An HREM study of the WO3/TiO2 monolayer catalyst system. Proposals for the overlayer structure

High resolution electron microscopy (HREM) has been used to characterise the WO₃/TiO₂ (anatase) catalyst system. Comparisons between pure samples of TiO₂ in the uncalcined and calcined states with titania in the catalyst (loaded with 10 wt% WO₃) indicate that the tungsten oxide overlayer preserves the surface roughness of the support (as observed in the pure uncalcined material). The calcination of pure anatase results in significant grain growth and surface smoothing. In the electron microscope, the tungsten oxide overlayer is revealed as 2D pseudo-hexagonal shaped clusters which appear to be epitaxially related to the support. After noting that the anatase support predominantly exposes {112}, {011}, {110} and (001) type facets we have combined this information with structural data on the overlayer derived from a previous EXAFS and XANES study by Hilbrig et al. that reported the presence of WO₄ species and six-coordinate WO₅ groups. By considering the arrangement of terminating oxygen atoms on each of the aforementioned anatase surfaces, we suggest ways in which the WO _x species may be linked together to form the tungsten oxide overlayer. This approach has led us to conclude that, with the exception of the (001) surface, the overlayer may consist of WO₄ dimers rather than chains of linked WO₅ groups terminated by WO₄ species.     

贝希特斯加登山野度假村,奥伯赛尔茨贝格,德国

自19世纪末以来,奥伯赛尔茨贝格山上就已有了用于接待的客房,吸引了不少社会名流。1938年,希特勒也来此修建私家宅邸。之后,他将这里定为＂前线＂,强行征购了所有地产,用于修建军营和亲信们的私宅,并挖掘了长达4000m的地下防空隧道。     

Autosomal Dominant Gyrate Atrophy-Like Choroidal Dystrophy Revisited: 45 Years Follow-Up and Association with a Novel C1QTNF5 Missense Variant

We present a long-term follow-up in autosomal dominant gyrate atrophy-like choroidal dystrophy (adGALCD) and propose a possible genotype/phenotype correlation. Ophthalmic examination of six patients from two families revealed confluent areas of choroidal atrophy resembling gyrate atrophy, starting in the second decade of life. Progression continued centrally, reaching the fovea at about 60 years of age. Subretinal deposits, retinal pigmentation or choroidal neovascularization as seen in late-onset retinal degeneration (LORD) were not observed. Whole genome sequencing revealed a novel missense variant in the C1QTNF5 gene (p.(Q180E)) which was found in heterozygous state in all affected subjects. Haplotype analysis showed that this variant found in both families is identical by descent. Three-dimensional modeling of the possible supramolecular assemblies of C1QTNF5 revealed that the p.(Q180E) variant led to the destabilization of protein tertiary and quaternary structures, affecting both the stability of the single protomer and the entire globular head, thus exerting detrimental effects on the formation of C1QTNF5 trimeric globular domains and their interaction. In conclusion, we propose that the p.(Q180E) variant causes a specific phenotype, adGALCD, that differs in multiple clinical aspects from LORD. Disruption of optimal cell-adhesion mechanisms is expected when analyzing the effects of the point mutation at the protein level.     

Organizational dynamics in adaptive distributed search processes: effects on performance and the role of complexity

In this paper, the effects of altering the organizational setting of distributed adaptive search processes in the course of search are investigated. We put particular emphasis on the complexity of interactions between partial search problems assigned to search agents. Employing an agent-based simulation based on the framework of NK landscapes we analyze different temporal change modes of the organizational set-up. The organizational properties under change include, for example, the coordination mechanisms among search agents. Results suggest that inducing organizational dynamics has the potential to increase the effectiveness of distributed adaptive search processes with respect to various performance measures like the final performance achieved at the end of the search, the chance to find the optimal solution of the search problem, or the average performance per period achieved during the search process. However, results also indicate that the mode of temporal change in conjunction with the complexity of the search problem considerably affects the order of magnitude of these beneficial effects. In particular, results suggest that organizational dynamics induces a shift towards more exploration, i.e., discovery of new areas in the fitness landscape, and less exploitation, i.e., stepwise improvement.     

Synthesis,characterization and properties evaluation of copolymers of 2,3,4,5,6‐pentafluorostyrene and N‐phenylmaleimide

Copolymers of 2,3,4,5,6‐pentafluorostyrene (PFS) having a combination of high hydrophobicity and high glass transition temperature (T_g) are reported here for the first time. The copolymerization was carried out using N‐phenylmaleimide (NPM) as the comonomer and azobisisobutyronitrile (AIBN) as the initiator under both conventional thermal heating and microwave heating. The initial copolymerization rate was found to be higher under microwave heating than under thermal heating. The copolymerization parameters were determined using the Fineman–Ross method and were found to be r₁ (NPM) = 0.28 and r₂ (PFS) = 0.86. Increased incorporation of NPM in the copolymers led to an increase in T_g of the copolymers without significantly affecting the hydrophobicity of poly(2,3,4,5,6‐pentafluorostyrene). Thermal stability of the copolymers is also reported. Copyright © 2005 Society of Chemical Industry     

ERK1/2 Activity Is Critical for the Outcome of Ischemic Stroke

Ischemic disorders are the leading cause of death worldwide. The extracellular signal-regulated kinases 1 and 2 (ERK1/2) are thought to affect the outcome of ischemic stroke. However, it is under debate whether activation or inhibition of ERK1/2 is beneficial. In this study, we report that the ubiquitous overexpression of wild-type ERK2 in mice (ERK2^wt) is detrimental after transient occlusion of the middle cerebral artery (tMCAO), as it led to a massive increase in infarct volume and neurological deficits by increasing blood–brain barrier (BBB) leakiness, inflammation, and the number of apoptotic neurons. To compare ERK1/2 activation and inhibition side-by-side, we also used mice with ubiquitous overexpression of the Raf-kinase inhibitor protein (RKIP^wt) and its phosphorylation-deficient mutant RKIP^S153A, known inhibitors of the ERK1/2 signaling cascade. RKIP^wt and RKIP^S153A attenuated ischemia-induced damages, in particular via anti-inflammatory signaling. Taken together, our data suggest that stimulation of the Raf/MEK/ERK1/2-cascade is severely detrimental and its inhibition is rather protective. Thus, a tight control of the ERK1/2 signaling is essential for the outcome in response to ischemic stroke.     

Interaction of Alpha Synuclein and Microtubule Organization Is Linked to Impaired Neuritic Integrity in Parkinson’s Patient-Derived Neuronal Cells

Parkinson’s disease (PD) is neuropathologically characterized by the loss of dopaminergic neurons and the deposition of aggregated alpha synuclein (aSyn). Mounting evidence suggests that neuritic degeneration precedes neuronal loss in PD. A possible underlying mechanism could be the interference of aSyn with microtubule organization in the neuritic development, as implied by several studies using cell-free model systems. In this study, we investigate the impact of aSyn on microtubule organization in aSyn overexpressing H4 neuroglioma cells and midbrain dopaminergic neuronal cells (mDANs) generated from PD patient-derived human induced pluripotent stem cells (hiPSCs) carrying an aSyn gene duplication (SNCA^Dupl). An unbiased mass spectrometric analysis reveals a preferential binding of aggregated aSyn conformers to a number of microtubule elements. We confirm the interaction of aSyn with beta tubulin III in H4 and hiPSC-derived mDAN cell model systems, and demonstrate a remarkable redistribution of tubulin isoforms from the soluble to insoluble fraction, accompanied by a significantly increased insoluble aSyn level. Concordantly, SNCA^Dupl mDANs show impaired neuritic phenotypes characterized by perturbations in neurite initiation and outgrowth. In summary, our findings suggest a mechanistic pathway, through which aSyn aggregation interferes with microtubule organization and induces neurite impairments.