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Functioning quantum dot (QD) sensitized solar cells have been fabricated using the vacuum deposition technique atomic layer deposition (ALD). Utilizing the incubation period of CdS growth by ALD on TiO2, we are able to grow QDs of adjustable size which act as sensitizers for solid‐state QD‐sensitized solar cells (ssQDSSC). The size of QDs, studied with transmission electron microscopy (TEM), varied with the number of ALD cycles from 1‐10 nm. Photovoltaic devices with the QDs were fabricated and characterized using a ssQDSSC device architecture with 2,2',7,7'‐tetrakis‐(N,N‐di‐p methoxyphenylamine) 9,9'‐spirobifluorene (spiro‐OMeTAD) as the solid‐state hole conductor. The ALD approach described here can be applied to fabrication of quantum‐confined structures for a variety of applications, including solar electricity and solar fuels. Because ALD provides the ability to deposit many materials in very high aspect ratio substrates, this work introduces a strategy by which material and optical properties of QD sensitizers may be adjusted not only by the size of the particles but also in the future by the composition.  相似文献   
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Free radical damage caused by ferrous iron is involved in the pathogenesis of secondary brain injury after intracerebral hemorrhage (ICH). NF‐E2‐related factor 2 (Nrf2), a major phase II gene regulator that binds to antioxidant response element, represents an important cellular cytoprotective mechanism against oxidative damage. We hypothesized that Nrf2 might protect astrocytes from damage by Fe2+. Therefore, we examined cytotoxicity in primary astrocytes induced by iron overload and evaluated the effects of Fe2+ on Nrf2 expression. The results demonstrated that 24‐h Fe2+ exposure exerted time‐ and concentration‐dependent cytotoxicity in astrocytes. Furthermore, Fe2+ exposure in astrocytes resulted in time‐ and concentration‐dependent increases in Nrf2 expression, which preceded Fe2+ toxicity. Nrf2‐specific siRNA further knocked down Nrf2 levels, resulting in greater Fe2+‐induced astrocyte cytotoxicity. These data indicate that induction of Nrf2 expression could serve as an adaptive self‐defense mechanism, although it is insufficient to completely protect primary astrocytes from Fe2+‐induced neurotoxicity.  相似文献   
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This study was aimed at understanding the main abiotic environmental factors controlling the distribution patterns of abundance and composition of phytoplankton (size less than 10 μm) assemblages in the coastal waters of south‐eastern Côte d'Ivoire. Data were collected during two cruises, in January (low‐water period) and October (high‐water period) of 2014. A total of 67 species were identified and assigned to Bacillariophyceae (49%), Cyanophyceae (21%), Chlorophyceae (13%), Euglenophyceae (10%), Dinophyceae (4%) and Chrysophyceae (3%). Three biotic zones (I, IIA and IIB) were distinguishable on a Kohonen self‐organizing map after an unsupervised learning process. The diatom genera Eunotia sp., Navicula sp. and Actinoptychus senarius are significantly associated with I, IIA and IIB biotic zones, respectively. A clear seasonal cum salinity trend was apparent in phytoplankton distribution patterns. Turbidity and nitrate levels were the main abiotic factors controlling phytoplankton distribution in I, the upland tidal regions of the lagoon. In regions along the lagoon–sea continuum, phosphate and turbidity exert the most control during the low‐water season (IIA), while total dissolved solids control phytoplankton distribution during the high‐water season (IIB). These are climate‐sensitive parameters whose concentrations depend on prevailing hydroclimatic processes. Therefore, seasonality can have important consequences on phytoplankton community and inadvertently the productivity of these systems.  相似文献   
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The self‐assembling MexA‐MexB‐OprM efflux pump system, encoded by the mexO operon, contributes to facile resistance of Pseudomonas aeruginosa by actively extruding multiple antimicrobials. MexR negatively regulates the mexO operon, comprising two adjacent MexR binding sites, and is as such highly targeted by mutations that confer multidrug resistance (MDR). To understand how MDR mutations impair MexR function, we studied MexR‐wt as well as a selected set of MDR single mutants distant from the proposed DNA‐binding helix. Although DNA affinity and MexA‐MexB‐OprM repression were both drastically impaired in the selected MexR‐MDR mutants, MexR‐wt bound its two binding sites in the mexO with high affinity as a dimer. In the MexR‐MDR mutants, secondary structure content and oligomerization properties were very similar to MexR‐wt despite their lack of DNA binding. Despite this, the MexR‐MDR mutants showed highly varying stabilities compared with MexR‐wt, suggesting disturbed critical interdomain contacts, because mutations in the DNA‐binding domains affected the stability of the dimer region and vice versa. Furthermore, significant ANS binding to MexR‐wt in both free and DNA‐bound states, together with increased ANS binding in all studied mutants, suggest that a hydrophobic cavity in the dimer region already shown to be involved in regulatory binding is enlarged by MDR mutations. Taken together, we propose that the biophysical MexR properties that are targeted by MDR mutations—stability, domain interactions, and internal hydrophobic surfaces—are also critical for the regulation of MexR DNA binding.  相似文献   
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