593 research outputs found

    Decay dynamics of excitonic polarons in InAs/GaAs quantum dots

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    This article may be downloaded for personal use only. Any other use requires prior permission of the author and AIP Publishing. This article appeared in Journal of Applied Physics 110, 074303 (2011) and may be found at https://doi.org/10.1063/1.3639310.We present time-resolved studies of the exciton-phonon interaction in self-assembled InAs/GaAs quantum dots. Different scattering and luminescence processes were investigated by time-resolved spectroscopy exciting resonantly into the quantum dot’s electronic structure. By studying the characteristic decay times of the ground state and of several phonon-assisted recombinations we were able to distinguish a resonant Raman process from a phonon-assisted photoluminescence process which are always simultaneously present and can interfere with each other. While lifetimes under 30 ps were observed for the coherent Raman process, the incoherent phonon-assisted recombination exhibited typical lifetimes of around 1 ns independently of the excitation energy. We conclude that under resonant excitation the dominant radiative recombination process in this system always involves an electronic state of the ground state of the quantum dot’s electronic structure. Combining temperature-dependent and time-resolved measurements we show that a weak phonon-bottleneck is present in the low temperature regime (< 130 K), while it disappears for higher temperatures.DFG, 43659573, SFB 787: Halbleiter - Nanophotonik: Materialien, Modelle, BauelementeDFG, 53182490, EXC 314: Unifying Concepts in Catalysi

    Anaerobic methanotrophic communities thrive in deep submarine permafrost

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    Thawing submarine permafrost is a source of methane to the subsurface biosphere. Methane oxidation in submarine permafrost sediments has been proposed, but the responsible microorganisms remain uncharacterized. We analyzed archaeal communities and identified distinct anaerobic methanotrophic assemblages of marine and terrestrial origin (ANME-2a/b, ANME-2d) both in frozen and completely thawed submarine permafrost sediments. Besides archaea potentially involved in anaerobic oxidation of methane (AOM) we found a large diversity of archaea mainly belonging to Bathyarchaeota, Thaumarchaeota, and Euryarchaeota. Methane concentrations and δ13C-methane signatures distinguish horizons of potential AOM coupled either to sulfate reduction in a sulfate-methane transition zone (SMTZ) or to the reduction of other electron acceptors, such as iron, manganese or nitrate. Analysis of functional marker genes (mcrA) and fluorescence in situ hybridization (FISH) corroborate potential activity of AOM communities in submarine permafrost sediments at low temperatures. Modeled potential AOM consumes 72–100% of submarine permafrost methane and up to 1.2 Tg of carbon per year for the total expected area of submarine permafrost. This is comparable with AOM habitats such as cold seeps. We thus propose that AOM is active where submarine permafrost thaws, which should be included in global methane budgets

    The left frontal cortex supports reserve in aging by enhancing functional network efficiency

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    Background: Recent evidence from fMRI studies suggests that functional hubs, i.e. highly connected brain regions, are important for mental health. We found recently that global connectivity of a hub in the left frontal cortex (LFC-connectivity) is associated with relatively preserved memory abilities and higher levels of protective factors (education, IQ) in normal aging and Alzheimer’s disease. These results suggest that LFC-connectivity supports reserve capacity alleviating memory decline. An open question is, however, why LFC-connectivity is beneficial and supports memory function in the face of neurodegeneration. We hypothesized that higher LFCconnectivity is associated with enhanced efficiency in connected major networks involved in episodic memory. We further hypothesized that higher LFC-related network efficiency predicts higher memory abilities. Methods: We assessed fMRI during a face-name association learning task in 26 healthy cognitively normal elderly participants. Using beta-series correlation analysis, we computed task-related LFC-connectivity to key memory networks including the default-mode network (DMN) and dorsal attention network (DAN). Network efficiency within the DMN and DAN was estimated by the graph theoretical small-worldness statistic. We applied linear regression analyses in order to test the association between LFC-connectivity to the DMN/DAN and small-worldness of these networks. Mediation analysis was applied to test LFC-connectivity to the DMN and DAN as a mediator of the association between education and higher DMN and DAN smallworldness. Lastly, we tested network small-worldness as a predictor of memory performance. Results: We found that higher LFC-connectivity to the DMN and DAN during successful memory encoding and recognition was associated with higher small-worldness of those networks. Higher task-related LFC-connectivity mediated the association between education and higher small-worldness in the DMN and DAN. Further, higher small-worldness of these networks predicted better performance in the memory task. Conclusions: The current results suggest that higher education-related LFC-connectivity to key memory networks during a memory task is associated with higher network efficiency and thus enhanced reserve of memory abilities in aging

    Keratinocyte-derived S100A9 modulates neutrophil infiltration and affects psoriasis-like skin and joint disease

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    [Objectives]: S100A9, an alarmin that can form calprotectin (CP) heterodimers with S100A8, is mainly produced by keratinocytes and innate immune cells. The contribution of keratinocyte-derived S100A9 to psoriasis (Ps) and psoriatic arthritis (PsA) was evaluated using mouse models, and the potential usefulness of S100A9 as a Ps/PsA biomarker was assessed in patient samples. [Methods]: Conditional S100A9 mice were crossed with DKO* mice, an established psoriasis-like mouse model based on inducible epidermal deletion of c-Jun and JunB to achieve additional epidermal deletion of S100A9 (TKO* mice). Psoriatic skin and joint disease were evaluated in DKO* and TKO* by histology, microCT, RNA and proteomic analyses. Furthermore, S100A9 expression was analysed in skin, serum and synovial fluid samples of patients with Ps and PsA. [Results]: Compared with DKO* littermates, TKO* mice displayed enhanced skin disease severity, PsA incidence and neutrophil infiltration. Altered epidermal expression of selective pro-inflammatory genes and pathways, increased epidermal phosphorylation of STAT3 and higher circulating TNFα were observed in TKO* mice. In humans, synovial S100A9 levels were higher than the respective serum levels. Importantly, patients with PsA had significantly higher serum concentrations of S100A9, CP, VEGF, IL-6 and TNFα compared with patients with only Ps, but only S100A9 and CP could efficiently discriminate healthy individuals, patients with Ps and patients with PsA. [Conclusions]: Keratinocyte-derived S100A9 plays a regulatory role in psoriatic skin and joint disease. In humans, S100A9/CP is a promising marker that could help in identifying patients with Ps at risk of developing PsA.The Wagner laboratory at the Medical University of Vienna (MUV) is supported by an ERC‐AdG 2016 CSI‐Fun‐741888, a H2020‐MSCA‐ITN 2019‐859860‐CANCERPREV grant and the MUV. GS and AR are supported by the Deutsche Forschungsgemeinschaft (DFG-FOR2886 PANDORA and the CRC1181 Checkpoints for Resolution of Inflammation). Additional funding was received by the Bundesministerium für Bildung und Forschung (BMBF; project MASCARA), the ERC-SyG 2018 (810316 4D Nanoscope), ERC-STG 2019 (853508 BARRIER BREAK) and the IMI-funded project Hippocrates. The Oxford Laboratory at the Biomolecular Research Centre at Boise State University was supported by the National Institutes of Health, NIGMS P20GM109095 and P20GM103408

    Impaired protein translation in Drosophila models for Charcot–Marie–Tooth neuropathy caused by mutant tRNA synthetases

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    Dominant mutations in five tRNA synthetases cause Charcot–Marie–Tooth (CMT) neuropathy, suggesting that altered aminoacylation function underlies the disease. However, previous studies showed that loss of aminoacylation activity is not required to cause CMT. Here we present a Drosophila model for CMT with mutations in glycyl-tRNA synthetase (GARS). Expression of three CMT-mutant GARS proteins induces defects in motor performance and motor and sensory neuron morphology, and shortens lifespan. Mutant GARS proteins display normal subcellular localization but markedly reduce global protein synthesis in motor and sensory neurons, or when ubiquitously expressed in adults, as revealed by FUNCAT and BONCAT. Translational slowdown is not attributable to altered tRNA[superscript Gly] aminoacylation, and cannot be rescued by Drosophila Gars overexpression, indicating a gain-of-toxic-function mechanism. Expression of CMT-mutant tyrosyl-tRNA synthetase also impairs translation, suggesting a common pathogenic mechanism. Finally, genetic reduction of translation is sufficient to induce CMT-like phenotypes, indicating a causal contribution of translational slowdown to CMT.National Institutes of Health (U.S.) (Grant GM17151

    Microbial community composition and abundance after millennia of submarine permafrost warming

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    Warming of the Arctic led to an increase in permafrost temperatures by about 0.3 �C during the last decade. Permafrost warming is associated with increasing sediment water content, permeability, and diffusivity and could in the long term alter microbial community composition and abundance even before permafrost thaws. We studied the long-term effect (up to 2500 years) of submarine permafrost warming on microbial communities along an onshore–offshore transect on the Siberian Arctic Shelf displaying a natural temperature gradient of more than 10 �C. We analysed the in situ development of bacterial abundance and community composition through total cell counts (TCCs), quantitative PCR of bacterial gene abundance, and amplicon sequencing and correlated the microbial community data with temperature, pore water chemistry, and sediment physicochemical parameters. On timescales of centuries, permafrost warming coincided with an overall decreasing microbial abundance, whereas millennia after warming microbial abundance was similar to cold onshore permafrost. In addition, the dissolved organic carbon content of all cores was lowest in submarine permafrost after millennial-scale warming. Based on correlation analysis, TCC, unlike bacterial gene abundance, showed a significant rank-based negative correlation with increasing temperature, while bacterial gene copy numbers showed a strong negative correlation with salinity. Bacterial community composition correlated only weakly with temperature but strongly with the pore water stable isotopes �18O and �D, as well as with depth. The bacterial community showed substantial spatial variation and an overall dominance of Actinobacteria, Chloroflexi, Firmicutes, Gemmatimonadetes, and Proteobacteria, which are amongst the microbial taxa that were also found to be active in other frozen permafrost environments. We suggest that, millennia after permafrost warming by over 10 �C, microbial community composition and abundance show some indications for proliferation but mainly reflect the sedimentation history and paleoenvironment and not a direct effect through warming

    Evaluation of the current knowledge limitations in breast cancer research: a gap analysis

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    BACKGROUND A gap analysis was conducted to determine which areas of breast cancer research, if targeted by researchers and funding bodies, could produce the greatest impact on patients. METHODS Fifty-six Breast Cancer Campaign grant holders and prominent UK breast cancer researchers participated in a gap analysis of current breast cancer research. Before, during and following the meeting, groups in seven key research areas participated in cycles of presentation, literature review and discussion. Summary papers were prepared by each group and collated into this position paper highlighting the research gaps, with recommendations for action. RESULTS Gaps were identified in all seven themes. General barriers to progress were lack of financial and practical resources, and poor collaboration between disciplines. Critical gaps in each theme included: (1) genetics (knowledge of genetic changes, their effects and interactions); (2) initiation of breast cancer (how developmental signalling pathways cause ductal elongation and branching at the cellular level and influence stem cell dynamics, and how their disruption initiates tumour formation); (3) progression of breast cancer (deciphering the intracellular and extracellular regulators of early progression, tumour growth, angiogenesis and metastasis); (4) therapies and targets (understanding who develops advanced disease); (5) disease markers (incorporating intelligent trial design into all studies to ensure new treatments are tested in patient groups stratified using biomarkers); (6) prevention (strategies to prevent oestrogen-receptor negative tumours and the long-term effects of chemoprevention for oestrogen-receptor positive tumours); (7) psychosocial aspects of cancer (the use of appropriate psychosocial interventions, and the personal impact of all stages of the disease among patients from a range of ethnic and demographic backgrounds). CONCLUSION Through recommendations to address these gaps with future research, the long-term benefits to patients will include: better estimation of risk in families with breast cancer and strategies to reduce risk; better prediction of drug response and patient prognosis; improved tailoring of treatments to patient subgroups and development of new therapeutic approaches; earlier initiation of treatment; more effective use of resources for screening populations; and an enhanced experience for people with or at risk of breast cancer and their families. The challenge to funding bodies and researchers in all disciplines is to focus on these gaps and to drive advances in knowledge into improvements in patient care
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