]thiophenediyl]])
solar cells in combination with current--voltage characteristics. We show that
the charge carrier density dependence of the mobility and the
recombination prefactor are different for PCBM at temperatures below
300K and PTB7:PCBM at room temperature. Therefore, in addition to
a detrapping limited recombination in systems with at least partial
donor--acceptor phase separation is required to explain the high recombination
orders.Comment: 7 pages, 4 figure
Trap Distribution and the Impact of Oxygen-induced Traps on the Charge Transport in Poly(3-Hexylthiophene)
The trap distribution in the conjugated polymer poly(3-hexylthiophene) was
investigated by fractional thermally stimulated current measurements. Two
defect states with activation energies of about 50 meV and 105 meV and Gaussian
energy distributions were revealed. The first is assigned to the tail of the
intrinsic density of states, whereas the concentration of second trap is
directly related to oxygen exposure. The impact of the oxygen induced traps on
the charge transport was examined by performing photo-induced charge carrier
extraction by linearly increasing voltage measurements, that exhibited a strong
decrease in the mobility with air exposure time.Comment: 4 pages, 3 figures, 2 table
Reversible and Irreversible Interactions of Poly(3-hexylthiophene) with Oxygen Studied by Spin-Sensitive Methods
Understanding of degradation mechanisms in polymer:fullerene
bulk-heterojunctions on the microscopic level aimed at improving their
intrinsic stability is crucial for the breakthrough of organic photovoltaics.
These materials are vulnerable to exposure to light and/or oxygen, hence they
involve electronic excitations. To unambiguously probe the excited states of
various multiplicities and their reactions with oxygen, we applied combined
magneto-optical methods based on multifrequency (9 and 275 GHz) electron
paramagnetic resonance (EPR), photoluminescence (PL), and PL-detected magnetic
resonance (PLDMR) to the conjugated polymer poly(3-hexylthiophene) (P3HT) and
polymer:fullerene bulk heterojunctions (P3HT:PCBM; PCBM =
[6,6]-phenyl-C61-butyric acid methyl ester). We identified two distinct
photochemical reaction routes, one being fully reversible and related to the
formation of polymer:oxygen charge transfer complexes, the other one,
irreversible, being related to the formation of singlet oxygen under
participation of bound triplet excitons on the polymer chain. With respect to
the blends, we discuss the protective effect of the methanofullerenes on the
conjugated polymer bypassing the triplet exciton generation
Kinetics of occupancy of defect states in poly(3-hexylthiophene): fullerene solar cells
Energetics and kinetics of defects in the effective band gap of organic bulk heterojunctions are determined by means of capacitance methods. The technique consists of calculating the junction capacitance derivative with respect to the angular frequency of the small voltage perturbation applied to thin film poly(3-hexylthiophene) (P3HT) and [6,6]-phenyl C61-butyric acid methyl ester solar cells, varying the temperature. The analysis reveals the presence of defect bands (shallow acceptors) centered at E0 = 35 meV above the highest-occupied molecular orbital level of P3HT. The total density of defects results of order 1016 cm− 3. Characteristic frequency is obtained to be situated within the range of 1–10 Hz. Defect bands acting as negatively charged levels are responsible for the p-doping of the active layer and the band-bending near the cathode contact, as derived from Mott–Schottky capacitance–voltage analysis
Variants of GCKR Affect Both β-Cell and Kidney Function in Patients With Newly Diagnosed Type 2 Diabetes: The Verona Newly Diagnosed Type 2 Diabetes Study 2
In genome-wide association studies, performed mostly in nondiabetic individuals, genetic variability of glucokinase regulatory protein (GCKR) affects type 2 diabetes-relatedphenotypes, kidney function, and risk of chronic kidney disease (CKD). We tested whether GCKR variability affects type 2 diabetes or kidney-related phenotypes in newly diagnosed type 2diabetes. In 509 GAD-negative patients with newly diagnosedtype 2 diabetes,we 1) genotyped six single nucleotide polymorphisms in GCKR genomic region: rs6717980, rs1049817, rs6547626, rs780094, rs2384628, and rs8731; 2) assessedclinical phenotypes, insulin sensitivity by the euglycemic insulin clamp, and b-cell function by state-of-the-art modeling of glucose/C-peptide curves during an oral glucose tolerance test;and 3) estimated glomerular filtration rate (eGFR) by the Modification of Diet in Renal Disease formula.The major alleles of rs6717980 and rs2384628 were associated with reduced b-cell function (P<0.05), with mutual additive effects of each variant (P<0.01). The minoralleles of rs1049817 and rs6547626 and the major allele of rs780094 were associated withreduced eGFR according to a recessive model (P<0.03), but with no mutual additive effects of the variants. Additional associations were found between rs780094 and 2-h plasma glucose(P<0.05) and rs8731 and insulin sensitivity (P<0.05) and triglycerides (P<0.05). Our findings are compatible with the idea that GCKR variability may play a pathogenetic role in both type 2 diabetes and CKD. Genotyping GCKR in patients withnewly diagnosed type 2 diabetes might help in identifying patients at high risk for metabolic derangements or CKD
SARS-CoV-2 structural coverage map reveals viral protein assembly, mimicry, and hijacking mechanisms
We modeled 3D structures of all SARS-CoV-2 proteins, generating 2,060 models that span 69% of the viral proteome and provide details not available elsewhere. We found that ˜6% of the proteome mimicked human proteins, while ˜7% was implicated in hijacking mechanisms that reverse post-translational modifications, block host translation, and disable host defenses; a further ˜29% self-assembled into heteromeric states that provided insight into how the viral replication and translation complex forms. To make these 3D models more accessible, we devised a structural coverage map, a novel visualization method to show what is-and is not-known about the 3D structure of the viral proteome. We integrated the coverage map into an accompanying online resource (https://aquaria.ws/covid) that can be used to find and explore models corresponding to the 79 structural states identified in this work. The resulting Aquaria-COVID resource helps scientists use emerging structural data to understand the mechanisms underlying coronavirus infection and draws attention to the 31% of the viral proteome that remains structurally unknown or dark
Charge Trapping in Mixed Organic Donor–Acceptor Semiconductor Thin Films
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109598/1/adma201403198.pd
SARS-CoV-2 structural coverage map reveals viral protein assembly, mimicry, and hijacking mechanisms
Abstract We modeled 3D structures of all SARS‐CoV‐2 proteins, generating 2,060 models that span 69% of the viral proteome and provide details not available elsewhere. We found that ˜6% of the proteome mimicked human proteins, while ˜7% was implicated in hijacking mechanisms that reverse post‐translational modifications, block host translation, and disable host defenses; a further ˜29% self‐assembled into heteromeric states that provided insight into how the viral replication and translation complex forms. To make these 3D models more accessible, we devised a structural coverage map, a novel visualization method to show what is—and is not—known about the 3D structure of the viral proteome. We integrated the coverage map into an accompanying online resource (https://aquaria.ws/covid) that can be used to find and explore models corresponding to the 79 structural states identified in this work. The resulting Aquaria‐COVID resource helps scientists use emerging structural data to understand the mechanisms underlying coronavirus infection and draws attention to the 31% of the viral proteome that remains structurally unknown or dark
DDRprot: a database of DNA damage response-related proteins
The DNA Damage Response (DDR) signalling network is an essential system that protects the genome’s integrity. The DDRprot database presented here is a resource that integrates manually curated information on the human DDR network and its sub-pathways. For each particular DDR protein, we present detailed information about its function. If involved in post-translational modifications (PTMs) with each other, we depict the position of the modified residue/s in the three-dimensional structures, when resolved structures are available for the proteins. All this information is linked to the original publication from where it was obtained. Phylogenetic information is also shown, including time of emergence and conservation across 47 selected species, family trees and sequence alignments of homologues. The DDRprot database can be queried by different criteria: pathways, species, evolutionary age or involvement in (PTM). Sequence searches using hidden Markov models can be also used.E.A.-L. was supported by the European Commission grant [FP7-REGPOT-2012-2013-1; A.A. was partially supported by the Spanish Ministry of Science and Innovation grant [PS09/02111].Peer reviewe
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