Local Defects in colloidal quantum dot thin films measured via spatially resolved multi-modal optoelectronic spectroscopy.

The morphology, chemical composition, and electronic uniformity of thin-film solution-processed optoelectronics are believed to greatly affect device performance. Although scanning probe microscopies can address variations on the micrometer scale, the field of view is still limited to well under the typical device area, as well as the size of extrinsic defects introduced during fabrication. Herein, a micrometer-resolution 2D characterization method with millimeter-scale field of view is demonstrated, which simultaneously collects photoluminescence spectra, photocurrent transients, and photovoltage transients. This high-resolution morphology mapping is used to quantify the distribution and strength of the local optoelectronic property variations in colloidal quantum dot solar cells due to film defects, physical damage, and contaminants across nearly the entire test device area, and the extent to which these variations account for overall performance losses. It is found that macroscopic defects have effects that are confined to their localized areas, rarely prove fatal for device performance, and are largely not responsible for device shunting. Moreover, quantitative analysis based on statistical partitioning methods of such data is used to show how defect identification can be automated while identifying variations in underlying properties such as mobilities and recombination strengths and the mechanisms by which they govern device behavior.DMR-1807342 - National Science Foundation; Hopkins Extreme Materials InstituteAccepted manuscrip

Concerted action of the Ubiquitin-Fusion Degradation Protein 1 (Ufd1) and Sumo-Targeted Ubiquitin Ligases (STUbLs) in the DNA-damage response

In eukaryotes many players in the DNA-damage response (DDR) catalyze protein sumoylation or ubiquitylation. Emphasis has been placed on how these modifications orchestrate the sequential recruitment of repair factors to sites of DNA damage or stalled replication forks. Here, we shed light on a pathway in which sumoylated factors are eliminated through the coupled action of Sumo-targeted ubiquitin ligases (STUbLs) and the ubiquitin-fusion degradation protein 1 (Ufd1). Ufd1 is a subunit of the Cdc48-Ufd1-Npl4 complex implicated in the sorting of ubiquitylated substrates for degradation by the proteasome. We find that in fission yeast, Ufd1 interacts physically and functionally with the Sumo-targeted ubiquitin ligase (STUbL) Rfp1, homologous to human RNF4, and with the Sumo E3 ligase Pli1, homologous to human PIAS1. Deleting a C-terminal domain of Ufd1 that mediates the interaction of Ufd1 with Rfp1, Pli1, and Sumo (ufd1ΔCt (213-342)) lead to an accumulation of high-molecular-weight Sumo conjugates and caused severe genomic instabilities. The spectrum of sensitivity of ufd1ΔCt (213-342) cells to genotoxins, the epistatic relationships of ufd1ΔCt (213-342) with mutations in DNA repair factors, and the localization of the repair factor Rad22 in ufd1ΔCt (213-342) cells point to ufd1ΔCt (213-342) cells accumulating aberrant structures during replication that require homologous recombination (HR) for their repair. We present evidence that HR is however often not successful in ufd1ΔCt (213-342) cells and we identify Rad22 as one of the high-molecular-weight conjugates accumulating in the ufd1ΔCt (213-342) mutant consistent with Rad22 being a STUbL/Ufd1 substrate. Suggesting a direct role of Ufd1 in the processing of Sumo-conjugates, Ufd1 formed nuclear foci colocalizing with Sumo during the DDR, and Sumo-conjugates accumulated in foci in the ufd1ΔCt (213-342) mutant. Broader functional relationships between Ufd1 and STUbLs conceivably affect numerous cellular processes beyond the DDR

2-[2-(4-Acetyl­phen­yl)hydrazinyl­idene]-1,3-diphenyl­propane-1,3-dione

In the title compound, C23H18N2O3, the inter­planar angle between the benzoyl units is 80.51 (6)° while the dihedral angles between the hydrazinyl­idene and benzoyl groups are 43.43 (6) and 54.16 (6)°. In the crystal, a strong resonance-assisted intra­molecular N—H⋯O hydrogen bond is observed. The mol­ecules form an inversion dimer via a pair of weak C—H⋯O hydrogen bonds and a π–π inter­action [centroid–centroid distance of 3.5719 (10) Å]. These dimers are linked via weak C—H⋯O contacts, forming chains along the b axis

2-[2-(4-Bromo­phen­yl)hydrazinyl­idene]-1,3-diphenyl­propane-1,3-dione

The conformation of the title mol­ecule, C21H15BrN2O2, is stabilized by a weak intra­molecular C—H⋯N hydrogen bond and a strong resonance-assisted N—H⋯O intra­molecular hydrogen bond. In the crystal, the mol­ecules are linked by weak inter­molecular C—H⋯O inter­actions, forming zigzag chains along the b axis

A second monoclinic polymorph of 2-[2-(4-meth­oxy­phen­yl)hydrazinyl­idene]-1,3-diphenyl­propane-1,3-dione

The title compound, C22H18N2O3 is the second monoclinic polymorph (P21/c) of the compound, the first being reported in space group P21 [Bertolasi et al. (1993 ▶). J. Chem. Soc. Perkin Trans. 2, pp. 2223–2228]. In the mol­ecular structure of the title compound, the inter­planar angle between the benzoyl units is 80.04 (5)°, while the corresponding angles between the phenyl­hydrazinyl­idene and benzoyl groups are 36.11 (5) and 55.77 (2)°. A strong resonance-assisted intra­molecular N—H⋯O hydrogen bond is found. In the crystal, the entire supra­molecular structure is constructed by weak inter­molecular C—H⋯O inter­actions and an inter-ring π–π inter­action [centroid–centroid distance = 3.6088 (8) Å]

A ‘higher order' of telomere regulation: telomere heterochromatin and telomeric RNAs

Protection of chromosome ends from DNA repair and degradation activities is mediated by specialized protein complexes bound to telomere repeats. Recently, it has become apparent that epigenetic regulation of the telomric chromatin template critically impacts on telomere function and telomere-length homeostasis from yeast to man. Across all species, telomeric repeats as well as the adjacent subtelomeric regions carry features of repressive chromatin. Disruption of this silent chromatin environment results in loss of telomere-length control and increased telomere recombination. In turn, progressive telomere loss reduces chromatin compaction at telomeric and subtelomeric domains. The recent discoveries of telomere chromatin regulation during early mammalian development, as well as during nuclear reprogramming, further highlights a central role of telomere chromatin changes in ontogenesis. In addition, telomeres were recently shown to generate long, non-coding RNAs that remain associated to telomeric chromatin and will provide new insights into the regulation of telomere length and telomere chromatin. In this review, we will discuss the epigenetic regulation of telomeres across species, with special emphasis on mammalian telomeres. We will also discuss the links between epigenetic alterations at mammalian telomeres and telomere-associated diseases

(E)-3,5-Dimethyl-1-p-tolyl-4-(p-tolyl­diazen­yl)-1H-pyrazole

There are two independent mol­ecules, A and B, in the asymmetric unit of the title compound, C19H20N4, in each of which the N=N double bond has an E conformation. The dihedral angles between the pyrazole ring and the p-tolyl rings in the 1- and 4-positions are 22.54 (8) and 35.73 (7)°, respectively, in mol­ecule A. The corresponding dihedral angles in mol­ecule B are 28.13 (8) and 22.18 (8)°. In the crystal, the A and B mol­ecules are linked by weak C—H⋯π inter­actions, leading to inversion dimers in each case

In Vitro Megakaryocyte Differentiation and Proplatelet Formation in Ph-Negative Classical Myeloproliferative Neoplasms: Distinct Patterns in the Different Clinical Phenotypes

Background: Ph-negative myeloproliferative neoplasms (MPNs) are clonal disorders that include primary myelofibrosis (PMF), polycythemia vera (PV) and essential thrombocythemia (ET). Although the pathogenesis of MPNs is still incompletely understood, an involvement of the megakaryocyte lineage is a distinctive feature. Methodology/Principal Findings: We analyzed the in vitro megakaryocyte differentiation and proplatelet formation in 30 PMF, 8 ET, 8 PV patients, and 17 healthy controls (CTRL). Megakaryocytes were differentiated from peripheral blood CD34+ or CD45+ cells in the presence of thrombopoietin. Megakaryocyte output was higher in MPN patients than in CTRL with no correlation with the JAK2 V617F mutation. PMF-derived megakaryocytes displayed nuclei with a bulbous appearance, were smaller than ET- or PV-derived megakaryocytes and formed proplatelets that presented several structural alterations. In contrast, ET- and PV-derived megakaryocytes produced more proplatelets with a striking increase in bifurcations and tips compared to both control and PMF. Proplatelets formation was correlated with platelet counts in patient peripheral blood. Patients with pre-fibrotic PMF had a pattern of megakaryocyte proliferation and proplatelet formation that was similar to that of fibrotic PMF and different from that of ET. Conclusions/Significance: In conclusion, MPNs are associated with high megakaryocyte proliferative potential. Profound differences in megakaryocyte morphology and proplatelet formation distinguish PMF, both fibrotic and prefibrotic, from ET and PV

Controlo químico de infestantes

Uma planta é considerada infestante quando nasce espontaneamente num local e momento indesejados, podendo interferir negativamente com a cultura instalada. As infestantes competem com as culturas para o espaço, a luz, água e nutrientes, podendo atrasar e prejudicar as operações de colheita, depreciar o produto final e assegurarem a reinfestação nas culturas seguintes. Dado o modo de propagação diferenciado das diversas espécies de infestantes, com as anuais a propagarem-se por semente e as perenes ou vivazes a assegurarem a sua propagação através de órgãos vegetativos (rizomas, bolbos, tubérculos, etc.), assim, também o seu controlo quer químico, quer mecânico terá que ser diferenciado, ou seja, para controlar infestantes anuais será suficiente destruir a sua parte aérea, enquanto para controlar infestantes perenes teremos que destruir os seus órgãos reprodutivos. O controlo de infestantes poderá ser químico, através da utilização de herbicidas, ou mecânico pela utilização de alfaias agrícolas, tais como a charrua de aivecas, a charrua de discos, a grade de discos, o escarificador e a fresa. Quando a técnica utilizada na instalação das culturas é a sementeira directa, o controlo das infestantes terá que ser obrigatoriamente químico, enquanto se o recurso à mobilização do solo for a técnica mais utilizada (sistema de mobilização tradicional ou sistema de mobilização reduzida), o controlo das infestantes tanto poderá ser químico como mecânico. Neste trabalho iremos abordar apenas, o controlo químico de infestantes