bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ‘Chip Shop Welsh’: Aspects of ‘Welsh Speaking’ Identity in Contemporary Wales
Authors: Madoc‐Jones Iolo , Parry Odette , Jones Dawn 
Published: December 2013

AbstractConsiderable research has explored the relationship between majority and minority language speaking communities in bilingual contexts. Comparatively little research, however, has explored relations within as opposed to between a language group in these contexts. Antecedent to a new order of social and cultural life in Wales, this article explores how two groups of Welsh speakers, one relatively privileged and one relatively marginalized, positioned themselves as they talked about ‘being Welsh speaking’. For all respondents the ability to speak Welsh was understood to confer sameness beyond linguistic competence on Welsh speakers. Claims to a strong Welsh‐speaking identity, however, were legitimized by drawing on different resources. Whilst the relatively privileged group identified themselves as ‘traditionally Welsh’ based on their linguistic and social practices, members of the more marginalized group were unable to define their own linguistic and social practices as ‘traditional’ for a Welsh speaker. In response they forged a distinctive social space for themselves by developing a class‐based communal Welsh identity. With reference to Bourdieu's work on the process of boundary construction and maintenance, this article makes a contribution to understanding ethnolinguistic diversity and how discourses about being Welsh speaking might be reproduced and negotiated in contemporary post‐diglossic Wales. It suggests that ethnolinguistic identity may become implicated in the process of classificatory struggle, with social groups emerging through a social space of hierarchical difference.
Measuring disparities in sanitation access: does the measure matter?
Authors: Rheingans Richard , Anderson John D. , Luyendijk Rolf , Cumming Oliver 
Published: December 2013

AbstractObjectiveInitiatives to monitor progress in health interventions like sanitation are increasingly focused on disparities in access. We explored three methodological challenges to monitoring changes in sanitation coverage across socio‐economic and demographic determinants: (i) confounding by wealth indices including water and sanitation assets, (ii) use of individual urban and rural settings versus national wealth indices and (iii) child‐level versus household‐level analyses.MethodsSanitation coverage by wealth for children and households across settings was estimated from recent Demographic and Health Surveys in six low‐income countries. Household assignment to wealth quintiles was based on principal components analyses of assets. Concordance in household quintile assignment and estimated distribution of improved sanitation was assessed using two wealth indices differing by inclusion or exclusion of water and sanitation assets and independently derived for each setting. Improved sanitation was estimated using under five children and households.ResultsWealth indices estimated with water, and sanitation assets are highly correlated with indices excluding them but can overstate disparities in sanitation access. Independently, derived setting wealth indices highly correlate with setting estimates of coverage using a single national index. Sanitation coverage and quintile disparities were consistently lower in household‐level estimates.ConclusionsStandard asset indices provide a reasonably robust measure of disparities in improved sanitation, although overestimation is possible. Separate setting wealth quintiles reveal important disparities in urban areas, but analysis of setting quintiles using a national index is sufficient. Estimates and disparities in household‐level coverage of improved sanitation can underestimate coverage for children under five.
Carbachol excites sublaterodorsal nucleus neurons projecting to the spinal cord
Authors: Weng F. J. , Williams R. H. , Hawryluk J. M. , Lu J. , Scammell T. E. , Saper C. B. , Arrigoni E. 
Published: December 2013

Key points
Activation of spinally projecting sublaterodorsal nucleus (SLD) neurons inhibits motor activity, in part through spinal inhibitory interneurons, to produce muscle atonia during rapid‐eye‐movement (REM) sleep.
It has long been hypothesized that acetylcholine released during REM sleep contributes to REM sleep atonia through activation of SLD neurons.
We show, using whole‐cell recordings in brainstem slices, that acetylcholine directly excites spinally projecting SLD neurons via M1 and M3 muscarinic receptors, and increases afferent excitatory synaptic input to these neurons.
These results suggest that acetylcholine contributes to REM sleep muscle atonia through excitation of spinally projecting SLD neurons.
AbstractConsiderable electrophysiological and pharmacological evidence has long suggested an important role for acetylcholine in the regulation of rapid‐eye‐movement (REM) sleep. For example, injection of the cholinergic agonist carbachol into the dorsomedial pons produces an REM sleep‐like state with muscle atonia and cortical activation, both of which are cardinal features of REM sleep. Located within this region of the pons is the sublaterodorsal nucleus (SLD), a structure thought to be both necessary and sufficient for generating REM sleep muscle atonia. Subsets of glutamatergic SLD neurons potently contribute to motor inhibition during REM sleep through descending projections to motor‐related glycinergic/GABAergic neurons in the spinal cord and ventromedial medulla. Prior electrophysiological and pharmacological studies examining the effects of acetylcholine on SLD neurons have, however, produced conflicting results. In the present study, we sought to clarify how acetylcholine influences the activity of spinally projecting SLD (SLDsp) neurons. We used retrograde tracing in combination with patch‐clamp recordings and recorded pre‐ and postsynaptic effects of carbachol on SLDsp neurons. Carbachol acted presynaptically by increasing the frequency of glutamatergic miniature excitatory postsynaptic currents. We also found that carbachol directly excited SLDsp neurons by activating an Na+–Ca2+ exchanger. Both pre‐ and postsynaptic effects were mediated by co‐activation of M1 and M3 muscarinic receptors. These observations suggest that acetylcholine produces synergistic, excitatory pre‐ and postsynaptic responses on SLDsp neurons that, in turn, probably serve to promote muscle atonia during REM sleep.
In Vitro
Analyses of Mild Heat Stress in Combination with Antifungal Agents against Aspergillus fumigatus Biofilm
Authors: Zeng Rong , Li Min , Chen Qing , Wang Le , Zhan Ping , Wang Chong , Lv Guixia , Shen Yongnian , Liu Weida 
Published: December 2013

ABSTRACT

Aspergillus fumigatus
biofilms still present a challenge for effective treatment in clinical settings. While mild heat stress has been introduced as a treatment for infectious diseases, the effectiveness of mild heat stress on
A. fumigatus
biofilm formation and antifungal susceptibility is still unknown. In the present study, confocal laser scanning microscopy (CLSM) was used to image and quantify
Aspergillus fumigatus
biofilm formation under three different regimens of continuous mild heat stress: at 37, 39, and 41°C. Furthermore, fungal growth has been investigated under the above conditions in combination with antifungal drugs (amphotericin B [AMB], micafungin [MCF], and voriconazole [VOC]) at early and late stages. CLSM analysis showed that higher temperatures induce earlier germination and greater hyphal elongation but poorer polar growth and reduced biofilm thickness. In the early stage of biofilm formation, the combination of treatment at 39 or 41°C with MCF or VOC produced no visible difference in biomass formation from similar treatments at 37°C with the same drug. Interestingly, AMB treatment at 37°C inhibited early stage biofilm formation to a much greater extent than at 39 and 41°C. At the late stage of biofilm formation, the mild heat treatments at 39 and 41°C with AMB, MCF, and VOC inhibited biomass formation compared to that at 37°C. The present data show that mild heat stress has a negative regulatory effect on biofilm formation
in vitro
, and antifungal drug improvement with mild heat treatment at late-stage biofilm formation provides useful indications of possible effective strategies for clinical management of aspergillosis.
vanO
, a New Glycopeptide Resistance Operon in Environmental Rhodococcus equi Isolates
Authors: Gudeta Dereje Dadi , Moodley Arshnee , Bortolaia Valeria , Guardabassi Luca 
Published: December 2013

ABSTRACT

We describe here the sequence and gene organization of a new glycopeptide resistance operon (
vanO
) in
Rhodococcus equi
from soil. The
vanO
operon has low homology to enterococcal
van
operons and harbors a
vanHOX
cluster transcribed in the direction opposite that of the
vanS-vanR
regulatory system and composed of three open reading frames with unknown function. This finding has clinical interest, since glycopeptides are used to treat
R. equi
infections and resistance has been reported in clinical isolates.
Induction of the Chlamydia muridarum Stress/Persistence Response Increases Azithromycin Treatment Failure in a Murine Model of Infection
Authors: Phillips-Campbell R. , Kintner J. , Schoborg R. V. 
Published: December 2013

ABSTRACT

Viable but noninfectious (stressed/persistent) chlamydiae are more resistant to azithromycin (AZM) in culture than are organisms in the normal developmental cycle.
Chlamydia muridarum
-infected mice were exposed to amoxicillin to induce the organisms to enter the persistent/stressed state and subsequently treated with AZM. AZM treatment failure was observed in 22% of persistently infected mice, with an average of 321,667 inclusion-forming units (IFU) shed after AZM treatment. Productively infected mice had a 9% rate of AZM treatment failure and shed an average of 12,083 IFU. These data suggest that stressed chlamydiae are more resistant to frontline antichlamydial drugs
in vivo
.
Identification and Characterization of a Bacitracin Resistance Network in Enterococcus faecalis
Authors: Gebhard Susanne , Fang Chong , Shaaly Aishath , Leslie David J. , Weimar Marion R. , Kalamorz Falk , Carne Alan , Cook Gregory M. 
Published: December 2013

ABSTRACT

Resistance of
Enterococcus faecalis
against antimicrobial peptides, both of host origin and produced by other bacteria of the gut microflora, is likely to be an important factor in the bacterium's success as an intestinal commensal. The aim of this study was to identify proteins with a role in resistance against the model antimicrobial peptide bacitracin. Proteome analysis of bacitracin-treated and untreated cells showed that bacitracin stress induced the expression of cell wall-biosynthetic proteins and caused metabolic rearrangements. Among the proteins with increased production, an ATP-binding cassette (ABC) transporter with similarity to known peptide antibiotic resistance systems was identified and shown to mediate resistance against bacitracin. Expression of the transporter was dependent on a two-component regulatory system and a second ABC transporter, which were identified by genome analysis. Both resistance and the regulatory pathway could be functionally transferred to
Bacillus subtilis
, proving the function and sufficiency of these components for bacitracin resistance. Our data therefore show that the two ABC transporters and the two-component system form a resistance network against antimicrobial peptides in
E. faecalis
, where one transporter acts as the sensor that activates the TCS to induce production of the second transporter, which mediates the actual resistance.
In Vitro
Activities of Ceftazidime-Avibactam and Aztreonam-Avibactam against 372 Gram-Negative Bacilli Collected in 2011 and 2012 from 11 Teaching Hospitals in China
Authors: Wang Xiaojuan , Zhang Feifei , Zhao Chunjiang , Wang Zhanwei , Nichols Wright W. , Testa Raymond , Li Henan , Chen Hongbin , He Wenqiang , Wang Qi , Wang Hui 
Published: December 2013

ABSTRACT

Ceftazidime-avibactam, aztreonam-avibactam, and comparators were tested by reference broth microdilution against 372 nonrepetitive Gram-negative bacilli (346 unselected plus 26 selected meropenem-nonsusceptible
Enterobacteriaceae
isolates) collected from 11 teaching hospitals in China in 2011 and 2012. Meropenem-nonsusceptible isolates produced extended-spectrum β-lactamases (ESBLs; e.g., CTX-M-14/3), AmpCs (e.g., CMY-2), and/or carbapenemases (e.g., KPC-2 and NDM-1). Avibactam potentiated the activity of ceftazidime against organisms with combinations of ESBLs, AmpCs, and KPC-2. Aztreonam-avibactam was active against all β-lactamase producers (including producers of NDM-1 and IMP-4/8) except
bla
OXA
-containing
Acinetobacter baumannii
and some
Pseudomonas aeruginosa
isolates.
Novel Composite Efficacy Measure To Demonstrate the Rationale and Efficacy of Combination Antiviral–Anti-Inflammatory Treatment for Recurrent Herpes Simplex Labialis
Authors: Hull Christopher M. , Levin Myron J. , Tyring Stephen K. , Spruance Spotswood L. 
Published: December 2013

ABSTRACTHistorically, the primary target for research and treatment of recurrent herpes simplex labialis (HSL) has been limited to inhibiting herpes simplex virus (HSV) replication. Antiviral monotherapy, however, has proven only marginally effective in curtailing the duration and severity of recurrent lesions. Recently, the role of inflammation in the progression and resolution of recurrences has been identified as an additional target. This was evaluated in a randomized study comparing combination topical 5% acyclovir-1% hydrocortisone cream (AHC) with 5% acyclovir alone (AC; in the AHC vehicle) and the vehicle. The efficacy of each topical therapy was evaluated for cumulative lesion size—a novel composite efficacy endpoint incorporating episode duration, lesion area, and proportion of nonulcerative lesions. In that study, cumulative lesion area was significantly decreased with AHC compared with AC (25% decrease;P< 0.05) and the vehicle (50% decrease;P< 0.0001). As research continues in this arena, cumulative lesion area should be included as a measure of efficacy in clinical trials of recurrent HSL therapies.
Role of Acinetobacter baumannii UmuD Homologs in Antibiotic Resistance Acquired through DNA Damage-Induced Mutagenesis
Authors: Aranda Jesús , López Mario , Leiva Enoy , Magán Andrés , Adler Ben , Bou Germán , Barbé Jordi 
Published: December 2013

ABSTRACT

The role of
Acinetobacter baumannii
ATCC 17978 UmuDC homologs A1S_0636-A1S_0637, A1S_1174-A1S_1173, and A1S_1389 (UmuD
Ab
) in antibiotic resistance acquired through UV-induced mutagenesis was evaluated. Neither the growth rate nor the UV-related survival of any of the three mutants was significantly different from that of the wild-type parental strain. However, all mutants, and especially the

umuD
Ab

mutant, were less able to acquire resistance to rifampin and streptomycin through the activities of their error-prone DNA polymerases. Furthermore, in the
A. baumannii
mutant defective in the

umuD
Ab

gene, the spectrum of mutations included a dramatic reduction in the frequency of transition mutations, the mutagenic signature of the DNA polymerase V encoded by
umuDC
.
Statistics in
Infection and Immunity
Revisited
Authors: Olsen Cara H. 
Published: December 2013

ABSTRACT

In 2003, a review of the use of statistics in
Infection and Immunity
(IAI) found that more than half of articles had errors of statistical analysis or reporting of statistical results. This updated review of recent articles identifies and discusses the most common statistical methods reported in IAI and provides examples of both good reporting and common mistakes. Furthermore, it expands on the criteria for statistical analysis and reporting presented in the IAI “Instructions to Authors,” with the goal of helping both readers and authors better understand and apply the criteria.
Assembly of NADPH Oxidase in Human Neutrophils Is Modulated by the Opacity-Associated Protein Expression State of Neisseria gonorrhoeae
Authors: Smirnov Asya , Daily Kylene P. , Criss Alison K. 
Published: December 2013

ABSTRACT

Neisseria gonorrhoeae
(the gonococcus, Gc) triggers a potent inflammatory response and recruitment of neutrophils to the site of infection. Gc survives exposure to neutrophils despite these cells' antimicrobial products, such as reactive oxygen species (ROS). ROS production in neutrophils is initiated by NADPH oxidase, which converts oxygen into superoxide. The subunits of NADPH oxidase are spatially separated between granules (gp91
phox
/p22
phox
) and the cytoplasm (p47
phox
, p67
phox
, and p40
phox
). Activation of neutrophils promotes the coassembly of NADPH oxidase subunits at phagosome and/or plasma membranes. While Gc-expressing opacity-associated (Opa) proteins can induce neutrophils to produce ROS, Opa-negative (Opa
−
) Gc does not stimulate neutrophil ROS production. Using constitutively Opa
−
and OpaD-positive (OpaD
+
) Gc bacteria in strain FA1090, we now show that the difference in ROS production levels in primary human neutrophils between these backgrounds can be attributed to differential assembly of NADPH oxidase. Neutrophils infected with Opa
−
Gc showed limited translocation of NADPH oxidase cytoplasmic subunits to cellular membranes, including the bacterial phagosome. In contrast, these subunits rapidly translocated to neutrophil membranes following infection with OpaD
+
Gc. gp91
phox
and p22
phox
were recruited to Gc phagosomes regardless of bacterial Opa expression. These results suggest that Opa
−
Gc interferes with the recruitment of neutrophil NADPH oxidase cytoplasmic subunits to membranes, in particular, the p47
phox
“organizing” subunit, to prevent assembly of the holoenzyme, resulting in an absence of the oxidative burst.
Role of Dectin-2 for Host Defense against Systemic Infection with Candida glabrata
Authors: Ifrim Daniela C. , Bain Judith M. , Reid Delyth M. , Oosting Marije , Verschueren Ineke , Gow Neil A. R. , van Krieken J. Han , Brown Gordon D. , Kullberg Bart-Jan , Joosten Leo A. B. , van der Meer Jos W. M. , Koentgen Frank , Erwig Lars P. , Quintin Jessica , Netea Mihai G. 
Published: December 2013

ABSTRACTAlthoughCandida glabratais an important pathogenicCandidaspecies, relatively little is known about its innate immune recognition. Here, we explore the potential role of Dectin-2 for host defense againstC. glabrata. Dectin-2-deficient (Dectin-2−/−) mice were found to be more susceptible toC. glabratainfections, showing a defective fungal clearance in kidneys but not in the liver. The increased susceptibility to infection was accompanied by lower production of T helper 1 (Th1) and Th17-derived cytokines by splenocytes of Dectin-2−/−mice, while macrophage-derived cytokines were less affected. These defects were associated with a moderate yet significant decrease in phagocytosis of the fungus by the Dectin-2−/−macrophages and neutrophils. Neutrophils of Dectin-2−/−mice also displayed lower production of reactive oxygen species (ROS) upon challenge with opsonizedC. glabrataorC. albicans. This study suggests that Dectin-2 is important in host defense againstC. glabrataand provides new insights into the host defense mechanisms against this important fungal pathogen.
Interleukin-17-Induced Protein Lipocalin 2 Is Dispensable for Immunity to Oral Candidiasis
Authors: Ferreira Maria Carolina , Whibley Natasha , Mamo Anna J. , Siebenlist Ulrich , Chan Yvonne R. , Gaffen Sarah L. 
Published: December 2013

ABSTRACT

Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused by the commensal microbe
Candida albicans
. Immunity to OPC is strongly dependent on CD4
+
T cells, particularly those of the Th17 subset. Interleukin-17 (IL-17) deficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of IL-17-mediated host defense remain unclear. Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced in response to inflammatory cytokines, particularly IL-17. Lcn2 plays a key role in preventing iron acquisition by bacteria that use catecholate-type siderophores, and lipocalin 2
−/−
mice are highly susceptible to infection by
Escherichia coli
and
Klebsiella pneumoniae
. The role of Lcn2 in mediating immunity to fungi is poorly defined. Accordingly, in this study, we evaluated the role of Lcn2 in immunity to oral infection with
C. albicans
. Lcn2 is strongly upregulated following oral infection with
C. albicans
, and its expression is almost entirely abrogated in mice with defective IL-17 signaling (IL-17RA
−/−
or Act1
−/−
mice). However, Lcn2
−/−
mice were completely resistant to OPC, comparably to wild-type (WT) mice. Moreover, Lcn2 deficiency mediated protection from OPC induced by steroid immunosuppression. Therefore, despite its potent regulation during
C. albicans
infection, Lcn2 is not required for immunity to mucosal candidiasis.
Janus Kinase 3 Activity Is Necessary for Phosphorylation of Cytosolic Phospholipase A2 and Prostaglandin E2 Synthesis by Macrophages Infected with Francisella tularensis Live Vaccine Strain
Authors: Brummett Ashley M. , Navratil Aaron R. , Bryan Joshua D. , Woolard Matthew D. 
Published: December 2013

ABSTRACT

Francisella tularensis
, the causative agent of tularemia, modulates the host immune response to gain a survival advantage within the host. One mechanism of immune evasion is the ability of
F. tularensis
to induce the synthesis of the small lipid mediator prostaglandin E2 (PGE
2
), which alters the host T cell response making the host more susceptible to
Francisella
growth. PGE
2
is synthesized by a tightly regulated biosynthetic pathway following stimulation. The synthesis of PGE
2
begins with the liberation of arachidonic acid (AA) from membrane phospholipids by cytosolic phospholipase A2 (cPLA
2
). AA is subsequently converted to the unstable intermediate PGH
2
by cyclooxygenase-2 (COX-2), and PGH
2
undergoes an isomerization reaction to generate PGE
2
. Our objective was to identify
F. tularensis
-activated host signaling pathways that regulate the activity of the enzymes in the PGE
2
-biosynthetic pathway. In this study, we show that cPLA
2
, p38 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for
F. tularensis
-induced PGE
2
production. Inhibition of JAK3 activity reduced the phosphorylation of cPLA
2
and COX-2 protein levels. In addition, JAK3 regulates cPLA
2
phosphorylation independent of transcription. Moreover, p38 MAPK activity is required for
F. tularensis
-induced COX-2 protein synthesis, but not for the phosphorylation of cPLA
2
. This research highlights a unique signaling axis in which JAK3 and p38 MAPK regulate the activity of multiple enzymes of the PGE
2
-biosynthetic pathway in macrophages infected with
F. tularensis
.