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Introduction Vaporization of the prostate (VP) and endoscopic enucleation of the prostate (EEP) are reliable and frequently used methods for BPO relief. Both surgeries utilize lasers and EAU recommends them in similar patient cohorts. Our objective was to compare intra- and perioperative results of patients who had undergone VP and EEP. Evidence acquisition A systematic literature search was performed in three databases (MEDLINE, Web of Science and Scopus). The detailed search strategy is available at Prospero, CRD42020204739. Primary outcomes were functional results (IPSS, QoL, PVR, Qmax), and secondary outcomes were intraoperative results, postoperative PSA and prostate volume, complications, and recurrence rate. Evidence synthesis VP required less operative time compared to EEP, mean difference=-5.51 (95%CI -7.52; -3.50). IPSS and Qmax for VP were worse after 12-month follow-up, mean difference=0.89 (95%CI 0.52; 1.27) and -3.7 (95%CI -4.56; -2.85), respectively, while QoL did not differ significantly. Postoperative PSA level was higher in the VP group, mean difference=2.28 (95%CI 2.00; 2.55). VP was associated with reduced Clavien-Dindo grade I (OR=4.16; 95%CI 2.96; 5.84) and grade II (OR=3.79; 95%CI 2.25; 6.39) complication rate, especially in terms of the percentage of blood transfusion and transient urinary incontinence. The rate of complications grade IIIa and higher was similar (3 - 6%). Reoperation rate was only estimated in one study and was significantly higher in the PVP group at 60 months of follow-up, 2.7% vs 0%, p Conclusions EEP and VP share the efficacy and safety in BPH management. Our meta-analysis shows comparable complication rate in Clavien-Dindo III, VP superiority in operation time, and EEP superiority in long-term functional outcomes and PSA reduction.

INTRODUCTION AND OBJECTIVE:Nowadays the most commonly used methods of BPH surgical treatment are vaporization (PVP) and enucleation of the prostate (EEP). We aimed to compare intra- and perioperati...

International audience; The identification of a functional molecular moiety relating the lipopolysaccharides (LPSs) to their capacity to induce inflammation-mediated metabolic diseases needed to be performed. We previously described a proportional increase in the relative abundance of the 16 SrDNA bacterial gene from the genus Ralstonia, within the microbiota from the adipose tissue stroma vascular fraction of obese patients, suggesting a causal role of the bacteria. Therefore, we first characterized the structures of the lipids A, the inflammatory inducing moieties of LPSs, of three Ralstonia species: Ralstonia eutropha, R. mannitolilytica and R. pickettii, and then compared each, in terms of in vitro inflammatory capacities. R. pickettii lipid A displaying only 5 Fatty Acids (FA) was a weaker inducer of inflammation, compared to the two other species harboring hexa-acylated lipids A, despite the presence of 2 AraN substituents on the phosphate groups. With regard to in vitro pro-inflammatory activities, TNF-alpha and IL-6 inducing capacities were compared on THP-1 cells treated with LPSs isolated from the three Ralstonia. R. pickettii, with low inflammatory capacities, and recently involved in nosocomial outcomes, could explain the low inflammatory level reported in previous studies on diabetic patients and animals. In addition, transmission electron microscopy was performed on the three Ralstonia species. It showed that the R. pickettii under-acylated LPSs, with a higher level of phosphate substitution had the capacity of producing more outer membrane vesicles (OMVs). The latter could facilitate transfer of LPSs to the blood and explain the increased low-grade inflammation observed in obese/diabetic patients. (C) 2019 Elsevier B.V. and Societe Francaise de Biochimie et Biologie Moleculaire (SFBBM). All rights reserved.

The structure of 166416 gene chains of various dimensions consisting of polylocus combinations of 12 polymorphic positions which forming cytokine gene network which associated with the development of uterine fibroids was studied. The structural and functional organization of the cytokine gene network, which associated with uterine fibroids resistance, was also studied for comparison. Computer modeling of network interactions of cytokine genotypes of various nature involved in the regulation of inflammation, angiogenesis, destruction and remodeling of connective tissue involved in the pathogenesis of polygenic diseases, including uterine fibroids, was performed using the Cytoscape bioinformatics platform. Analysis of the topology of this gene network allowed us to identify the main genes and the main intergenic interactions that make the greatest contribution to the development of uterine fibroids. The main genes for the development of uterine fibroids can be 3 polymorphisms: IL1B-31TC, VEGF+936CT and IL10-592CA. These genes form the main nodes in the gene network because they have the most interactions with other genes. The main intergenic interactions are the following paired combinations of polymorphisms: [IL1B-31TC : IL10-592CA] (13,5%), [TNF-238GG : IL1B-31TC] (12,0%), [IL1B-31TC : IL10-1082AG] (10,5%), [TNF-863CC : IL1B-31TC] (9,7%), [TNF-238GG : VEGF+936CT] (9,0%), since they account for 55% of all major interactions in the gene network associated with uterine fibroids development. These composite gene patterns can determine the predisposition to the uterine fibroids development, affecting the intensity of immune inflammation processes and the activity of neoangiogenesis in the myometrium. On the other hand, a characteristic feature of the structural and functional organization of the cytokine gene network, which associated with uterine fibroids resistance, is its ability to self-regulate the levels of promoter activity of angiogenesis and inflammation regulator genes due to regulatory circuits with a common hub in the form of the homozygous VEGF+936CC genotype. The most frequent intergenic interactions are associated with this vertex: [TNF-238 GG : VEGF+936 CC] (13.2%), [TNF-863 CC : VEGF+936 CC] (13.2%), [IL4-590 CC :VEGF+936 CC] (7.9%), and [VEGF+936 CC : MMP9-1562 CC] (7.9%). This gene network ensures the balanced flow of angiogenesis processes, the functioning of the extracellular matrix and the processes of inflammation in the myometrium, which prevents the development of uterine fibroids.

In open environments such as water, enterohemorrhagic Escherichia coli O157:H7 responds to inorganic phosphate (P(i)) starvation by inducing the Pho regulon controlled by PhoB. This activates the phosphate-specific transport (Pst) system that contains a high-affinity P(i) transporter. In the Δpst mutant, PhoB is constitutively activated and regulates the expression of genes in the Pho regulon. Here, we show that P(i) starvation and deletion of the pst system enhance E. coli O157:H7 biofilm formation. Among differentially expressed genes of EDL933 grown under P(i) starvation conditions and in the Δpst mutant, we have found that a member of the PhoB regulon, waaH, predicted to encode a glycosyltransferase, was highly expressed. Interestingly, WaaH contributed to biofilm formation of E. coli O157:H7 during both P(i) starvation and in the Δpst mutant. In the Δpst mutant, the presence of waaH was associated with lipopolysaccharide (LPS) R3 core type modifications, whereas in E. coli O157:H7, waaH overexpression had no effect on LPS structure during P(i) starvation. Therefore, waaH participates in E. coli O157:H7 biofilm formation during P(i) starvation, but its biochemical role remains to be clarified. This study highlights the importance of the P(i) starvation stress response to biofilm formation, which may contribute to the persistence of E. coli O157:H7 in the environment. IMPORTANCE Enterohemorrhagic Escherichia coli O157:H7 is a human pathogen that causes bloody diarrhea that can result in renal failure. Outside of mammalian hosts, E. coli O157:H7 survives for extended periods of time in nutrient-poor environments, likely as part of biofilms. In E. coli K-12, the levels of free extracellular P(i) affect biofilm formation; however, it was unknown whether P(i) influences biofilm formation by E. coli O157:H7. Our results show that upon P(i) starvation, PhoB activates waaH expression, which favors biofilm formation by E. coli O157:H7. These findings suggest that WaaH is a target for controlling biofilm formation. Altogether, our work demonstrates how adaptation to P(i) starvation allows E. coli O157:H7 to occupy different ecological niches.

In open environments such as water, enterohemorrhagicEscherichia coliO157:H7 responds to inorganic phosphate (Pi) starvation by inducing the Pho regulon controlled by PhoB. The phosphate-specific transport (Pst) system is the high-affinity Pi transporter. In the Δpstmutant, PhoB is constitutively activated and regulates the expression of genes from the Pho regulon. InE. coliO157:H7, the Δpstmutant, biofilm, and autoagglutination were increased. In the double-deletion mutant ΔpstΔphoB, biofilm and autoagglutination were similar to the wild-type strain, suggesting that PhoB is involved. We investigated the relationship between PhoB activation and enhanced biofilm formation by screening a transposon mutant library derived from Δpstmutant for decreased autoagglutination and biofilms mutants. Lipopolysaccharide (LPS) genes involved in the synthesis of the LPS core were identified. Transcriptomic studies indicate the influence of Pi-starvation andpstmutation on LPS biosynthetic gene expression. LPS analysis indicated that the O-antigen was deficient in the Δpstmutant. Interestingly,waaH, encoding a glycosyltransferase associated with LPS modifications inE. coliK-12, was highly expressed in the Δpstmutant ofE. coliO157:H7. Deletion ofwaaHfrom the Δpstmutant and from the wild-type strain grown in Pi-starvation conditions decreased the biofilm formation but without affecting LPS. Our findings suggest that LPS core is involved in the autoagglutination and biofilm phenotypes of the Δpstmutant and that WaaH plays a role in biofilm in response to Pi-starvation. This study highlights the importance of Pi-starvation in biofilm formation of E. coli O157:H7, which may affect its transmission and persistence.IMPORTANCEEnterohemorrhagicEscherichia coliO157:H7 is a human pathogen responsible for bloody diarrhea and renal failures. In the environment, O157:H7 can survive for prolonged periods of time under nutrient-deprived conditions. Biofilms are thought to participate in this environmental lifestyle. Previous reports have shown that the availability of extracellular inorganic phosphate (Pi) affected bacterial biofilm formation; however, nothing was known about O157:H7 biofilm formation. Our results show that O157:H7 membrane undergoes modifications upon PhoB activation leading to increased biofilm formation. A mutation in the Pst system results in reduced amount of the smooth type LPS and that this could influence the biofilm composition. This demonstrates how theE. coliO157:H7 adapts to Pi starvation increasing its ability to occupy different ecological niches.

During the evolution of Gram-negative bacteria, their outermost and major membrane components, lipopolysaccharides (LPS), the constituents of the so-called endotoxin, adapted to environmental changes. This helped pathogenic bacteria evade detection by the host immune system. The modifications were numerous and occurred in all three distinct LPS regions: lipid A, core, and O-chains.

Endotoxin (lipopolysaccharide, LPS) is, in general, composed of two moieties: a hydrophilic polysaccharide linked to a hydrophobic lipid A terminal unit and forms a major surface component of Gram-negative bacteria. The structural features of LPS moieties play a role in pathogenesis and also involve immunogenicity and diagnostic serology. The major toxic factor of LPS resides in the lipid A moiety, anchored in the outer layer of the bacterium, and its relative biological activity is critically related to fine structural features within the molecule. In establishing relationships between structural features and biological activities of LPS it is of the utmost importance to develop new analytical methods that can be applied to the complete unambiguous characterization of a specific LPS molecule. Herein is presented a practical rapid and sensitive analytical procedure for the mass spectral screening of LPS using triethylamine citrate as an agent for both disaggregation and mild hydrolysis of LPS. It provides improved matrix-assisted laser desorption/ionization (MALDI) mass spectra and, in particular, affords the identification of fragments retaining labile substituents present in the native macromolecular LPS structures. The methods were developed and applied using purified LPS of Escherichia coli and Salmonella enterica, as well as more complex LPS of Actnobacillus pleuropneumoniae. Copyright © 2011 John Wiley & Sons, Ltd.

Pseudomonas entomophila is an entomopathogenic bacterium that is lethal to Drosophila melanogaster within 1-2 days of ingestion of high doses. Flies orally infected with P. entomophila rapidly succumb despite the induction of both local and systemic immune responses. Recent studies suggest that its virulence relies on its ability to cause irreversible damages to the intestinal epithelium, in contrast to what is observed with milder pathogenic bacteria such as Erwinia carotovora carotovora Ecc15 or Pseudomonas aeruginosa PA14. The GacS/GacA two-component system plays a key role in P. entomophila pathogenicity. Here, we report the identification of the pvf genes, whose products are involved in production of a secondary metabolite involved in P. entomophila virulence. A pvf mutant is impaired in its ability to persist within the gut, to trigger the fly immune responses and to inflict gut damages. The expression of several genes is affected in a pvf mutant, independently of the Gac system. Moreover, growing a pvf mutant in medium supplemented with supernatant extracts from either the wild-type strain or a gacA mutant restore its pathogenicity. Collectively, our results indicate that we identified genes involved in the synthesis of a signalling molecule that controls P. entomophila virulence independently from the Gac system.

Bordetella pertussis endotoxin is a key modulator of the host immune response, mainly due to the role of its lipid A moiety in Toll-like receptor 4 (TLR4)-mediated signaling. We have previously demonstrated that the lipid A phosphate groups of B. pertussis BP338 can be substituted with glucosamine in a BvgAS-regulated manner. Here we examined the effect of this lipid A modification on the biological activity of B. pertussis endotoxin. We compared purified endotoxin and heat-killed B. pertussis BP338 whole cells that have modified lipid A phosphate groups to an isogenic mutant lacking this modification with respect to their capacities to induce the release of inflammatory cytokines by human and murine macrophages and to participate in the TLR4-mediated activation of NF-κB in transfected HEK-293 cells. We found inactivated B. pertussis cells to be stronger inducers of proinflammatory cytokines in THP-1-derived macrophages when lipid A was modified. Most notably, lack of lipid A modification abolished the ability of purified B. pertussis endotoxin to induce the release of inflammatory cytokines by human THP-1-derived macrophages but led to only slightly reduced inflammatory cytokine levels when stimulating murine (RAW 264.7) macrophages. Accordingly, upon stimulation of HEK-293 cells with inactivated bacteria and purified endotoxin, lack of lipid A modification led to impaired NF-κB activation only when human, and not when murine, TLR4-MD-2-CD14 was expressed. We speculate that in B. pertussis , lipid A modification has evolved to benefit the bacteria during human infection by modulating immune defenses rather than to evade innate immune recognition.

International audience; To determine whether growth of bacteria in biofilms triggers a specific immune response, we compared cytokine induction in human monocytes and mouse macrophages by planktonic and biofilm bacteria. We compared Pseudomonas aeruginosa and Staphylococcus aureus, two bacteria often colonizing the airways of cystic fibrosis patients. Planktonic and biofilm S. aureus induced equivalent amounts of cytokine in human monocytes. In contrast, biofilm-forming P. aeruginosa induced a higher production of tumor necrosis factor and interleukin-6 than their planktonic counterpart, both for clinical isolates and laboratory strains. This increased cytokine production was partly dependent on phagocytosis. In contrast, no difference in cytokine induction was observed with mouse macrophages. We investigated the structures of the lipopolysaccharides (LPSs) of these Gram-negative bacteria in biofilm and planktonic cultures of P. aeruginosa. Switch between the two life-styles was shown to cause several reversible LPS structure modifications affecting the lipid A and polysaccharide moieties of both clinical isolates and laboratory strains. In addition, LPS isolated from biofilm-grown bacteria induced slightly more inflammatory cytokines than that extracted from its planktonic counterpart. Our results, therefore, show that P. aeruginosa biofilm LPS undergoes structural modifications that only partially contribute to an increased inflammatory response from human monocytes.

Endotoxins [lipopolysaccharides (LPSs)] are part of the outer cell membrane of Gram-negative bacteria. Their biological activities are associated mainly with the lipid component (lipid A) and even more specifically with discrete aspects of their fine structure. The need for a rapid and small-scale analysis of lipid A motivated us to develop a procedure that combines direct isolation of lipids A from bacterial cells with sequential release of their ester-linked fatty acids by a mild alkali treatment followed by MALDI-MS analysis. This method avoids the multiple-step LPS extraction procedure and lipid A isolation. The whole process can be performed in a working day and applied to lyophilized bacterial samples as small as 1 mg. We illustrate the method by applying it to the analysis of lipids A of three species of Citrobacter that were found to be identical. On the other hand, when applied to two batches of Bordetella bronchiseptica strain 4650, it highlighted the presence, in one of them, of hitherto unreported hexosamine residues substituting the lipid A phosphate groups, possibly a new camouflage opportunity to escape a host defense system.

The purpose of this paper is to consider personality traits as the factors of social perception determining the characteristics of ethnic stereotypes and prejudices in multinational university students. Based on an analysis of the published data we suppose that such personality traits as self-confidence and aggression are connected with the peculiarities of the social perception in general and ethnic perceptions in particular. A total of 95 respondents took part in the research, including 36 young men and 59 young women. All the respondents were the first, second and third year Russian students of various departments of the multinational university (PFUR). The age of the respondents is from 18 to 21 years, the average age is 19 years. The self-confidence and aggression levels were measured by the Questionnaires developed by A. Krupnov (Krupnov, 2008) in accordance with the System-Functional Model. The features of the ethnic stereotypes of Russian students were measured by the technique of the Semantic Differential (Osgood, Suci, Tannenbaum, 1957). We used a modified version of the semantic differential called “Personal Differential” (Fetiskin, Kozlov, Manuilov, 2002). The Mann–Whitney U-test and regression analysis were used for statistical analysis. Summing up the results of the study, it can be concluded that the characteristics of the ethnic stereotypes and prejudices of the Russian students are more associated with the degree of self-confidence they have, rather than aggressiveness. DOI: 10.5901/jesr.2014.v4n2p72

Lipopolysaccharides (LPSs) are major components of the external membrane of Gram-negative bacteria, and act as an effective permeability barrier. They are essentially composed of a hydrophilic polysaccharide region linked to an hydrophobic one, termed lipid A. Depending on their individual variable fine structures, they may be potent immunomodulators. Because of the structural importance and role of lipid A in bacterial pathogenesis, herein we describe two rapid practical micromethods for structural analysis. The first method allows the direct isolation of lipid A from whole bacteria cell mass; the second describes conditions for the sequential release of fatty acids, enabling the determination of their substitution position in the lipid A structure to be determined by matrix-assisted laser desorption/ionization mass spectrometry. Examples are given with reference to two major pathogens: Bordetella pertussis and Pseudomonas aeruginosa.