bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of orthopedic reinforced gloves versus double standard gloves on contamination events during small animal orthopedic surgery
Authors: Hayes Galina , Singh Ameet , Gibson Tom , Moens Noel , Oblak Michelle , Ogilvie Adam , Reynolds Debbie 
Published: July 2017

AbstractObjectiveTo determine the influence of orthopedic reinforced gloves on contamination events during small animal orthopedic surgery.Study designProspective randomized controlled trialSample populationTwo hundred and thirty‐seven pairs of orthopedic gloves (474 gloves) and 203 pairs of double standard gloves (812 gloves) worn during 193 orthopedic procedures.MethodsPrimary and assistant surgeons were randomized to wear either orthopedic reinforced gloves or double gloves. Gloves were leak tested to identify perforations at the end of procedures. Perforations detected intraoperatively or postoperatively were recorded. A contamination event was defined as at least one perforation on either hand for orthopedic reinforced gloves, or a perforation of both the inner and outer glove on the same hand for double gloves.ResultsBaseline characteristics between the 2 intervention groups were similar. There was no difference in contamination events between the double‐gloved and orthopedic gloved groups (OR = 0.95, 95% CI = 0.49‐1.87,P = .89). The same percentage of contamination events (8% glove pairs used) occurred in the double gloved group (17 contamination events) and in the orthopedic gloved group (19 contamination events). The odds of a contamination event increased by 1.02 (95% CI 1.01‐1.03,P < .001) with each additional minute of surgery.ConclusionOrthopedic reinforced gloves and double standard gloving were equally effective at preventing contamination events in small animal orthopedic procedures.Clinical relevanceSurgeons reluctant to double glove due to perceptions of decreased dexterity and discomfort may safely opt for wearing orthopedic gloves, which may improve their compliance.
Imposed Environmental Stresses Facilitate Cell-Free Nanoparticle Formation by Deinococcus radiodurans
Authors: Chen Angela , Contreras Lydia M. , Keitz Benjamin K. 
Published: July 2017

ABSTRACTThe biological synthesis of metal nanoparticles has been examined in a wide range of organisms, due to increased interest in green synthesis and environmental remediation applications involving heavy metal ion contamination.Deinococcus radioduransis particularly attractive for environmental remediation involving metal reduction, due to its high levels of resistance to radiation and other environmental stresses. However, few studies have thoroughly examined the relationships between environmental stresses and the resulting effects on nanoparticle biosynthesis. In this work, we demonstrate cell-free nanoparticle production and study the effects of metal stressor concentrations and identity, temperature, pH, and oxygenation on the production of extracellular silver nanoparticles byD. radioduransR1. We also report the synthesis of bimetallic silver and gold nanoparticles following the addition of a metal stressor (silver or gold), highlighting how production of these particles is enabled through the application of environmental stresses. Additionally, we found that both the morphology and size of monometallic and bimetallic nanoparticles were dependent on the environmental stresses imposed on the cells. The nanoparticles produced byD. radioduransexhibited antimicrobial activity comparable to that of pure silver nanoparticles and displayed catalytic activity comparable to that of pure gold nanoparticles. Overall, we demonstrate that biosynthesized nanoparticle properties can be partially controlled through the tuning of applied environmental stresses, and we provide insight into how their application may affect nanoparticle production inD. radioduransduring bioremediation.IMPORTANCEBiosynthetic production of nanoparticles has recently gained prominence as a solution to rising concerns regarding increased bacterial resistance to antibiotics and a desire for environmentally friendly methods of bioremediation and chemical synthesis. To date, a range of organisms have been utilized for nanoparticle formation. The extremophileD. radiodurans, which can withstand significant environmental stresses and therefore is more robust for metal reduction applications, has yet to be exploited for this purpose. Thus, this work improves our understanding of the impact of environmental stresses on biogenic nanoparticle morphology and composition during metal reduction processes in this organism. This work also contributes to enhancing the controlled synthesis of nanoparticles with specific attributes and functions using biological systems.
Deficiency of RgpG Causes Major Defects in Cell Division and Biofilm Formation, and Deficiency of LytR-CpsA-Psr Family Proteins Leads to Accumulation of Cell Wall Antigens in Culture Medium by Streptococcus mutans
Authors: De Arpan , Liao Sumei , Bitoun Jacob P. , Roth Randy , Beatty Wandy L. , Wu Hui , Wen Zezhang T. 
Published: July 2017

ABSTRACT

Streptococcus mutans
is known to possess rhamnose-glucose polysaccharide (RGP), a major cell wall antigen.
S. mutans
strains deficient in
rgpG
, encoding the first enzyme of the RGP biosynthesis pathway, were constructed by allelic exchange. The
rgpG
deficiency had no effect on growth rate but caused major defects in cell division and altered cell morphology. Unlike the coccoid wild type, the
rgpG
mutant existed primarily in chains of swollen, “squarish” dividing cells. Deficiency of
rgpG
also causes significant reduction in biofilm formation (
P
< 0.01). Double and triple mutants with deficiency in
brpA
and/or
psr
, genes coding for the LytR-CpsA-Psr family proteins BrpA and Psr, which were previously shown to play important roles in cell envelope biogenesis, were constructed using the
rgpG
mutant. There were no major differences in growth rates between the wild-type strain and the
rgpG brpA
and
rgpG psr
double mutants, but the growth rate of the
rgpG brpA psr
triple mutant was reduced drastically (
P
< 0.001). Under transmission electron microscopy, both double mutants resembled the
rgpG
mutant, while the triple mutant existed as giant cells with multiple asymmetric septa. When analyzed by immunoblotting, the
rgpG
mutant displayed major reductions in cell wall antigens compared to the wild type, while little or no signal was detected with the double and triple mutants and the
brpA
and
psr
single mutants. These results suggest that RgpG in
S. mutans
plays a critical role in cell division and biofilm formation and that BrpA and Psr may be responsible for attachment of cell wall antigens to the cell envelope.

IMPORTANCE
Streptococcus mutans
, a major etiological agent of human dental caries, produces rhamnose-glucose polysaccharide (RGP) as the major cell wall antigen. This study provides direct evidence that deficiency of RgpG, the first enzyme of the RGP biosynthesis pathway, caused major defects in cell division and morphology and reduced biofilm formation by
S. mutans
, indicative of a significant role of RGP in cell division and biofilm formation in
S. mutans
. These results are novel not only in
S. mutans
, but also other streptococci that produce RGP. This study also shows that the LytR-CpsA-Psr family proteins BrpA and Psr in
S. mutans
are involved in attachment of RGP and probably other cell wall glycopolymers to the peptidoglycan. In addition, the results also suggest that BrpA and Psr may play a direct role in cell division and biofilm formation in
S. mutans
. This study reveals new potential targets to develop anticaries therapeutics.
Genome-Scale Model and Omics Analysis of Metabolic Capacities of
Akkermansia muciniphila
Reveal a Preferential Mucin-Degrading Lifestyle
Authors: Ottman Noora , Davids Mark , Suarez-Diez Maria , Boeren Sjef , Schaap Peter J. , Martins dos Santos Vitor A. P. , Smidt Hauke , Belzer Clara , de Vos Willem M. 
Published: July 2017

ABSTRACT

The composition and activity of the microbiota in the human gastrointestinal tract are primarily shaped by nutrients derived from either food or the host. Bacteria colonizing the mucus layer have evolved to use mucin as a carbon and energy source. One of the members of the mucosa-associated microbiota is
Akkermansia muciniphila
, which is capable of producing an extensive repertoire of mucin-degrading enzymes. To further study the substrate utilization abilities of
A. muciniphila
, we constructed a genome-scale metabolic model to test amino acid auxotrophy, vitamin biosynthesis, and sugar-degrading capacities. The model-supported predictions were validated by
in vitro
experiments, which showed
A. muciniphila
to be able to utilize the mucin-derived monosaccharides fucose, galactose, and
N
-acetylglucosamine. Growth was also observed on
N
-acetylgalactosamine, even though the metabolic model did not predict this. The uptake of these sugars, as well as the nonmucin sugar glucose, was enhanced in the presence of mucin, indicating that additional mucin-derived components are needed for optimal growth. An analysis of whole-transcriptome sequencing (RNA-Seq) comparing the gene expression of
A. muciniphila
grown on mucin with that of the same bacterium grown on glucose confirmed the activity of the genes involved in mucin degradation and revealed most of these to be upregulated in the presence of mucin. The transcriptional response was confirmed by a proteome analysis, altogether revealing a hierarchy in the use of sugars and reflecting the adaptation of
A. muciniphila
to the mucosal environment. In conclusion, these findings provide molecular insights into the lifestyle of
A. muciniphila
and further confirm its role as a mucin specialist in the gut.

IMPORTANCE
Akkermansia muciniphila
is among the most abundant mucosal bacteria in humans and in a wide range of other animals. Recently,
A. muciniphila
has attracted considerable attention because of its capacity to protect against diet-induced obesity in mouse models. However, the physiology of
A. muciniphila
has not been studied in detail. Hence, we constructed a genome-scale model and describe its validation by transcriptomic and proteomic approaches on bacterial cells grown on mucus and glucose, a nonmucus sugar. The results provide detailed molecular insight into the mucus-degrading lifestyle of
A. muciniphila
and further confirm the role of this mucin specialist in producing propionate and acetate under conditions of the intestinal tract.
Host Specificity of Flagellins from Segmented Filamentous Bacteria Affects Their Patterns of Interaction with Mouse Ileal Mucosal Proteins
Authors: Chen Huahai , Yin Yeshi , Wang Yanling , Wang Xin , Xiang Charlie 
Published: July 2017

ABSTRACT

Segmented filamentous bacteria (SFB) are known modulators of the mammalian immune system. Currently, the technology for investigating SFB culture
in vitro
is immature, and as a result, the mechanisms of SFB colonization and immune regulation are not yet fully elucidated. In this study, we investigated the gene diversity and host specificity of SFB flagellin genes. The
fliC1
and
fliC2
genes are relatively conserved, while the
fliC3
and
fliC4
genes are more variable, especially at the central and C-terminal regions. Host specificity analysis demonstrated that the
fliC1
genes do not cluster together based on the host organism, whereas the
fliC3
and
fliC4
genes were host specific at the nucleotide and deduced amino acid levels. SFB flagellin protein expression in the ileum mucosa and cecal contents was detected by using fluorescence
in situ
hybridization (FISH) combined with immunohistochemical (IHC) analysis, immunoblotting, and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Although the purified SFB FliC3 protein originating from both mouse and rat was able to activate Toll-like receptor 5 (TLR5)-linked NF-κB signaling, no host specificity was observed. Interestingly, the patterns of interaction with mouse ileum mucosal proteins were different for mouse FliC3 (mFliC3) and rat FliC3 (rFliC3). Gene Ontology (GO) and KEGG analyses indicated that more adherence-related proteins interacted with mFliC3, while more lysosome- and proteolysis-related proteins interacted with rFliC3.
In vitro
degradation experiments indicated that the stability of rFliC3 was lower than that of mFliC3 when they were incubated with mouse ileum mucosal proteins. In summary, the gene diversity and host specificity of SFB flagellin genes were investigated, and SFB flagellin expression was detected in gut samples.

IMPORTANCE
Since SFB genomes contain only one copy of each FliC gene, the diversity of FliC is representative of SFB strain diversity. Currently, little is known regarding the diversity and specificity of members of the group of SFB. The work presented herein demonstrates that select SFB strains, exhibiting unique FliC patterns, are present in a variety of mammalian hosts. SFB
fliC
genes were found to interact with a number of unique targets, providing further evidence for SFB host selection. Together, this work represents a major advancement in identifying SFB and delineating how members of the group of SFB interact with the host. Future examination of FliC genes will likely enhance our knowledge of intestinal colonization by the gut microbiota.
High Temporal and Spatial Variability of Atmospheric-Methane Oxidation in Alpine Glacier Forefield Soils
Authors: Chiri Eleonora , Nauer Philipp A. , Rainer Edda-Marie , Zeyer Josef , Schroth Martin H. 
Published: July 2017

ABSTRACTGlacier forefield soils can provide a substantial sink for atmospheric CH4, facilitated by aerobic methane-oxidizing bacteria (MOB). However, MOB activity, abundance, and community structure may be affected by soil age, MOB location in different forefield landforms, and temporal fluctuations in soil physical parameters. We assessed the spatial and temporal variability of atmospheric-CH4oxidation in an Alpine glacier forefield during the snow-free season of 2013. We quantified CH4flux in soils of increasing age and in different landforms (sandhill, terrace, and floodplain forms) by using soil gas profile and static flux chamber methods. To determine MOB abundance and community structure, we employedpmoAgene-based quantitative PCR and targeted amplicon sequencing. Uptake of CH4increased in magnitude and decreased in variability with increasing soil age. Sandhill soils exhibited CH4uptake rates ranging from −3.7 to −0.03 mg CH4m−2day−1. Floodplain and terrace soils exhibited lower uptake rates and even intermittent CH4emissions. Linear mixed-effects models indicated that soil age and landform were the dominating factors shaping CH4flux, followed by cumulative rainfall (weighted sum ≤4 days prior to sampling). Of 31 MOB operational taxonomic units retrieved, ∼30% were potentially novel, and ∼50% were affiliated with upland soil clusters gamma and alpha. The MOB community structures in floodplain and terrace soils were nearly identical but differed significantly from the highly variable sandhill soil communities. We concluded that soil age and landform modulate the soil CH4sink strength in glacier forefields and that recent rainfall affects its short-term variability. This should be taken into account when including this environment in future CH4inventories.IMPORTANCEOxidation of methane (CH4) in well-drained, “upland” soils is an important mechanism for the removal of this potent greenhouse gas from the atmosphere. It is largely mediated by aerobic, methane-oxidizing bacteria (MOB). Whereas there is abundant information on atmospheric-CH4oxidation in mature upland soils, little is known about this important function in young, developing soils, such as those found in glacier forefields, where new sediments are continuously exposed to the atmosphere as a result of glacial retreat. In this field-based study, we investigated the spatial and temporal variability of atmospheric-CH4oxidation and associated MOB communities in Alpine glacier forefield soils, aiming at better understanding the factors that shape the sink for atmospheric CH4in this young soil ecosystem. This study contributes to the knowledge on the dynamics of atmospheric-CH4oxidation in developing upland soils and represents a further step toward the inclusion of Alpine glacier forefield soils in global CH4inventories.
Injury epidemiology of tennis players at the 2011–2016 Australian Open Grand Slam
Authors: Gescheit Danielle T , Cormack Stuart J , Duffield Rob , Kovalchik Stephanie , Wood Tim O , Omizzolo Melanie , Reid Machar 
Published: July 2017

AimTo examine the epidemiology and in-event treatment frequency of injury at the 2011–2016 Australian Open tournaments.MethodsInjury incidence was defined as a medical consultation by a tournament physician and in-event treatment frequency as the mean total number of follow-up medical/physiotherapy consultations (2013–2016 tournaments only). Data were collated by sex, injury region and type and reported as frequencies per 10 000 game exposures. Incidence rate s± 95% CI and rate ratios were used to test effects for injury, sex and year.ResultsFemale players experienced more injuries than male players (201.7 vs 148.6). The shoulder (5.1±1.1 injuries per year), foot (3.2±1.1), wrist (3.1±1.5) and knee (3.1±1.1) were the most commonly injured regions among females. Knee (3.5±1.6), ankle (2.3±1.3) and thigh (2.3±1.5) were the most prevalent male injuries. Upper arm injuries and in-event treatment frequency increased by ≥2.4 times in both sexes over the 5-year period. Muscle injuries were most frequent. There was a greater than twofold increase in men and women with stress fractures over the 5-year period. The torso region, including the neck, thoracic spine, trunk and abdominal, lumbar spine, hip and groin, pelvis/buttock, attracted high in-event treatment frequencies in both sexes.ConclusionInvestigation of injury at the Australian Open suggests that females are more commonly injured than males. Upper and lower extremity injuries affected females while lower limb injuries were more prominent in males. There was an increasing rate of in-event treatments of upper limb and torso injuries as well as stress fractures during the observation period.
Cancer-Associated Fibroblasts Share Characteristics and Protumorigenic Activity with Mesenchymal Stromal Cells
Authors: Borriello Lucia , Nakata Rie , Sheard Michael A. , Fernandez G. Esteban , Sposto Richard , Malvar Jemily , Blavier Laurence , Shimada Hiroyuki , Asgharzadeh Shahab , Seeger Robert C. , DeClerck Yves A. 
Published: July 2017

Abstract
Cancer-associated fibroblasts (CAF) have been suggested to originate from mesenchymal stromal cells (MSC), but their relationship with MSCs is not clear. Here, we have isolated from primary human neuroblastoma tumors a population of αFAP- and FSP-1–expressing CAFs that share phenotypic and functional characteristics with bone marrow–derived MSCs (BM-MSC). Analysis of human neuroblastoma tumors also confirmed the presence of αFAP- and FSP-1–positive cells in the tumor stroma, and their presence correlated with that of M2 tumor-associated macrophages. These cells (designated CAF-MSCs) enhanced in vitro neuroblastoma cell proliferation, survival, and resistance to chemotherapy and stimulated neuroblastoma tumor engraftment and growth in immunodeficient mice, indicating an effect independent of the immune system. The protumorigenic activity of MSCs in vitro and in xenografted mice was dependent on the coactivation of JAK2/STAT3 and MEK/ERK1/2 in neuroblastoma cells. In a mouse model of orthotopically implanted neuroblastoma cells, inhibition of JAK2/STAT3 and MEK/ERK/1/2 by ruxolitinib and trametinib potentiated tumor response to etoposide and increased overall survival. These data point to a new type of protumorigenic CAF in the tumor microenvironment of neuroblastoma and to STAT3 and ERK1/2 as mediators of their activity. Cancer Res; 77(18); 5142–57. ©2017 AACR.
Huwe1 Sustains Normal Ovarian Epithelial Cell Transformation and Tumor Growth through the Histone H1.3-H19 Cascade
Authors: Yang Dong , Sun Bin , Zhang Xiaohong , Cheng Daomei , Yu Xiaoping , Yan Lanzhen , Li Lei , An Sanqi , Jiang Hua , Lasorella Anna , Iavarone Antonio , Zhang Shu , Zou Fangdong , Zhao Xudong 
Published: July 2017

Abstract
Ubiquitination-directed protein degradation is important in many cancers for tumor initiation and maintenance, and E3 ligases containing HECT domains are emerging as new therapeutic targets. In contrast to many other E3 ligases, the role of HUWE1 in ovarian cancer where HUWE1 is dysregulated has been unclear. Here we report that genetic deletion of Huwe1 in the mouse inhibits transformation of ovary surface epithelium cells without significantly affecting cell survival and apoptosis, and that Huwe1 deletion after tumors have been initiated inhibits tumor growth. In Huwe1-deficient cells, expression of histone H1.3 increased, inhibiting the expression of noncoding RNA H19. H19 silencing phenocopied the effects of Huwe1 deficiency, whereas H1.3 silencing partially rescued the expression of H19 and the Huwe1-null phenotype. Inducible silencing of HUWE1 in human ovarian cancer cells produced a similar phenotype. Mechanistically, HUWE1 bound and ubiquitinated H1.3, which was consequently marked for destruction by proteasomes. Our results establish that HUWE1 plays an essential role in promoting ovarian cancer. Cancer Res; 77(18); 4773–84. ©2017 AACR.
Resistance to the Antibody–Drug Conjugate T-DM1 Is Based in a Reduction in Lysosomal Proteolytic Activity
Authors: Ríos-Luci Carla , García-Alonso Sara , Díaz-Rodríguez Elena , Nadal-Serrano Mercedes , Arribas Joaquín , Ocaña Alberto , Pandiella Atanasio 
Published: July 2017

Abstract
Trastuzumab-emtansine (T-DM1) is an antibody–drug conjugate (ADC) that was approved recently to treat HER2+ breast cancers. Despite its impressive clinical efficacy in many patients, intrinsic and acquired resistance to T-DM1 has emerged as a challenge. To identify mechanisms of T-DM1 resistance, we isolated several resistant HER2+ clones exhibiting stable drug refractoriness in vitro and in vivo. Genomic comparisons showed substantial differences among three of the isolated clones, indicating several potential mechanisms of resistance to T-DM1. However, we observed no differences in HER2 levels and signaling among the resistant models and parental HER2+ cells. Bioinformatics studies suggested that intracellular trafficking of T-DM1 could underlie resistance to T-DM1, and systematic analysis of the path followed by T-DM1 showed that the early steps in the internalization of the drug were unaltered. However, in some of the resistant clones, T-DM1 accumulated in lysosomes. In these clones, lysosomal pH was increased and the proteolytic activity of these organelles was deranged. These results were confirmed in T-DM1–resistant cells from patient-derived HER2+ samples. We postulate that resistance to T-DM1 occurs through multiple mechanisms, one of which is impaired lysosomal proteolytic activity. Because other ADC may use the same internalization-degradation pathway to deliver active payloads, strategies aimed at restoring lysosomal functionality might overcome resistance to ADC-based therapies and improve their effectiveness. Cancer Res; 77(17); 4639–51. ©2017 AACR.