bluuebunny/crossref_metadata_2025_split huggingface dataset:
“The Sigh of the East”: A Sense of Empire and Other Lingerings*
Authors: Wong Yoke‐Sum 
Published: February 2011

L'étude des récits de voyageurs qui sont allés à Singapour au XIXe siècle révèle de quelle manière l'odorat, le toucher et le goût ont influé sur la subjectivité des voyageurs occidentaux et sur I'idée qu'ils se faisaient de Singapour et de la Malaisie britannique à cette période. Souvent, le même endroit suscitait différents sentiments: soit une admiration pour la nature, soit un dégoût pour l'état de délabrement qui régnait, et parfois même un sentiment ambivalent. En s'appuyant sur des fictions et sur plusieurs récits, cet article démontre que, si l'Orient a été orientalisé par les expériences de ces voyageurs, les identités de ces mêmes voyageurs se sont construites dans la sensualité de leurs relations avec le milieu.An examination of travellers' accounts of 19th‐century Singapore reveals how smell, feel, touch and taste impacted upon the subjectivities of Western travellers and their conception of 19th‐century Singapore and British Malaya. Often the same location would evoke different conceptions: either a celebration of nature or disgust with the dilapidated conditions, and sometimes even ambivalence. The paper argues, through the use of fiction and several narrative accounts, that as much as the East was orientalized through such travellers' experiences, the travellers' identities were constituted by their sensuous interaction with their environment.
Brucella melitensis Infection Following Military Duty in Iraq
Authors: Bechtol D. , Carpenter L. R. , Mosites E. , Smalley D. , Dunn J. R. 
Published: February 2011

SummaryBrucellosis is a common zoonotic disease worldwide; however, few cases are reported in the US. Brucella melitensis infections are primarily acquired via consumption of high‐risk foods or travel to endemic areas. We describe a case of B. melitensis infection in a Tennessee soldier following deployment in Iraq. Initial symptoms included knee and back pain. Culture of an aspirate of the left sacroiliac joint yielded B. melitensis. Genetic analysis indicated that this isolate came from the Middle East. Investigation of laboratory workers identified risky exposures and positive serology prompting post‐exposure prophylaxis. Military personnel and other travellers should be advised to reduce risk regarding food consumption and animal contact in endemic areas. Additionally, medical providers should remain vigilant for non‐endemic zoonoses among recent travellers.
Activities of Triazole-Echinocandin Combinations against Candida Species in Biofilms and as Planktonic Cells
Authors: Chatzimoschou Athanasios , Katragkou Αspasia , Simitsopoulou Maria , Antachopoulos Charalampos , Georgiadou Elpiniki , Walsh Thomas J. , Roilides Emmanuel 
Published: February 2011

ABSTRACT

Biofilm formation complicates the treatment of various infections caused by
Candida
species. We investigated the effects of simultaneous or sequential combinations of two triazoles, voriconazole (VRC) and posaconazole (PSC), with two echinocandins, anidulafungin (AND) and caspofungin (CAS), against
Candida albicans
and
Candida parapsilosis
biofilms in comparison to their planktonic counterparts. Antifungal activity was assessed by the 2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]2H-tetrazolium-5-carboxanilide (XTT) metabolic assay. Antifungal-agent interactions were analyzed by the Bliss independence model in the simultaneous-treatment studies and by analysis of variance (ANOVA) in the sequential-treatment studies. Against
C. albicans
planktonic cells, the simultaneous combination of PSC (32 to 128 mg/liter) and CAS (0.008 to 0.25 mg/liter) was synergistic; the combinations of PSC (128 to 1,024 mg/liter) with AND (0.03 to 0.5 mg/liter) and VRC (32 to 512 mg/liter) with AND (0.008 to 0.03 mg/liter) were antagonistic. Against
C. parapsilosis
planktonic cells, the interaction between VRC (32 to 1,024 mg/liter) and CAS (1 to 16 mg/liter) was antagonistic. All simultaneous antifungal combinations demonstrated indifferent interactions against biofilms of both
Candida
species. Damage to biofilms of both species increased (
P
< 0.01) in the presence of subinhibitory concentrations of echinocandins (0.008 to 0.064 mg/liter), followed by the addition of PSC (512 mg/liter for
C. albicans
and 64 to 512 mg/liter for
C. parapsilosis
) or VRC (256 to 512 mg/liter for
C. albicans
and 512 mg/liter for
C. parapsilosis
). Triazole-echinocandin combinations do not appear to produce antagonistic effects against
Candida
sp. biofilms, while various significant interactions occur with their planktonic counterparts.
Differential Requirement of the Transcription Factor Mcm1 for Activation of the Candida albicans Multidrug Efflux Pump
MDR1
by Its Regulators Mrr1 and Cap1
Authors: Mogavero Selene , Tavanti Arianna , Senesi Sonia , Rogers P. David , Morschhäuser Joachim 
Published: February 2011

ABSTRACT

Overexpression of the multidrug efflux pump Mdr1 causes increased fluconazole resistance in the pathogenic yeast
Candida albicans
. The transcription factors Mrr1 and Cap1 mediate
MDR1
upregulation in response to inducing stimuli, and gain-of-function mutations in Mrr1 or Cap1, which render the transcription factors hyperactive, result in constitutive
MDR1
overexpression. The essential MADS box transcription factor Mcm1 also binds to the
MDR1
promoter, but its role in inducible or constitutive
MDR1
upregulation is unknown. Using a conditional mutant in which Mcm1 can be depleted from the cells, we investigated the importance of Mcm1 for
MDR1
expression. We found that Mcm1 was dispensable for
MDR1
upregulation by H
2
O
2
but was required for full
MDR1
induction by benomyl. A C-terminally truncated, hyperactive Cap1 could upregulate
MDR1
expression both in the presence and in the absence of Mcm1. In contrast, a hyperactive Mrr1 containing a gain-of-function mutation depended on Mcm1 to cause
MDR1
overexpression. These results demonstrate a differential requirement for the coregulator Mcm1 for Cap1- and Mrr1-mediated
MDR1
upregulation. When activated by oxidative stress or a gain-of-function mutation, Cap1 can induce
MDR1
expression independently of Mcm1, whereas Mrr1 requires either Mcm1 or an active Cap1 to cause overexpression of the
MDR1
efflux pump. Our findings provide more detailed insight into the molecular mechanisms of drug resistance in this important human fungal pathogen.
Comparative Genome Sequencing of an Isogenic Pair of USA800 Clinical Methicillin-Resistant Staphylococcus aureus Isolates Obtained before and after Daptomycin Treatment Failure
Authors: Boyle-Vavra Susan , Jones Marcus , Gourley Brett L. , Holmes Michael , Ruf Rebecca , Balsam Ashley R. , Boulware David R. , Kline Susan , Jawahir Selina , DeVries Aaron , Peterson Scott N. , Daum Robert S. 
Published: February 2011

ABSTRACT

We describe here a clinical daptomycin treatment failure in a patient with recurrent methicillin-resistant
Staphylococcus aureus
(MRSA) bacteremia in whom daptomycin was administered after a failed empirical treatment course with vancomycin and piperacillin-tazobactam. We had the opportunity to compare the genome sequences of an isogenic pair of daptomycin-susceptible and -resistant MRSA isolates obtained before and after initiation of daptomycin therapy, respectively. The genotype of both isolates was USA800, ST5, SCC
mec
type IV,
agr
type II. There was no increase in cell wall thickness in the daptomycin-resistant strain despite having decreased susceptibility to both vancomycin and daptomycin. By comparing the genome sequences by pyrosequencing, we identified a polymorphism (S337L) in the tenth transmembrane segment of the multiple peptide resistance factor, MprF, encoding lysyl phosphatidylglycerol transferase. This enzyme has been shown previously to promote repulsion of daptomycin at the cell surface by addition of positively charged lysine to phosphatidylglycerol. Also, the
hlb
open reading frame (ORF) encoding the β-toxin was interrupted by a prophage in the daptomycin-susceptible strain; this phage was missing in the daptomycin-resistant isolate and the
hlb
ORF was restored. Loss of the phage in the resistant isolate also resulted in loss of the virulence factor genes
clpP
,
scn
, and
sak
. This is the first study to use pyrosequencing to compare the genomes of a daptomycin-susceptible/resistant MRSA isolate pair obtained during failed daptomycin therapy in humans.
Multistep Resistance Development Studies of Ceftaroline in Gram-Positive and -Negative Bacteria
Authors: Clark Catherine , McGhee Pamela , Appelbaum Peter C. , Kosowska-Shick Klaudia 
Published: February 2011

ABSTRACT

Ceftaroline, the active component of the prodrug ceftaroline fosamil, is a novel broad-spectrum cephalosporin with bactericidal activity against Gram-positive and -negative isolates. This study evaluated the potential for ceftaroline and comparator antibiotics to select for clones of
Streptococcus pneumoniae
,
Streptococcus pyogenes
,
Haemophilus influenzae
,
Moraxella catarrhalis
,
Klebsiella pneumoniae
,
Staphylococcus aureus
, and
Enterococcus faecalis
with elevated MICs.
S. pneumoniae
and
S. pyogenes
isolates in the present study were highly susceptible to ceftaroline (MIC range, 0.004 to 0.25 μg/ml). No streptococcal strains yielded ceftaroline clones with increased MICs (defined as an increase in MIC of >4-fold) after 50 daily passages. Ceftaroline MICs for
H. influenzae
and
M. catarrhalis
were 0.06 to 2 μg/ml for four strains and 8 μg/ml for a β-lactamase-positive, efflux-positive
H. influenzae
with a mutation in L22. One
H. influenzae
clone with an increased ceftaroline MIC (quinolone-resistant, β-lactamase-positive) was recovered after 20 days. The ceftaroline MIC for this isolate increased 16-fold, from 0.06 to 1 μg/ml. MICs for
S. aureus
ranged from 0.25 to 1 μg/ml. No
S. aureus
isolates tested with ceftaroline had clones with increased MIC (>4-fold) after 50 passages. Two
E. faecalis
isolates tested had ceftaroline MICs increased from 1 to 8 μg/ml after 38 days and from 4 to 32 μg/ml after 41 days, respectively. The parental ceftaroline MIC for the one
K. pneumoniae
extended-spectrum β-lactamase-negative isolate tested was 0.5 μg/ml and did not change after 50 daily passages.
In Vitro
Activity of Fusidic Acid (CEM-102, Sodium Fusidate) against Staphylococcus aureus Isolates from Cystic Fibrosis Patients and Its Effect on the Activities of Tobramycin and Amikacin against Pseudomonas aeruginosa and Burkholderia cepacia
Authors: McGhee Pamela , Clark Catherine , Credito Kim , Beachel Linda , Pankuch Glenn A. , Appelbaum Peter C. , Kosowska-Shick Klaudia 
Published: February 2011

ABSTRACT

We tested the MICs of fusidic acid (CEM-102) plus other agents against 40 methicillin-resistant
Staphylococcus aureus
(MRSA) isolates from cystic fibrosis patients and the activities of fusidic acid with or without tobramycin or amikacin against
Pseudomonas aeruginosa
, MRSA, and
Burkholderia cepacia
isolates from cystic fibrosis patients in a 24-h time-kill study. Fusidic acid was potent (MICs, 0.125 to 0.5 μg/ml; a single 500-mg dose of fusidic acid at 8 h averaged 8 to 12. 5 μg/ml with 91 to 97% protein binding) against all MRSA strains. No antagonism was observed; synergy occurred for one MRSA strain treated with fusidic acid plus tobramycin.
Neuraminidase Inhibitor Sensitivity and Receptor-Binding Specificity of Cambodian Clade 1 Highly Pathogenic H5N1 Influenza Virus
Authors: Naughtin M. , Dyason J. C. , Mardy S. , Sorn S. , von Itzstein M. , Buchy P. 
Published: February 2011

ABSTRACTThe evolution of the highly pathogenic H5N1 influenza virus produces genetic variations that can lead to changes in antiviral susceptibility and in receptor-binding specificity. In countries where the highly pathogenic H5N1 virus is endemic or causes regular epidemics, the surveillance of these changes is important for assessing the pandemic risk. In Cambodia between 2004 and 2010, there have been 26 outbreaks of highly pathogenic H5N1 influenza virus in poultry and 10 reported human cases, 8 of which were fatal. We have observed naturally occurring mutations in hemagglutinin (HA) and neuraminidase (NA) of Cambodian H5N1 viruses that were predicted to alter sensitivity to neuraminidase inhibitors (NAIs) and/or receptor-binding specificity. We tested H5N1 viruses isolated from poultry and humans between 2004 and 2010 for sensitivity to the NAIs oseltamivir (Tamiflu) and zanamivir (Relenza). All viruses were sensitive to both inhibitors; however, we identified a virus with a mildly decreased sensitivity to zanamivir and have predicted that a V149A mutation is responsible. We also identified a virus with a hemagglutinin A134V mutation, present in a subpopulation amplified directly from a human sample. Using reverse genetics, we verified that this mutation is adaptative for human α2,6-linked sialidase receptors. The importance of an ongoing surveillance of H5N1 antigenic variance and genetic drift that may alter receptor binding and sensitivities of H5N1 viruses to NAIs cannot be underestimated while avian influenza remains a pandemic threat.
Critical Role of cRel Subunit of NF-κB in Sepsis Survival
Authors: Courtine Emilie , Pène Frédéric , Cagnard Nicolas , Toubiana Julie , Fitting Catherine , Brocheton Jessy , Rousseau Christophe , Gerondakis Steve , Chiche Jean-Daniel , Ouaaz Fatah , Mira Jean-Paul 
Published: February 2011

ABSTRACT

NF-κB is a critical regulator of gene expression during severe infections. NF-κB comprises homo- and heterodimers of proteins from the Rel family. Among them, p50 and p65 have been clearly implicated in the pathophysiology of sepsis. In contrast, the role of cRel in sepsis is still controversial and has been poorly studied in single-pathogen infections. We aimed to investigate the consequences of cRel deficiency in a cecal ligation and puncture (CLP) model of sepsis. We have approached the underlying mechanisms of host defense by analyzing bacterial clearance, systemic inflammation, and the distribution of spleen dendritic cell subsets. Moreover, by using a genome-wide technology, we have also analyzed the CLP-induced modifications in gene expression profiles both in wild-type (wt) and in
rel
−/−
mice. The absence of cRel enhances mortality due to polymicrobial sepsis. Despite normal pathogen clearance, cRel deficiency leads to an altered systemic inflammatory response associated with a sustained loss of the spleen lymphoid dendritic cells. Furthermore, a whole-blood microarray study reveals that the differential outcome between wt and
rel

−/−

mice during sepsis is preceded by remarkable changes in the expression of hundreds of genes involved in aspects of host-pathogen interaction, such as host survival and lipid metabolism. In conclusion, cRel is a key NF-κB member required for host antimicrobial defenses and a regulatory transcription subunit that controls the inflammatory and immune responses in severe infection.
Atypical Enteropathogenic Escherichia coli That Contains Functional Locus of Enterocyte Effacement Genes Can Be Attaching-and-Effacing Negative in Cultured Epithelial Cells
Authors: Rocha Sérgio P. D. , Abe Cecilia M. , Sperandio Vanessa , Bando Silvia Y. , Elias Waldir P. 
Published: February 2011

ABSTRACT

Enteropathogenic
Escherichia coli
(EPEC) induces a characteristic histopathology on enterocytes known as the attaching-and-effacing (A/E) lesion, which is triggered by proteins encoded by the locus of enterocyte effacement (LEE). EPEC is currently classified as typical EPEC (tEPEC) and atypical EPEC (aEPEC), based on the presence or absence of the EPEC adherence factor plasmid, respectively. Here we analyzed the LEE regions of three aEPEC strains displaying the localized adherence-like (LAL), aggregative adherence (AA), and diffuse adherence (DA) patterns on HEp-2 cells as well as one nonadherent (NA) strain. The adherence characteristics and the ability to induce A/E lesions were investigated with HeLa, Caco-2, T84, and HT29 cells. The adherence patterns and fluorescent actin staining (FAS) assay results were reproducible with all cell lines. The LEE region was structurally intact and functional in all strains regardless of their inability to cause A/E lesions. An EspF
U
-expressing plasmid (pKC471) was introduced into all strains, demonstrating no influence of this protein on either the adherence patterns or the capacity to cause A/E of the adherent strains. However, the NA strain harboring pKC471 expressed the LAL pattern and was able to induce A/E lesions on HeLa cells. Our data indicate that FAS-negative aEPEC strains are potentially able to induce A/E
in vivo
, emphasizing the concern about this test for the determination of aEPEC virulence. Also, the presence of EspF
U
was sufficient to provide an adherent phenotype for a nonadherent aEPEC strain via the direct or indirect activation of the
LEE4
and
LEE5
operons.
Structure-Function Analysis of the TibA Self-Associating Autotransporter Reveals a Modular Organization
Authors: Côté Jean-Philippe , Mourez Michael 
Published: February 2011

ABSTRACT

Some enterotoxigenic
Escherichia coli
strains express the TibA adhesin/invasin, a multifunctional autotransporter that mediates the autoaggregation of bacteria, biofilm formation, adhesion to cultured epithelial cells, and invasion of these cells. To elucidate the structure-function relationship in TibA, we generated mutants by transposon-based linker scanning mutagenesis and by site-directed mutagenesis. Several insertion mutants had a defect in either adhesion or autoaggregation. Mutants with a defect in autoaggregation were found in the N-terminal half of the extracellular domain, while mutants with a defect in adhesion were found in the C-terminal half. The deletion of the putative N-terminal autoaggregation domain abolished the autoaggregation of the bacteria but did not affect adhesion. The deletion of a proline-rich region located at the C terminus of the extracellular domain abolished the adhesion properties of TibA but did not affect invasion. This finding suggests that adhesion and invasion may rely on distinct mechanisms. Thus, our results reveal that TibA possesses a modular organization, with the extracellular domain being separated into an autoaggregation module and an adhesion module.
High Parasite Burdens Cause Liver Damage in Mice following Plasmodium berghei ANKA Infection Independently of CD8+T Cell-Mediated Immune Pathology
Authors: Haque Ashraful , Best Shannon E. , Amante Fiona H. , Ammerdorffer Anne , de Labastida Fabian , Pereira Tamara , Ramm Grant A. , Engwerda Christian R. 
Published: February 2011

ABSTRACTInfection of C57BL/6 mice withPlasmodium bergheiANKA induces a fatal neurological disease commonly referred to as experimental cerebral malaria. The onset of neurological symptoms and mortality depend on pathogenic CD8+T cells and elevated parasite burdens in the brain. Here we provide clear evidence of liver damage in this model, which precedes and is independent of the onset of neurological symptoms. Large numbers of parasite-specific CD8+T cells accumulated in the liver followingP. bergheiANKA infection. However, systemic depletion of these cells at various times during infection, while preventing neurological symptoms, failed to protect against liver damage or ameliorate it once established. In contrast, rapid, drug-mediated removal of parasites prevented hepatic injury if administered early and quickly resolved liver damage if administered after the onset of clinical symptoms. These data indicate that CD8+T cell-mediated immune pathology occurs in the brain but not the liver, while parasite-dependent pathology occurs in both organs duringP. bergheiANKA infection. Therefore, we show thatP. bergheiANKA infection of C57BL/6 mice is a multiorgan disease driven by the accumulation of parasites, which is also characterized by organ-specific CD8+T cell-mediated pathology.
How To Become a Top Model: Impact of Animal Experimentation on Human Salmonella Disease Research
Authors: Tsolis Renée M. , Xavier Mariana N. , Santos Renato L. , Bäumler Andreas J. 
Published: February 2011

ABSTRACT

Salmonella
serotypes are a major cause of human morbidity and mortality worldwide. Over the past decades, a series of animal models have been developed to advance vaccine development, provide insights into immunity to infection, and study the pathogenesis of human
Salmonella
disease. The successive introduction of new animal models, each suited to interrogate previously neglected aspects of
Salmonella
disease, has ushered in important conceptual advances that continue to have a strong and sustained influence on the ideas driving research on
Salmonella
serotypes. This article reviews important milestones in the use of animal models to study human
Salmonella
disease and identify research needs to guide future work.
Quality of ethical guidelines and ethical content in clinical guidelines: the example of end-of-life decision-making
Authors: Strech Daniel , Schildmann Jan 
Published: February 2011

BackgroundWhile there are many guidelines on how to make ethical decisions at the end of life, there is little evidence regarding the quality of this sort of ethical guidelines.ObjectivesFirst, this study aims to demonstrate the conceptual transferability of the Appraisal of Guidelines for Research and Evaluation (AGREE) instrument for the quality assessment of ethical guidelines. Second, it aims to illustrate the status quo of the quality of guidelines on end-of-life decision-making by using the AGREE instrument in a first practice test.MethodThe transferability of the AGREE instrument on the quality assessment of ethical guidelines is demonstrated by conceptual analysis. Guidelines on end-of-life decisions in medicine are identified through a systematic search in MEDLINE (from June 1999 to June 2009). The quality of all included guidelines was assessed with a slightly modified AGREE instrument.ResultsOf 103 guidelines identified, 34 were included as relevant. The majority of the guidelines analysed in this study were assessed as qualitatively insufficient in five out of six AGREE quality domains. A few guidelines demonstrated, however, that a high level of quality in accordance with the AGREE requirements is possible.ConclusionThis review concludes that the quality of many ethical guidelines should and can be improved in all quality domains specified by the AGREE instrument. Furthermore, conceptual analysis indicates that a slightly modified AGREE instrument is transferable to the comprehensive evaluation of the quality of ethical guidelines. Nevertheless, future research is needed to improve the assessment of the presentation of the guidelines' normative basis.