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With the emergence of multi-drug resistant bacteria the use of bacteriophages (phages) is gaining renewed interest as promising anti-microbial agents. The aim of this study was to isolate and characterize phages from human fecal samples. Three new coliphages, ɸAPCEc01, ɸAPCEc02 and ɸAPCEc03, were isolated. Their phenotypic and genomic characteristics, and lytic activity against biofilm, and in combination with ciprofloxacin, were investigated. All three phages reduced the growth of E. coli strain DPC6051 at multiplicity of infection (MOI) between 10-3 and 105. A cocktail of all three phages completely inhibited the growth of E. coli. The phage cocktail also reduced biofilm formation and prevented the emergence of phage-resistant mutants which occurred with single phage. When combined with ciprofloxacin, phage alone or in cocktail inhibited the growth of E. coli and prevented the emergence of resistant mutants. These three new phages are promising biocontrol agents for E. coli infections.

This review discusses the role of galectin-1 in the tumor microenvironment. First, the structure and function of galectin-1 are discussed. Galectin-1, a member of the galectin family of lectins, is a functionally dimeric galactoside-binding protein. Although galectin-1 has both intracellular and extracellular functions, the defining carbohydrate-binding role occurs extracellularly. In this review, the extracellular roles of galectin-1 in cancer processes are discussed. In particular, the importance of multivalent interactions in galectin-1 mediated cellular processes is reviewed. Multivalent interactions involving galectin-1 in cellular adhesion, mobility and invasion, tumor-induced angiogenesis, and apoptosis are presented. Although the mechanisms of action of galectin-1 in these processes are still not well understood, the overexpression of galectin-1 in cancer progression indicates that the role of galectin-1 is significant. To conclude this review, synthetic frameworks that have been used to modulate galectin-1 processes are reviewed. Small molecule oligomers of carbohydrates, carbohydrate-functionalized pseudopolyrotaxanes, cyclodextrins, calixarenes, and glycodendrimers are presented. These synthetic multivalent systems serve as important tools for studying galectin-1 mediated cancer cellular functions.

\"A set of researchers on a compound that is itself a sociological experiment in systems theory face danger and rising chaos as they discover that an unknown computer scientist lurks among them\"-- Provided by publisher.

Metabolic Endotoxemia Initiates Obesity and Insulin Resistance Patrice D. Cani 1 2 , Jacques Amar 3 , Miguel Angel Iglesias 1 , Marjorie Poggi 4 , Claude Knauf 1 , Delphine Bastelica 4 , Audrey M. Neyrinck 2 , Francesca Fava 5 , Kieran M. Tuohy 5 , Chantal Chabo 1 , Aurélie Waget 1 , Evelyne Delmée 2 , Béatrice Cousin 6 , Thierry Sulpice 7 , Bernard Chamontin 3 , Jean Ferrières 3 , Jean-François Tanti 8 , Glenn R. Gibson 5 , Louis Casteilla 6 , Nathalie M. Delzenne 2 , Marie Christine Alessi 4 and Rémy Burcelin 1 1 Institute of Molecular Medicine, I2MR Toulouse, France 2 Unité Pharmacokinetics, Metabolism, Nutrition, and Toxicology-73/69, Université catholique de Louvain, Brussels, Belgium 3 Institut National de la Santé et de la Recherche Médicale (INSERM) 558, Toulouse, France 4 INSERM U 626, Marseille, France 5 Food Microbial Sciences Unit, Department of Food Biosciences, University of Reading, Reading, U.K 6 Unité Mixte de Recherche 5241, Centre National de la Recherche Scientifique, Université Paul Sabatier, Toulouse, France 7 Physiogenex S.A.S., Labège Innopole, France 8 INSERM U 568, Nice, France Address correspondence and reprint requests to Rémy Burcelin, I2MR U858, IFR 31, Hôpital Rangueil, BP 84225, Toulouse 31432 Cedex 4, France. E-mail: burcelin{at}toulouse.inserm.fr Abstract Diabetes and obesity are two metabolic diseases characterized by insulin resistance and a low-grade inflammation. Seeking an inflammatory factor causative of the onset of insulin resistance, obesity, and diabetes, we have identified bacterial lipopolysaccharide (LPS) as a triggering factor. We found that normal endotoxemia increased or decreased during the fed or fasted state, respectively, on a nutritional basis and that a 4-week high-fat diet chronically increased plasma LPS concentration two to three times, a threshold that we have defined as metabolic endotoxemia. Importantly, a high-fat diet increased the proportion of an LPS-containing microbiota in the gut. When metabolic endotoxemia was induced for 4 weeks in mice through continuous subcutaneous infusion of LPS, fasted glycemia and insulinemia and whole-body, liver, and adipose tissue weight gain were increased to a similar extent as in high-fat–fed mice. In addition, adipose tissue F4/80-positive cells and markers of inflammation, and liver triglyceride content, were increased. Furthermore, liver, but not whole-body, insulin resistance was detected in LPS-infused mice. CD14 mutant mice resisted most of the LPS and high-fat diet–induced features of metabolic diseases. This new finding demonstrates that metabolic endotoxemia dysregulates the inflammatory tone and triggers body weight gain and diabetes. We conclude that the LPS/CD14 system sets the tone of insulin sensitivity and the onset of diabetes and obesity. Lowering plasma LPS concentration could be a potent strategy for the control of metabolic diseases. IKK, inhibitor of κB kinase IL, interleukin LPS, lipopolysaccharide PAI, plasminogen activator inhibitor TLR4, toll-like receptor 4 TNF, tumor necrosis factor Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 24 April 2007. DOI: 10.2337/db06-1491. P.D.C., J.A., and M.A.I. contributed equally to this article. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted April 13, 2007. Received October 24, 2006. DIABETES

\"This is an illustrated dictionary of over 850 gestures from around the world. Gestures often convey meanings that transcend borders, but sometimes they bear vastly different meanings from one continent to another. A dictionary, then, of bodily signs made voluntarily in order to communicate in a open manner: not sign language, no involuntary psychoanalytic \"tells,\" no dance moves, and no secret means of exchange (for example, the recent appropriation of the same \"a-ok\" gesture mentioned above by white supremecists) or professional codes (military, for example). Which is not to make this book sound limited, but rather to explain that the overall guiding principle is the way we go about joining words to gestures throughout the world in our everyday lives (gestures don't constitute a language in and of themselves), with a side interest in the fact that there are no universals in the realm of the gesture. All entries are illustrated in a how-to manner via drawings (utilizing men, women, and children from all cultures, reflecting the book's global coverage), while illustrations from other sources showing gestures being performed in various cultural contexts throughout history are also scattered throughout the book and the introduction. Entries are organized by body parts and body regions, from head to foot (with everything in between: chin, nose, thumb, buttocks, and 33 other body parts), with an index for intention and interpretation of the different gestures (i.e., Complicity, Despair, Homosexuality, Indifference, Satisfaction, and so on) that makes for a different means of taxonomy\"-- Provided by publisher.

The transcription factor NF-E2 p45-related factor 2 (NRF2; encoded by NFE2L2) and its principal negative regulator, the E3 ligase adaptor Kelch-like ECH-associated protein 1 (KEAP1), are critical in the maintenance of redox, metabolic and protein homeostasis, as well as the regulation of inflammation. Thus, NRF2 activation provides cytoprotection against numerous pathologies including chronic diseases of the lung and liver; autoimmune, neurodegenerative and metabolic disorders; and cancer initiation. One NRF2 activator has received clinical approval and several electrophilic modifiers of the cysteine-based sensor KEAP1 and inhibitors of its interaction with NRF2 are now in clinical development. However, challenges regarding target specificity, pharmacodynamic properties, efficacy and safety remain.

This is an illustrated guide to more than 850 gestures and their meanings around the world, from a nod of the head to a click of the heels.

Attosecond light pulses in the extreme ultraviolet have drawn a great deal of attention due to their ability to interrogate electronic dynamics in real time. Nevertheless, to follow charge dynamics and excitations in materials, element selectivity is a prerequisite, which demands such pulses in the soft X-ray region, above 200 eV, to simultaneously cover several fundamental absorption edges of the constituents of the materials. Here, we experimentally demonstrate the exploitation of a transient phase matching regime to generate carrier envelope controlled soft X-ray supercontinua with pulse energies up to 2.9±0.1 pJ and a flux of (7.3±0.1) × 10 7 photons per second across the entire water window and attosecond pulses with 13 as transform limit. Our results herald attosecond science at the fundamental absorption edges of matter by bridging the gap between ultrafast temporal resolution and element specific probing. Attosecond soft X-ray pulses hold promise for probing electronic dynamics in real time, but it is challenging to achieve element sensitivity while maintaining temporal resolution. Teichmann et al . report the cover of carbon, nitrogen and oxygen absorption edges with an isolated pulse supporting 13 as duration.