bluuebunny/crossref_metadata_2025_split huggingface dataset:
Resonance frequency analysis and damping capacity assessment
Authors: Lachmann Stefan , Jäger Berthold , Axmann Detlef , Gomez‐Roman German , Groten Martin , Weber Heiner 
Published: August 2005

AbstractObjectives: The aims of this in vitro study were to evaluate reliability of the Osstell™ and Periotest™ devices in the assessment of implant stability and to perform a method comparison.Material and methods: Commercial dental implants were inserted into bovine rib segments of different anatomical origins and densities. Repeated measurements were performed, varying (a) the torque‐in force of the devices' attachment screw (the Osstell™ transducer and the ball attachment, insert for the Periotest™ device), (b) the insertion site bone quality, and (c) the thread exposure in simulated peri‐implant bone defects.Results: Both methods were comparably reliable and showed a strong association to each other in the classification of implant stability. As opposed to torque‐forced screw attachment, the variations in bone composition, differences in inter‐implant stability of adjacent implants, and peri‐implant bone reduction were statistically significant for both methods.Conclusions: Both non‐invasive diagnostic devices seem to be useful in the long‐term follow‐up of implant integration.
Resonance frequency analysis and damping capacity assessment
Authors: Lachmann Stefan , Yves Laval Johannes , Jäger Berthold , Axmann Detlef , Gomez‐Roman German , Groten Martin , Weber Heiner 
Published: August 2005

AbstractObjective: We compared the performance of damping capacity assessment (Periotest™ device) to resonance frequency analysis (Osstell™ device) in the assessment of peri‐implant bone loss in an in vitro experiment.Material and methods: Screw‐type oral implants were polymerized into acrylic blocks. Peri‐implant bone loss was simulated by successively removing defined portions of material surrounding the implants in millimeter increments. Measurement values of both devices were compared by assessing the associated measurement errors, by calculating correlation analyses and drawing scatterplots, and by means of regression analysis referring to increasing bone loss.Results: Both devices produced comparable results suggesting agreement of the measured implant stability values to the actual loss of peri‐implant resin. There was a noticeable correlation of the Periotest™ and Osstell™ implant stability values.Conclusion: The results of this experiment suggest agreement in predicting the actual implant stability with both the instruments with the Osstell™ instrument being the more precise device.
Gliding Motility Leads to Active Cellular Invasion byCryptosporidium parvumSporozoites
Authors: Wetzel Dawn M. , Schmidt Joann , Kuhlenschmidt Mark S. , Dubey J. P. , Sibley L. David 
Published: August 2005

ABSTRACTWe examined gliding motility and cell invasion by an early-branching apicomplexan,Cryptosporidium parvum, which causes diarrheal disease in humans and animals. Real-time video microscopy demonstrated thatC. parvumsporozoites undergo circular and helical gliding, two of the three stereotypical movements exhibited byToxoplasma gondiitachyzoites.C. parvumsporozoites moved more rapidly thanT. gondiisporozoites, which showed the same rates of motility as tachyzoites. Motility byC. parvumsporozoites was prevented by latrunculin B and cytochalasin D, drugs that depolymerize the parasite actin cytoskeleton, and by the myosin inhibitor 2,3-butanedione monoxime. Imaging of the initial events in cell entry byCryptosporidiumrevealed that invasion occurs rapidly; however, the parasite does not enter deep into the cytosol but rather remains at the cell surface in a membrane-bound compartment. Invasion did not stimulate rearrangement of the host cell cytoskeleton and was inhibited by cytochalasin D, even in host cells that were resistant to the drug. Our studies demonstrate thatC. parvumrelies on a conserved actin-myosin motor for motility and active penetration of its host cell, thus establishing that this is a widely conserved feature of the Apicomplexa.
Concurrent Infection with an Intestinal Helminth Parasite Impairs Host Resistance to EntericCitrobacter rodentiumand EnhancesCitrobacter-Induced Colitis in Mice
Authors: Chen Chien-Chang , Louie Steve , McCormick Beth , Walker W. Allan , Shi Hai Ning 
Published: August 2005

ABSTRACTInfections with intestinal helminth and bacterial pathogens, such as enteropathogenicEscherichia coli, continue to be a major global health threat for children. To test the hypothesis that intestinal helminth infection may be a risk factor for enteric bacterial infection, a murine model was established by using the intestinal helminthHeligomosomoides polygyrus. To analyze the modulatory effect of a Th2-inducing helminth on the outcome of enteric bacteriumCitrobacter rodentiuminfection, BALB/c and STAT 6 knockout (KO) mice were infected withH. polygyrus,C. rodentium, or both. We found that only BALB/c mice coinfected withH. polygyrusandC. rodentiumdisplayed a marked morbidity and mortality. The enhanced susceptibility toC. rodentiumand intestinal injury of coinfected BALB/c mice were shown to be associated with a significant increase in helminth-driven Th2 responses, mucosally and systemically, and correlated with a significant downregulation of protective gamma interferon and with a dramatic upregulation of the proinflammatory tumor necrosis factor alpha response. In addition,C. rodentium-associated colonic pathology in coinfected BALB/c mice was significantly enhanced, whereas bacterial burden was increased and clearance was delayed. In contrast, coinfection in STAT 6 KO mice failed to promoteC. rodentiuminfection or to induce a more severe intestinal inflammation and tissue injury, demonstrating a mechanism by which helminth influences the development of host protective immunity and susceptibility to bacterial infections. We conclude thatH. polygyruscoinfection can promoteC. rodentium-associated disease and colitis through a STAT 6-mediated immune mechanism.
Host Immune Status Influences the Development of Attaching and Effacing Lesions in Weaned Pigs
Authors: Girard Francis , Oswald Isabelle P. , Taranu Ionélia , Hélie Pierre , Appleyard Greg D. , Harel Josée , Fairbrother John M. 
Published: August 2005

ABSTRACT

Attaching and effacing
Escherichia
coli (AEEC) has been associated with naturally occurring attaching and effacing (A/E) lesions in weaned pigs, and although A/E lesions have been experimentally reproduced in newborn piglets, such lesions have been much more difficult to induce in older conventional pigs. Hence, the aim of this study was to examine the effect of oral administration of dexamethasone on the development of A/E lesions in weaned pigs challenged with a porcine enteropathogenic
E. coli
(PEPEC) strain and to investigate the involvement of local intestinal cytokine response. Dexamethasone, given orally at a dosage of 3 mg kg of body weight
−1
, significantly enhanced both the colonization of the challenge strain and the prevalence of foci of intimately adherent bacteria, resulting in extensive A/E lesions in the ileum, cecum, and colon of challenged pigs. We also confirmed the expression of both intimin and Tir by PEPEC strain ECL1001 in A/E lesions in vivo, which is, to our knowledge, the first report of the involvement of the latter proteins in any AEEC infections in vivo. Moreover, semiquantitative reverse transcription-PCR demonstrated that interleukin 1β (IL-1β), IL-6, IL-8, and, to a lesser extent, IL-12p40 are significantly upregulated in the ileum following challenge with strain ECL1001, whereas dexamethasone blocks such upregulation. Taken together, our results strongly suggested that host immune status influences the development of A/E lesions in weaned pigs, and it appears that IL-1β, IL-6, IL-8, and, to a lesser extent, IL-12p40 are expressed during infection of weaned pigs by PEPEC and may contribute to the natural resistance of the host against PEPEC infection.
Systematic Targeted Mutagenesis ofBrucella melitensis16M Reveals a Major Role for GntR Regulators in the Control ofVirulence
Authors: Haine Valérie , Sinon Audrey , Van Steen Frédéric , Rousseau Stéphanie , Dozot Marie , Lestrate Pascal , Lambert Christophe , Letesson Jean-Jacques , De Bolle Xavier 
Published: August 2005

ABSTRACTIn order to identify transcriptional regulators involved in virulence gene control inBrucella melitensis, we generated a collection of 88 mutants in the AraC, ArsR, Crp, DeoR, GntR, IclR, LysR, MerR, RpiR, and TetR families of regulators. This collection was named LiMuR (library ofmutants forregulators). We developed a method to test several mutants simultaneously in one animal in order to identify those unable to survive. This method, called the plasmid-tagged mutagenesis method, was used to test the residual virulence of mutants after 1 week in a mouse model of infection. Ten attenuated mutants, of which six and three belong to the GntR and LysR families, respectively, were identified and individually confirmed to replicate at lower rates in mice. Among these 10 mutants, onlygntR10andarsR6are attenuated in cellular models. The LiMuR also allows simple screenings to identify regulators of a particular gene or operon. As a first example, we analyzed the expression of thevirBoperon in the LiMuR mutants. We carried out Western blottings of whole-cell extracts to analyze the production of VirB proteins using polyclonal antisera against VirB proteins. Four mutants produced small amounts of VirB proteins, and one mutant overexpressed VirB proteins compared to the wild-type strain. In these five mutants, reporter analysis using thevirBpromoter fused tolacZshowed that three mutants controlvirBat the transcriptional level. The LiMuR is a resource that will provide straightforward identification of regulators involved in the control of genes of interest.
SalmonellaPathogenicity Island 2-Dependent Expression of Suppressor of Cytokine Signaling 3 in Macrophages
Authors: Uchiya Kei-ichi , Nikai Toshiaki 
Published: August 2005

ABSTRACTSalmonellapathogenicity island 2 (SPI-2), which is located at centisome 30.7 on the chromosome ofSalmonella entericaserovar Typhimurium, is required for growth within macrophages and systemic infection in mice. We recently reported that the infection of macrophages withSalmonellainduces the expression of cyclooxygenase-2 in a manner dependent on SPI-2 (K. Uchiya and T. Nikai, Infect. Immun.72:6860-6869, 2004). In the present study, gene expression analysis using a cDNA array further showed the involvement of SPI-2 in the expression of suppressor of cytokine signaling 3 (SOCS-3), which is involved in the inhibition of cytokine signaling via the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. A high level of SOCS-3 expression was induced in J774 macrophages infected with wild-typeSalmonellacompared to that in macrophages infected with a strain carrying a mutation in thespiCgene within SPI-2. Other members of the SOCS family were not detected inSalmonella-infected macrophages. The SPI-2-induced up-regulation of SOCS-3 expression was dependent on activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Furthermore, the inhibition of gamma-interferon-induced STAT-1 and interleukin-6-induced STAT-3 tyrosine phosphorylation correlated with the expression of SOCS-3. Taken together, these results indicate thatSalmonellacauses SPI-2-dependent activation of ERK1/2, leading to SOCS-3 expression, which in turn inhibits cytokine signaling via the JAK/STAT pathway.
Experimental Infection Model for Johne's Disease in Sheep
Authors: Begg D. J. , O'Brien R. , Mackintosh C. G. , Griffin J. F. T. 
Published: August 2005

ABSTRACTJohne's disease in ruminants results in chronic enteritis caused by the pathogenic bacteriumMycobacterium aviumsubsp.paratuberculosis. This study examined twoM. aviumsubsp.paratuberculosisstrains (JD3 and W), using different doses and routes of infection, to establish the optimal time postchallenge when predictable levels of infection, gut lesions, and clinical disease occur in a large proportion of sheep. While a small proportion (25%) of sheep challenged with a low-passage-number laboratory culture ofM. aviumsubsp.paratuberculosis(strain W) became infected, no infection was found in animals exposed to a high-passage-number culture isolate of strain W. In contrast, a primary tissue homogenate ofM. aviumsubsp.paratuberculosis(JD3) resulted in high (90%) infection rates and gut histopathology following oral or intratonsillar challenge. The optimal conditions necessary to produce Johne's disease involve oral inoculation of 3-month-old lambs with four doses of 5 × 108CFU ofM. aviumsubsp.paratuberculosisisolated directly from the gut lymphatic tissues of clinically affected sheep. This resulted in consistent gut histopathology at 9 months and the onset of clinical disease by 11 months postchallenge.
Bovine NK Cells Can Produce Gamma Interferon in Response to the Secreted Mycobacterial Proteins ESAT-6 and MPP14 but Not in Response to MPB70
Authors: Olsen Ingrid , Boysen Preben , Kulberg Siri , Hope Jayne C. , Jungersen Gregers , Storset Anne K. 
Published: August 2005

ABSTRACTBovine NK cells have recently been characterized and the present study describes the interaction between NK cells, antigen-presenting cells, and secreted mycobacterial proteins. Gamma interferon (IFN-γ) production by NK cells was seen in approximately 30% of noninfected calves in response to theMycobacterium tuberculosiscomplex-specific protein ESAT-6, MPP14 fromMycobacterium aviumsubsp.paratuberculosis, and purified protein derivative (PPD) fromM. tuberculosis. In contrast, no response was induced by MPB70, which is anotherM. tuberculosiscomplex-specific secreted antigen. The production of IFN-γ by NK cells in whole blood in response to ESAT-6 and MPP14 was demonstrated using intracellular staining together with surface labeling for the NK cell-specific receptor, NKp46, or CD3. Furthermore, the depletion of NK cells from peripheral blood mononuclear cells completely abolished the IFN-γ production. The response was mediated through stimulation of adherent cells and was largely independent of contact between adherent cells and the NK cells. Neutralization of interleukin-12 only partly inhibited IFN-γ production, showing that other cytokines were also involved. The demonstration of NK cell-mediated IFN-γ production in young cattle provides an explanation for the nonspecific IFN-γ response frequently encountered in young cattle when using the IFN-γ test in diagnosis of mycobacterial infections.
Characterization of
Vibrio cholerae
RyhB: the RyhB Regulon and Role of
ryhB
in Biofilm Formation
Authors: Mey Alexandra R. , Craig Stephanie A. , Payne Shelley M. 
Published: August 2005

ABSTRACT

Vibrio cholerae
encodes a small RNA with homology to
Escherichia coli
RyhB. Like
E. coli ryhB
,
V. cholerae ryhB
is negatively regulated by iron and Fur and is required for repression of genes encoding the superoxide dismutase SodB and multiple tricarboxylic acid cycle enzymes. However,
V. cholerae
RyhB is considerably longer (>200 nucleotides) than the
E. coli
RNA (90 nucleotides), and it regulates the expression of a variety of genes that are not known to be regulated by RyhB in
E. coli
, including genes involved in motility, chemotaxis, and biofilm formation. A mutant with a deletion in
ryhB
had reduced chemotactic motility in low-iron medium and was unable to form wild-type biofilms. The defect in biofilm formation was suppressed by growing the mutant in the presence of excess iron or succinate. The wild-type strain showed reduced biofilm formation in iron-deficient medium, further supporting a role for iron in normal biofilm formation. The
ryhB
mutant was not defective for colonization in a mouse model and appeared to be at a slight advantage when competing with the wild-type parental strain. Other genes whose expression was influenced by RyhB included those encoding the outer membrane porins OmpT and OmpU, several iron transport systems, and proteins containing heme or iron-sulfur clusters. These data indicate that
V. cholerae
RyhB has diverse functions, ranging from iron homeostasis to the regulation of biofilm formation.
Pathogenicity and Immunogenicity of a Vaccine Strain ofListeria monocytogenesThat Relies on a Suicide Plasmid To Supply an Essential Gene Product
Authors: Zhao Xinyan , Li Zhongxia , Gu Baiyan , Frankel Fred R. 
Published: August 2005

ABSTRACTListeria monocytogenesis a bacterial pathogen that elicits a strong cellular immune response and thus has potential use as a vaccine vector. An attenuated strain,L. monocytogenes dal dat, produced by deletion of two genes (dalanddat) used ford-alanine synthesis, induces cytotoxic T lymphocytes and protective immunity in mice following infection in the presence ofd-alanine. In order to obviate the dependence ofL. monocytogenes dal daton supplementald-alanine yet retain its attenuation and immunogenicity, we explored mechanisms to allow transient endogenous synthesis of the amino acid. Here, we report on a derivative strain,L. monocytogenes dal dat/pRRR, that expresses adalgene and synthesizesd-alanine under highly selective conditions. We constructed the suicide plasmid pRRR carrying adalgene surrounded by twores1sites and a resolvase gene,tnpR, which acts at theres1sites. The resolvase gene is regulated by a promoter activated upon exposure to host cell cytosol.L. monocytogenes dal dat/pRRR was thus able to grow in liquid culture and to infect host cells withoutd-alanine supplementation. However, after infection of these cells, resolvase-mediated excision of thedalgene resulted in strong down-regulation of racemase expression. As a result, this system allowed only transient growth ofL. monocytogenes dal dat/pRRR in infected cells and survival in animals for only 2 to 3 days. Nevertheless, mice immunized withL. monocytogenes dal dat/pRRR generated listeriolysin O-specific effector and memory CD8+T cells and were protected against lethal challenge by wild-typeListeria. This vector may be an attractive vaccine candidate for the induction of protective cellular immune responses.
Vaccination with theLeishmania infantumAcidic Ribosomal P0 Protein plus CpG Oligodeoxynucleotides Induces Protection against Cutaneous Leishmaniasis in C57BL/6 Mice but Does Not Prevent Progressive Disease in BALB/c Mice
Authors: Iborra Salvador , Carrión Javier , Anderson Charles , Alonso Carlos , Sacks David , Soto Manuel 
Published: August 2005

ABSTRACTWe have examined the efficacy of the administration in mice of a molecularly defined vaccine based on theLeishmania infantumacidic ribosomal protein P0 (rLiP0). Two different challenge models of murine cutaneous leishmaniasis were used: (i) subcutaneous inoculation ofL. majorparasites in susceptible BALB/c mice (a model widely used for vaccination analysis) and (ii) the intradermal inoculation of a low infective dose in resistant C57BL/6 mice (a model that more accurately reproduces theL. majorinfection in natural reservoirs and in human hosts). First, we demonstrated that C57BL/6 mice vaccinated with LiP0-DNA or rLiP0 protein plus CpG oligodeoxynucleotides (ODN) were protected against the development of dermal pathology and showed a reduction in the parasite load. This protection was associated with production of gamma interferon (IFN-γ) in the dermal site. Secondly, we showed that immunization with rLiP0 plus CpG ODN is able to induce only partial protection in BALB/c, since these mice finally developed a progressive disease. Further, we demonstrated that LiP0 vaccination induces a Th1 immunological response in both strains of mice. In both cases, the antibodies against LiP0 were predominantly of the immunoglobulin G2a isotype, which was correlated with an rLiP0-stimulated production of IFN-γ in draining lymph nodes. Finally, we demonstrated that LiP0 vaccination does not prevent the Th2 response induced byL. majorinfection in BALB/c mice. Taken together, these data indicate that the BALB/c model of cutaneous leishmaniasis may undervalue the potential efficacy of some vaccines based on defined proteins, making C57BL/6 a suitable alternative model to test vaccine candidates.
Brucella abortusVirB12 Is Expressed during Infection but Is Not an Essential Component of the Type IV Secretion System
Authors: Sun Yao-Hui , Rolán Hortensia G. , den Hartigh Andreas B. , Sondervan David , Tsolis Renée M. 
Published: August 2005

ABSTRACTTheBrucella abortus virBoperon, consisting of 11 genes,virB1tovirB11, and two putative genes,orf12(virB12) andorf13, encodes a type IV secretion system (T4SS) that is required for intracellular replication and persistent infection in the mouse model. This study was undertaken to determine whetherorf12(virB12) encodes an essential part of the T4SS apparatus. ThevirB12gene was found to encode a 17-kDa protein, which was detected in vitro inB. abortusgrown to stationary phase. Mice infected withB. abortus2308 produced an antibody response to the protein encoded byvirB12, showing that this gene is expressed during infection. Expression ofvirB12was not required for survival in J774 macrophages. VirB12 was also dispensable for the persistence ofB. abortus,B. melitensis, andB. suisin mice up to 4 weeks after infection, since deletion mutants lackingvirB12were recovered from splenic tissue at wild-type levels. These results show that VirB12 is not essential for the persistence of the human-pathogenicBrucellaspp. in the mouse and macrophage models of infection.
Arginase I Induction duringLeishmania majorInfection Mediates the Development of Disease
Authors: Iniesta Virginia , Carcelén Jesualdo , Molano Isabel , Peixoto Pablo M. V. , Redondo Eloy , Parra Pilar , Mangas Marina , Monroy Isabel , Campo Maria Luisa , Nieto Carlos Gómez , Corraliza Inés 
Published: August 2005

ABSTRACTIn a previous work, we demonstrated that the induction of arginase I favored the replication ofLeishmaniainside macrophages. Now we have analyzed the differential expression of this enzyme in the mouse model ofL. majorinfection. Ours results show that arginase I is induced in both susceptible and resistant mice during the development of the disease. However, in BALB/c-infected tissues, the induction of this protein parallels the time of infection, while in C57BL/6 mice, the enzyme is upregulated only during footpad swelling. The induction of the host arginase in both strains is mediated by the balance between interleukin-4 (IL-4) and IL-12 and opposite to nitric oxide synthase II expression. Moreover, inhibition of arginase reduces the number of parasites and delays disease outcome in BALB/c mice, while treatment withl-ornithine increases the susceptibility of C57BL/6 mice. Therefore, arginase I induction could be considered a marker of disease in leishmaniasis.
Viability of a Capsule- and Lipopolysaccharide-Deficient Mutant of
Neisseria meningitidis
Authors: Bos Martine P. , Tommassen Jan 
Published: August 2005

ABSTRACT

Neisseria meningitidis
is the only lipopolysaccharide (LPS)-producing gram-negative bacterial species shown to be viable also without LPS. It was thought that the presence of capsular polysaccharide is necessary for this unusual feature. However, we show now that no part of the capsule gene cluster is required for maintaining LPS deficiency in
N. meningitidis
.