bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spread and Transmission of Bacterial Pathogens in Experimental Populations of the Nematode Caenorhabditis elegans
Authors: Diaz S. Anaid , Restif Olivier 
Published: June 2014

ABSTRACTCaenorhabditis elegansis frequently used as a model species for the study of bacterial virulence and innate immunity. In recent years, diverse mechanisms contributing to the nematode's immune response to bacterial infection have been discovered. Yet despite growing interest in the biochemical and molecular basis of nematode-bacterium associations, many questions remain about their ecology. Although recent studies have demonstrated that free-living nematodes could act as vectors of opportunistic pathogens in soil, the extent to which worms may contribute to the persistence and spread of these bacteria has not been quantified. We conducted a series of experiments to test whether colonization of and transmission betweenC. elegansnematodes could enable two opportunistic pathogens (Salmonella entericaandPseudomonas aeruginosa) to spread on agar plates occupied byEscherichia coli. We monitored the transmission ofS. entericaandP. aeruginosafrom single infected nematodes to their progeny and measured bacterial loads both within worms and on the plates. In particular, we analyzed three factors affecting the dynamics of bacteria: (i) initial source of the bacteria, (ii) bacterial species, and (iii) feeding behavior of the host. Results demonstrate that worms increased the spread of bacteria through shedding and transmission. Furthermore, we found that despiteP. aeruginosa's relatively high transmission rate among worms, its pathogenic effects reduced the overall number of worms colonized. This study opens new avenues to understand the role of nematodes in the epidemiology and evolution of pathogenic bacteria in the environment.
Suicin 90-1330 from a Nonvirulent Strain of Streptococcus suis: a Nisin-Related Lantibiotic Active on Gram-Positive Swine Pathogens
Authors: LeBel Geneviève , Vaillancourt Katy , Frenette Michel , Gottschalk Marcelo , Grenier Daniel 
Published: June 2014

ABSTRACT

Streptococcus suis
serotype 2 is known to cause severe infections (meningitis, endocarditis, and septicemia) in pigs and is considered an emerging zoonotic agent. Antibiotics have long been used in the swine industry for disease treatment/prevention and growth promoters. This pattern of utilization resulted in the spread of antibiotic resistance in
S. suis
worldwide. Interestingly, pigs may harbor
S. suis
in their tonsils without developing diseases, while North American strains belonging to the sequence type 28 (ST28) are nonvirulent in animal models. Consequently, the aim of this study was to purify and characterize a bacteriocin produced by a nonvirulent strain of
S. suis
serotype 2, with a view to a potential therapeutic and preventive application.
S. suis
90-1330 belonging to ST28 and previously shown to be nonvirulent in an animal model exhibited antibacterial activity toward all
S. suis
pathogenic isolates tested. The bacteriocin produced by this strain was purified to homogeneity by cationic exchange and reversed-phase fast protein liquid chromatography. Given its properties (molecular mass of <4 kDa, heat, pH and protease stability, and the presence of modified amino acids), the bacteriocin, named suicin 90-1330, belongs to the lantibiotic class. Using a DNA-binding fluorophore, the bacteriocin was found to possess a membrane permeabilization activity. When tested on other swine pathogens, the suicin showed activity against
Staphylococcus hyicus
and
Staphylococcus aureus
, whereas it was inactive against all Gram-negative bacteria tested. Amino acid sequencing of the purified bacteriocin showed homology (90.9% identity) with nisin U produced by
Streptococcus uberis
. The putative gene cluster involved in suicin production was amplified by PCR and sequence analysis revealed the presence of 11 open reading frames, including the structural gene and those required for the modification of amino acids, export, regulation, and immunity. Further studies will evaluate the ability of suicin 90-1330 or the producing strain to prevent experimental
S. suis
infections in pigs.
Multilocus Sequence Analysis of the Marine Bacterial Genus Tenacibaculum Suggests Parallel Evolution of Fish Pathogenicity and Endemic Colonization of Aquaculture Systems
Authors: Habib Christophe , Houel Armel , Lunazzi Aurélie , Bernardet Jean-François , Olsen Anne Berit , Nilsen Hanne , Toranzo Alicia E. , Castro Nuria , Nicolas Pierre , Duchaud Eric 
Published: June 2014

ABSTRACT

The genus
Tenacibaculum
, a member of the family
Flavobacteriaceae
, is an abundant component of marine bacterial ecosystems that also hosts several fish pathogens, some of which are of serious concern for marine aquaculture. Here, we applied multilocus sequence analysis (MLSA) to 114 representatives of most known species in the genus and of the worldwide diversity of the major fish pathogen
Tenacibaculum maritimum
. Recombination hampers precise phylogenetic reconstruction, but the data indicate intertwined environmental and pathogenic lineages, which suggests that pathogenicity evolved independently in several species. At lower phylogenetic levels recombination is also important, and the species
T. maritimum
constitutes a cohesive group of isolates. Importantly, the data reveal no trace of long-distance dissemination that could be linked to international fish movements. Instead, the high number of distinct genotypes suggests an endemic distribution of strains. The MLSA scheme and the data described in this study will help in monitoring
Tenacibaculum
infections in marine aquaculture; we show, for instance, that isolates from tenacibaculosis outbreaks in Norwegian salmon farms are related to
T. dicentrarchi
, a recently described species.
LitR Is a Repressor of syp Genes and Has a Temperature-Sensitive Regulatory Effect on Biofilm Formation and Colony Morphology in Vibrio (Aliivibrio) salmonicida
Authors: Hansen Hilde , Bjelland Ane Mohn , Ronessen Maria , Robertsen Espen , Willassen Nils Peder 
Published: June 2014

ABSTRACT

Vibrio
(
Aliivibrio
)
salmonicida
is the etiological agent of cold water vibriosis, a disease in farmed Atlantic salmon (
Salmo salar
) that is kept under control due to an effective vaccine. A seawater temperature below 12°C is normally required for disease development. Quorum sensing (QS) is a cell density-regulated communication system that bacteria use to coordinate activities involved in colonization and pathogenesis, and we have previously shown that inactivation of the QS master regulator LitR attenuates the
V. salmonicida
strain LFI1238 in a fish model. We show here that strain LFI1238 and a panel of naturally occurring
V. salmonicida
strains are poor biofilm producers. Inactivation of
litR
in the LFI1238 strain enhances medium- and temperature-dependent adhesion, rugose colony morphology, and biofilm formation. Chemical treatment and electron microscopy of the biofilm identified an extracellular matrix consisting mainly of a fibrous network, proteins, and polysaccharides. Further, by microarray analysis of planktonic and biofilm cells, we identified a number of genes regulated by LitR and, among these, were homologues of the
Vibrio fischeri
symbiosis polysaccharide (
syp
) genes. The
syp
genes were regulated by LitR in both planktonic and biofilm lifestyle analyses. Disruption of
syp
genes in the
V. salmonicida
Δ
litR
mutant alleviated adhesion, rugose colony morphology, and biofilm formation. Hence, LitR is a repressor of
syp
transcription that is necessary for expression of the phenotypes examined. The regulatory effect of LitR on colony morphology and biofilm formation is temperature sensitive and weak or absent at temperatures above the bacterium's upper threshold for pathogenicity.
A Pseudomonas putida Strain Genetically Engineered for 1,2,3-Trichloropropane Bioremediation
Authors: Samin Ghufrana , Pavlova Martina , Arif M. Irfan , Postema Christiaan P. , Damborsky Jiri , Janssen Dick B. 
Published: June 2014

ABSTRACT

1,2,3-Trichloropropane (TCP) is a toxic compound that is recalcitrant to biodegradation in the environment. Attempts to isolate TCP-degrading organisms using enrichment cultivation have failed. A potential biodegradation pathway starts with hydrolytic dehalogenation to 2,3-dichloro-1-propanol (DCP), followed by oxidative metabolism. To obtain a practically applicable TCP-degrading organism, we introduced an engineered haloalkane dehalogenase with improved TCP degradation activity into the DCP-degrading bacterium
Pseudomonas putida
MC4. For this purpose, the dehalogenase gene (
dhaA31
) was cloned behind the constitutive
dhlA
promoter and was introduced into the genome of strain MC4 using a transposon delivery system. The transposon-located antibiotic resistance marker was subsequently removed using a resolvase step. Growth of the resulting engineered bacterium,
P. putida
MC4-5222, on TCP was indeed observed, and all organic chlorine was released as chloride. A packed-bed reactor with immobilized cells of strain MC4-5222 degraded >95% of influent TCP (0.33 mM) under continuous-flow conditions, with stoichiometric release of inorganic chloride. The results demonstrate the successful use of a laboratory-evolved dehalogenase and genetic engineering to produce an effective, plasmid-free, and stable whole-cell biocatalyst for the aerobic bioremediation of a recalcitrant chlorinated hydrocarbon.
Design and Validation of Four New Primers for Next-Generation Sequencing To Target the 18S rRNA Genes of Gastrointestinal Ciliate Protozoa
Authors: Ishaq Suzanne L. , Wright André-Denis G. 
Published: June 2014

ABSTRACT

Four new primers and one published primer were used to PCR amplify hypervariable regions within the protozoal 18S rRNA gene to determine which primer pair provided the best identification and statistical analysis. PCR amplicons of 394 to 498 bases were generated from three primer sets, sequenced using Roche 454 pyrosequencing with Titanium, and analyzed using the BLAST database (NCBI) and MOTHUR version 1.29. The protozoal diversity of rumen contents from moose in Alaska was assessed. In the present study, primer set 1, P-SSU-316F and GIC758R (amplicon of 482 bases), gave the best representation of diversity using BLAST classification, and the set amplified
Entodinium simplex
and
Ostracodinium
spp., which were not amplified by the other two primer sets. Primer set 2, GIC1080F and GIC1578R (amplicon of 498 bases), had similar BLAST results and a slightly higher percentage of sequences that were identified with a higher sequence identity. Primer sets 1 and 2 are recommended for use in ruminants. However, primer set 1 may be inadequate to determine protozoal diversity in nonruminants. The amplicons created by primer set 1 were indistinguishable for certain species within the genera
Bandia
,
Blepharocorys
,
Polycosta
, and
Tetratoxum
and between
Hemiprorodon gymnoprosthium
and
Prorodonopsis
coli
, none of which are normally found in the rumen.
Role of Bacillus subtilis Error Prevention Oxidized Guanine System in Counteracting Hexavalent Chromium-Promoted Oxidative DNA Damage
Authors: Santos-Escobar Fernando , Gutiérrez-Corona J. Félix , Pedraza-Reyes Mario 
Published: June 2014

ABSTRACT

Chromium pollution is potentially detrimental to bacterial soil communities, compromising carbon and nitrogen cycles that are essential for life on earth. It has been proposed that intracellular reduction of hexavalent chromium [Cr(VI)] to trivalent chromium [Cr(III)] may cause bacterial death by a mechanism that involves reactive oxygen species (ROS)-induced DNA damage; the molecular basis of the phenomenon was investigated in this work. Here, we report that
Bacillus subtilis
cells lacking a functional error prevention oxidized guanine (GO) system were significantly more sensitive to Cr(VI) treatment than cells of the wild-type (WT) strain, suggesting that oxidative damage to DNA is involved in the deleterious effects of the oxyanion. In agreement with this suggestion, Cr(VI) dramatically increased the ROS concentration and induced mutagenesis in a GO-deficient
B. subtilis
strain. Alkaline gel electrophoresis (AGE) analysis of chromosomal DNA of WT and ΔGO mutant strains subjected to Cr(VI) treatment revealed that the DNA of the ΔGO strain was more susceptible to DNA glycosylase Fpg attack, suggesting that chromium genotoxicity is associated with 7,8-dihydro-8-oxodeoxyguanosine (8-oxo-G) lesions. In support of this notion, specific monoclonal antibodies detected the accumulation of 8-oxo-G lesions in the chromosomes of
B. subtilis
cells subjected to Cr(VI) treatment. We conclude that Cr(VI) promotes mutagenesis and cell death in
B. subtilis
by a mechanism that involves radical oxygen attack of DNA, generating 8-oxo-G, and that such effects are counteracted by the prevention and repair GO system.
Cross Talk between NDR Kinase Pathways Coordinates Cytokinesis with Cell Separation in Schizosaccharomyces pombe
Authors: Gupta Sneha , Govindaraghavan Meera , McCollum Dannel 
Published: June 2014

ABSTRACT

NDR (nuclear Dbf-2-related) kinases constitute key regulatory nodes in signaling networks that control multiple biological processes such as growth, proliferation, mitotic exit, morphogenesis, and apoptosis. Two NDR pathways called the septation initiation network (SIN) and the morphogenesis Orb6 network (MOR) exist in the fission yeast
Schizosaccharomyces pombe
. The SIN promotes cytokinesis, and the MOR drives cell separation at the end of cytokinesis and polarized growth during interphase. We showed previously that cross talk exists between these two pathways, with the SIN inhibiting the MOR during cytokinesis through phosphorylation of the MOR component Nak1 by the SIN Sid2 kinase. The reason for this inhibition remained uncertain. We show here that failure to inhibit MOR signaling during cytokinesis results in cell lysis at the site of septum formation. Time-lapse analysis revealed that MOR signaling during cytokinesis causes cells to prematurely initiate septum degradation/cell separation. The cell lysis phenotype is due to premature initiation of cell separation because it can be rescued by mutations in genes required for cell separation/septum degradation. We also shed further light on how the SIN inhibits the MOR. Sid2 phosphorylation of the MOR proteins Sog2 and Nak1 is required to prevent cell lysis during cytokinesis. Together, these results show that SIN inhibition of the MOR enforces proper temporal ordering of cytokinetic events.
Multicentre observational cohort study of NSAIDs as risk factors for postoperative adverse events in gastrointestinal surgery
Authors: Nepogodiev Dmitri , Chapman Stephen J , Glasbey James C D , Kelly Michael , Khatri Chetan , Fitzgerald J Edward , Bhangu Aneel 
Published: June 2014

IntroductionNon-steroidal anti-inflammatory drugs (NSAIDs) are recommended as postoperative analgesia by the Enhanced Recovery After Surgery Society. Recent studies have raised concerns that NSAID administration following colorectal anastomosis may be associated with increased risk of anastomotic leak. This multicentre study aims to determine NSAIDs’ safety profile following gastrointestinal resection.Methods and analysisThis prospective, multicentre cohort study will be performed over a 2-week period utilising a collaborative methodology. Consecutive adults undergoing open or laparoscopic, elective or emergency gastrointestinal resection will be included. The primary end point will be the 30-day morbidity, assessed using the Clavien-Dindo classification. This study will be disseminated through medical student networks, with an anticipated recruitment of at least 900 patients. The study will be powered to detect a 10% increase in complication rates with NSAID use.Ethics and disseminationFollowing the Research Ethics Committee Chairperson's review, a formal waiver was received. This study will be registered as a clinical audit or service evaluation at each participating hospital. Dissemination will take place through previously described novel research collaborative networks.
Effect of hyperglycaemia in pregnancy on adiposity in their infants in India: a protocol of a multicentre cohort study
Authors: Babu Giridhara R , Garadi Lavanya , Murthy G V S , Kinra Sanjay 
Published: June 2014

IntroductionThe carbohydrate ‘fuel’ metabolism in a pregnant woman may have a long-term impact on the development of her offspring (‘fuel-mediated teratogenesis’ hypothesis) including in utero exposure to maternal hyperglycaemia leading to fetal hyperinsulinaemia, and the consequent increase in fetal fat cells. Therefore, a feed-forward loop can exist of rising adiposity and hyperinsulinaemia throughout childhood, perhaps leading to obesity and diabetes in later life. There is a need for prospective examination of body fat distribution in children born to mothers with different glycaemic levels to understand the plausible association between glucose metabolism and future risk of diabetes in offspring. The hypothesis is that maternal glucose levels in pregnant women are related to skinfold thickness in their infants.Methods and analysisHyperglycaemia in pregnancy and adiposity in infants is a multicentre cohort study to evaluate the effects of glucose levels in pregnancy on the risk of adverse infant outcomes, especially in predicting the risk of chronic diseases in infants. The study aims to recruit 1045 participants over a period of 1 year, who will be followed up irrespective of their glycaemia status for a period of 15 months, beginning in the 24th week of gestation. The glucose levels in pregnant women would be obtained through oral glucose tolerance testing. The primary outcome of our study was skinfold thickness in infants at the age of 6 weeks, 3rd and 9th month (as a proxy for fat distribution/adiposity).Ethics and disseminationThe institutional review board at The Indian Institute of Public Health (IIPH)-Hyderabad, Public Health Foundation of India has approved the protocol. All participants are required to provide written informed consent.
Asymptotic Law of thejth Records in the Bivariate Exponential Case
Authors: Azedine Grine 
Published: July 2014

We consider a sequence(Xi,Yi)1⩽i⩽nof independent and identically distributed random variables with joint cumulative distribution H(x,y), which has exponential marginalsF(x)andG(y)with parameterλ=1. We also assume thatXi(ω)≠Yi(ω),∀i∈N, andω∈Ω. We denoteRk(j)k⩾1andSk(j)k⩾1by the sequences of thejth records in the sequences(Xi)1⩽i⩽n,(Yi)1⩽i⩽n, respectively. The main result of of the paper is to prove the asymptotic independence ofRk(j)k⩾1andSk(j)k⩾1using the property of stopping time of thejth record times and that of the exponential distribution.
Afatinib Enhances the Efficacy of Conventional Chemotherapeutic Agents by Eradicating Cancer Stem–like Cells
Authors: Wang Xiao-kun , He Jie-hua , Xu Jing-hong , Ye Sheng , Wang Fang , Zhang Hui , Huang Zhen-cong , To Kenneth Kin Wah , Fu Li-wu 
Published: June 2014

Abstract
Cancer stem cells (CSC) have garnered significant attention as a therapeutic focus, based on evidence that they may represent an etiologic root of treatment-resistant cells. Indeed, expression of the multidrug resistance protein ATP-binding cassette subfamily G member 2 (ABCG2) confers chemoresistance to CSCs, where it serves as a potential biomarker and therapeutic target. Here, we show that afatinib, a small-molecule inhibitor of the tyrosine kinases EGFR, HER2, and HER4, preferentially eliminated side population cells with CSC character, in both cell lines and patient-derived leukemia cells, by decreasing ABCG2 expression. In these cells, afatinib also acted in parallel to suppress self-renewal capacity and tumorigenicity. Combining afatinib with the DNA-damaging drug topotecan enhanced the antitumor effect of topotecan in vitro and in vivo. Mechanistic investigations suggested that ABCG2 suppression by afatinib did not proceed by proteolysis through the ubiquitin-dependent proteosome, lysosome, or calpain. Instead, we found that afatinib increased DNA methyltransferase activity, thereby leading to methylation of the ABCG2 promoter and to a decrease in ABCG2 message level. Taken together, our results advocate the use of afatinib in combination with conventional chemotherapeutic drugs to improve efficacy by improving CSC eradication. Cancer Res; 74(16); 4431–45. ©2014 AACR.
Body Size, Physical Activity, Early-Life Energy Restriction, and Associations with Methylated Insulin-like Growth Factor–Binding Protein Genes in Colorectal Cancer
Authors: Simons Colinda C.J.M. , van den Brandt Piet A. , Stehouwer Coen D.A. , van Engeland Manon , Weijenberg Matty P. 
Published: June 2014

Abstract
Background: We investigated body size, physical activity, and early-life energy restriction in relation to colorectal tumors with and without methylated insulin-like growth factor–binding protein (IGFBP) genes, which are putative tumor-suppressor genes.
Methods: We determined IGFBP2, IGFBP3, and IGFBP7 promoter CpG island hypermethylation in tumors of 733 colorectal cancer cases from the Netherlands Cohort Study (N = 120,852). Participants self-reported lifestyle and dietary factors at baseline in 1986. Using a case–cohort approach (N subcohort = 5,000), we estimated hazard ratios (HR) for colorectal cancer by extent of IGFBP methylation.
Results: Comparison of the highest versus lowest sex-specific tertiles of adult body mass index (BMI) gave multivariable-adjusted HRs [95% confidence intervals (CI)] for colorectal cancers with 0 (18.7%), 1 (29.5%), 2 (32.4%), and 3 (19.5%) methylated genes of 1.39 (0.88–2.19), 1.11 (0.77–1.62), 1.67 (1.17–2.38), and 2.07 (1.29–3.33), respectively. Other anthropometric measures and physical activity were not associated with colorectal cancer risk by extent of IGFBP methylation, except height in sex-specific analyses for women. Exposure to energy restriction during the Dutch Hunger Winter versus nonexposure gave HRs (95% CIs) for colorectal cancers with 0, 1, 2, and 3 methylated genes of 1.01 (0.67–1.53), 1.03 (0.74–1.44), 0.72 (0.52–0.99), and 0.50 (0.32–0.78), respectively.
Conclusions: Adult BMI, height (in women only), and early-life energy restriction were associated with the risk of having a colorectal tumor characterized by IGFBP methylation.
Impact: Body size may particularly increase the risk of IGFBP gene–methylated colorectal tumors; this finding might facilitate more targeted approaches to prevent obesity-related colorectal cancers. Cancer Epidemiol Biomarkers Prev; 23(9); 1852–62. ©2014 AACR.