Nanometer scale wire structures fabricated by diffusion-induced selective disordering of a GaAs(AlGaAs) quantum well

A shallow zinc diffusion technique is used to selectively disorder a GaAs quantum well creating nanometer scale wire structures. Spectrally resolved cathodoluminescence images of the structures are presented as well as local spectra of cathodoluminescence emission from the structures. Blue shifting of the luminescence from the wire structures is observed

Bacterial travellers’ diarrhoea: A narrative review of literature published over the past 10 years

Travellers' diarrhoea (TD) is the most frequent illness experienced by international travellers to lower-income countries with bacterial agents considered to account for 80-90% of cases. In this review, we summarise evidence published on bacterial TD over the past 10 years, focusing on the epidemiology and aetiology of TD. Diarrhoeagenic Escherichia coli (DEC) continue to be the most commonly implicated bacteria in TD, although Enteropathogenic E. coli (EPEC) and Enteroaggregative E. coli (EAEC) now appear to be predominant where Enterotoxigenic E. coli (ETEC) was previously considered most prevalent globally. Where fluroquinolone resistance had primarily been documented for Campylobacter in Southeast Asia, widespread resistance has been observed in most regions of the world for multiple enteropathogens, including Shigella, Salmonella, ETEC and EAEC. Implementation of novel molecular methods for pathogen detection has led to identification of bacterial pathogens, including Clostridium difficile (with and without the use of prior antibiotics), Arcobacter species and Bacteroides fragilis, as aetiological agents in TD. The widespread resistance to first-line antibiotics in multiple bacterial enteropathogens warrants continued surveillance and re-evaluation of current treatment practices. Further investigations are required to determine the prevalence and geographical distribution of bacterial enteropathogens that have been more recently implicated in TD

Biochemical and structural characterization of the novel sialic acid-binding site of Escherichia coli heat-labile enterotoxin LT-IIb

International audienc

Quantum wire and quantum dot semiconductor lasers

There is currently great interest in fabrication of structures that are two and three dimensional analogs of the conventional quantum well. We review here the physics behind the use of arrays of such lower dimensional structures in semiconductor laser active layers. Methods which are currently under investigation for producing such structures will be discussed

Retrospective Analysis of Serotype Switching of Vibrio cholerae O1 in a Cholera Endemic Region Shows It Is a Non-random Process.

Genomic data generated from clinical Vibrio cholerae O1 isolates collected over a five year period in an area of Kolkata, India with seasonal cholera outbreaks allowed a detailed genetic analysis of serotype switching that occurred from Ogawa to Inaba and back to Ogawa. The change from Ogawa to Inaba resulted from mutational disruption of the methyltransferase encoded by the wbeT gene. Re-emergence of the Ogawa serotype was found to result either from expansion of an already existing Ogawa clade or reversion of the mutation in an Inaba clade. Our data suggests that such transitions are not random events but rather driven by as yet unidentified selection mechanisms based on differences in the structure of the O1 antigen or in the serotype-determining wbeT gene

Quantum wire and quantum dot semiconductor lasers

There is currently great interest in fabrication of structures that are two and three dimensional analogs of the conventional quantum well. We review here the physics behind the use of arrays of such lower dimensional structures in semiconductor laser active layers. Methods which are currently under investigation for producing such structures will be discussed

Sulfatide Recognition by Colonization Factor Antigen CS6 from Enterotoxigenic Escherichia coli

The first step in the pathogenesis of enterotoxigenic Escherichia coli (ETEC) infections is adhesion of the bacterium to the small intestinal epithelium. Adhesion of ETEC is mediated by a number of antigenically distinct colonization factors, and among these, one of the most commonly detected is the non-fimbrial adhesin coli surface antigen 6 (CS6). The potential carbohydrate recognition by CS6 was investigated by binding of recombinant CS6-expressing E. coli and purified CS6 protein to a large number of variant glycosphingolipids separated on thin-layer chromatograms. Thereby, a highly specific binding of the CS6-expressing E. coli, and the purified CS6 protein, to sulfatide (SO3-3Galβ1Cer) was obtained. The binding of the CS6 protein and CS6-expressing bacteria to sulfatide was inhibited by dextran sulfate, but not by dextran, heparin, galactose 4-sulfate or galactose 6-sulfate. When using recombinantly expressed and purified CssA and CssB subunits of the CS6 complex, sulfatide binding was obtained with the CssB subunit, demonstrating that the glycosphingolipid binding capacity of CS6 resides within this subunit. CS6-binding sulfatide was present in the small intestine of species susceptible to CS6-mediated infection, e.g. humans and rabbits, but lacking in species not affected by CS6 ETEC, e.g. mice. The ability of CS6-expressing ETEC to adhere to sulfatide in target small intestinal epithelium may thus contribute to virulence

The utilization of C[sub]14-C[sub]16 n-alkanes by microorganisms

Microorganisms capable of growth using n-alkanes as sole carbon and energy source were isolated from the environment. Subsequently selected organisms from those isolated were subjected to morphological and biochemical surveys that involved electron microscopy and assays of enzymes concerned with n-alkane degradation and assimilation. The alcohol and aldehyde dehydrogenases associated with the growth of a pseudomonad on n-alkanes were partially purified and shown to be NAD(P) independent. Genetic manipulations were attempted to produce mutants of a coryneform bacterium, by chemical and U .V. mutagenesis, that were blocked at specific points in the n-alkane degradation pathway which were shown to be chromosomally borne. Appropriate selection procedures were devised and mutations identified by product accumulation by whole cells. Evidence is also presented for the presence of a large plasmid that may carry genes for n-alkane assimilation in a pseudomonad under investigation

Proteomic analysis of cholera toxin adjuvant-stimulated human monocytes identifies Thrombospondin-1 and Integrin-beta 1 as strongly upregulated molecules involved in adjuvant activity

Cholera Toxin (CT) as well as its related non-toxic mmCT and dmLT mutant proteins have been shown to be potent adjuvants for mucosally administered vaccines. Their adjuvant activity involves activation of cAMP/protein kinase A (PKA) signaling and inflammasome/IL-1 beta pathways in antigen presenting cells (APC). To get a further understanding of the signal transduction and downstream pathways activated in APCs by this group of adjuvants we have, employing quantitative proteomic analytic tools, investigated human monocytes at various time points after treatment with CT. We report the activation of three main biological pathways among upregulated proteins, peaking at 16 hours of CT treatment: cellular organization, metabolism, and immune response. Specifically, in the further analyzed immune response pathway we note a strong upregulation of thrombospondin 1 (THBS1) and integrin beta 1 (ITGB1) in response to CT as well as to mmCT and dmLT, mediated via cAMP/PKA and NFKB signaling. Importantly, inhibition in vitro of THSB1 and ITGB1 in monocytes or primary dendritic cells using siRNA abrogated the ability of the treated APCs to promote an adjuvant-stimulated Th17 cell response when co-cultured with peripheral blood lymphocytes indicating the involvement of these molecules in the adjuvant action on APCs by CT, mmCT and dmLT

Requirement for Cyclic AMP/Protein Kinase A-Dependent Canonical NFκB Signaling in the Adjuvant Action of Cholera Toxin and Its Non-toxic Derivative mmCT

Cholera toxin (CT) is widely used as an effective adjuvant in experimental immunology for inducing mucosal immune responses; yet its mechanisms of adjuvant action remain incompletely defined. Here, we demonstrate that mice lacking NFκB, compared to wild-type (WT) mice, had a 90% reduction in their systemic and mucosal immune responses to oral immunization with a model protein antigen [Ovalbumin (OVA)] given together with CT. Further, NFκB−/− mouse dendritic cells (DCs) stimulated in vitro with CT showed reduced expression of MHCII and co-stimulatory molecules, such as CD80 and CD86, as well as of IL-1β, and other pro-inflammatory cytokines compared to WT DCs. Using a human monocyte cell line THP1 with an NFκB activation reporter system, we show that CT induced NFκB signaling in human monocytes, and that inhibition of the cyclic AMP—protein kinase A (cAMP-PKA) pathway abrogated the activation and nuclear translocation of NFκB. In a human monocyte-CD4+ T cell co-culture system we further show that the strong Th17 response induced by CT treatment of monocytes was abolished by blocking the classical but not the alternative NFκB signaling pathway of monocytes. Our results indicate that activation of classical (canonical) NFκB pathway signaling in antigen-presenting cells (APCs) by CT is important for CT's adjuvant enhancement of Th17 responses. Similar findings were obtained using the almost completely detoxified mmCT mutant protein as adjuvant. Altogether, our results demonstrate that activation of the classical NFκB signal transduction pathway in APCs is important for the adjuvant action of both CT and mmCT