Optical, morphological and photocatalytic properties of biobased tractable films of chitosan/donor-acceptor polymer blends

Biobased tractable films consisting of blends of chitosan (CS) with polymer bearing carbazole derivatives as pendant groups and fluorene-thiophene as donor-acceptor units (referred to as DA) were prepared, and their optical, morphological and photocatalytic properties were studied. DA was dissolved in tetrahydrofuran (THF) and mixed with an acidified aqueous solution containing chitosan to obtain chitosan/DA (CS/DA) films by solution casting. The fabricated biobased films were characterized using spectroscopic techniques (FT-IR and UV–vis), thermogravimetry, mechanical assays, contact angle analysis, and atomic force microscopy (AFM). The effects of varying DA compositions and the results of exposure to visible-light irradiation of the films were also analyzed. The results indicated the existence of interactions between chitosan and DA and a potentially profitable light-driven response of these biobased films. This behavior was reflected in the optical, topographical, and contact angle properties of the films, which exhibited different characteristics before and after visible-light exposure. Finally, the photocatalytic performance of the biobased films was tested via the decomposition of methyl orange (MO), as a reaction model system. Our results revealed a significant photocatalytic activity (according to biobased film composition, approximately 64 % and 87 % of methyl orange were degraded under continuous visible-light irradiation for 120 min) of the films which is attributed to the combined presence and synergetic effects of the film-forming ability of chitosan and the photoproperties of DA

Burkholderia cenocepacia BC2L-C Is a Super Lectin with Dual Specificity and Proinflammatory Activity

Lectins and adhesins are involved in bacterial adhesion to host tissues and mucus during early steps of infection. We report the characterization of BC2L-C, a soluble lectin from the opportunistic pathogen Burkholderia cenocepacia, which has two distinct domains with unique specificities and biological activities. The N-terminal domain is a novel TNF-α-like fucose-binding lectin, while the C-terminal part is similar to a superfamily of calcium-dependent bacterial lectins. The C-terminal domain displays specificity for mannose and l-glycero-d-manno-heptose. BC2L-C is therefore a superlectin that binds independently to mannose/heptose glycoconjugates and fucosylated human histo-blood group epitopes. The apo form of the C-terminal domain crystallized as a dimer, and calcium and mannose could be docked in the binding site. The whole lectin is hexameric and the overall structure, determined by electron microscopy and small angle X-ray scattering, reveals a flexible arrangement of three mannose/heptose-specific dimers flanked by two fucose-specific TNF-α-like trimers. We propose that BC2L-C binds to the bacterial surface in a mannose/heptose-dependent manner via the C-terminal domain. The TNF-α-like domain triggers IL-8 production in cultured airway epithelial cells in a carbohydrate-independent manner, and is therefore proposed to play a role in the dysregulated proinflammatory response observed in B. cenocepacia lung infections. The unique architecture of this newly recognized superlectin correlates with multiple functions including bacterial cell cross-linking, adhesion to human epithelia, and stimulation of inflammation

Comparative analyses imply that the enigmatic sigma factor 54 is a central controller of the bacterial exterior

Contains fulltext : 95738.pdf (publisher's version ) (Open Access)BACKGROUND: Sigma-54 is a central regulator in many pathogenic bacteria and has been linked to a multitude of cellular processes like nitrogen assimilation and important functional traits such as motility, virulence, and biofilm formation. Until now it has remained obscure whether these phenomena and the control by Sigma-54 share an underlying theme. RESULTS: We have uncovered the commonality by performing a range of comparative genome analyses. A) The presence of Sigma-54 and its associated activators was determined for all sequenced prokaryotes. We observed a phylum-dependent distribution that is suggestive of an evolutionary relationship between Sigma-54 and lipopolysaccharide and flagellar biosynthesis. B) All Sigma-54 activators were identified and annotated. The relation with phosphotransfer-mediated signaling (TCS and PTS) and the transport and assimilation of carboxylates and nitrogen containing metabolites was substantiated. C) The function annotations, that were represented within the genomic context of all genes encoding Sigma-54, its activators and its promoters, were analyzed for intra-phylum representation and inter-phylum conservation. Promoters were localized using a straightforward scoring strategy that was formulated to identify similar motifs. We found clear highly-represented and conserved genetic associations with genes that concern the transport and biosynthesis of the metabolic intermediates of exopolysaccharides, flagella, lipids, lipopolysaccharides, lipoproteins and peptidoglycan. CONCLUSION: Our analyses directly implicate Sigma-54 as a central player in the control over the processes that involve the physical interaction of an organism with its environment like in the colonization of a host (virulence) or the formation of biofilm

Institutional pioneers in world politics: Regional institution building and the influence of the European Union

What drives processes of institution building within regional international organizations? We challenge those established theories of regionalism, and of institutionalized cooperation more broadly, that treat different organizations as independent phenomena whose evolution is conditioned primarily by internal causal factors. Developing the basic premise of ‘diffusion theory’ — meaning that decision-making is interdependent across organizations — we argue that institutional pioneers, and specifically the European Union, shape regional institution-building processes in a number of discernible ways. We then hypothesize two pathways — active and passive — of European Union influence, and stipulate an endogenous capacity for institutional change as a key scope condition for their operation. Drawing on a new and original data set on the institutional design of 34 regional international organizations in the period from 1950 to 2010, the article finds that: (1) both the intensity of a regional international organization’s structured interaction with the European Union (active influence) and the European Union’s own level of delegation (passive influence) are associated with higher levels of delegation within other regional international organizations; (2) passive European Union influence exerts a larger overall substantive effect than active European Union influence does; and (3) these effects are strongest among those regional international organizations that are based on founding contracts containing open-ended commitments. These findings indicate that the creation and subsequent institutional evolution of the European Union has made a difference to the evolution of institutions in regional international organizations elsewhere, thereby suggesting that existing theories of regionalism are insufficiently able to account for processes of institution building in such contexts.peerReviewe

Depletion of the ubiquitin-binding adaptor molecule SQSTM1/p62 from macrophages harboring cftr ΔF508 mutation improves the delivery of Burkholderia cenocepacia to the autophagic machinery

Cystic fibrosis is the most common inherited lethal disease in Caucasians. It is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the cftr ΔF508 mutation is the most common. ΔF508 macrophages are intrinsically defective in autophagy because of the sequestration of essential autophagy molecules within unprocessed CFTR aggregates. Defective autophagy allows Burkholderia cenocepacia (B. cepacia) to survive and replicate in ΔF508 macrophages. Infection by B. cepacia poses a great risk to cystic fibrosis patients because it causes accelerated lung inflammation and, in some cases, a lethal necrotizing pneumonia. Autophagy is a cell survival mechanism whereby an autophagosome engulfs non-functional organelles and delivers them to the lysosome for degradation. The ubiquitin binding adaptor protein SQSTM1/p62 is required for the delivery of several ubiquitinated cargos to the autophagosome. In WT macrophages, p62 depletion and overexpression lead to increased and decreased bacterial intracellular survival, respectively. In contrast, depletion of p62 in ΔF508 macrophages results in decreased bacterial survival, whereas overexpression of p62 leads to increased B. cepacia intracellular growth. Interestingly, the depletion of p62 from ΔF508 macrophages results in the release of the autophagy molecule beclin1 (BECN1) from the mutant CFTR aggregates and allows its redistribution and recruitment to the B. cepacia vacuole, mediating the acquisition of the autophagy marker LC3 and bacterial clearance via autophagy. These data demonstrate that p62 differentially dictates the fate of B. cepacia infection in WT and ΔF508 macrophages

Burkholderia cenocepacia O polysaccharide chain contributes to caspase-1-dependent IL-1β production in macrophages

B. cenocepacia O antigen, host TLR4 and caspase-1 contribute to IL-1β production by infected macrophage