bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neoliberalism: The Whys and Wherefores … and Future Directions
Authors: Birch Kean 
Published: July 2015

AbstractNeoliberalism means many things to many people. Often used indiscriminately to mean anything ‘bad’, neoliberalism is in need of dissection as an analytical category and a way of understanding the transformation of society over the last few decades. This paper is a brief introduction to neoliberalism and a number of key analytical approaches used to study it, including governmentality, Marxism, ideational analysis, history and philosophy of economics, institutional analysis, state/regulation theory, and human geography. It finishes with some suggestions for areas of further and future research.
What's Going on? Making Sense of the Role of the Media in the Arab Uprisings
Authors: Robertson Alexa 
Published: July 2015

AbstractThe article reviews recent scholarship on the role of the media in the Arab uprisings. After a summary of events, it sets out the debate between researchers who attribute a central and significant role to social media in the mobilizations that spread from Tunisia to Egypt and beyond in early 2011, and those who are more sceptical of such ‘techno‐enthusiasm’. Different theoretical perspectives on the media and protest are then presented, followed by an overview of empirical approaches to the topic. It is argued that the impact of social media must be viewed in relation to how they fit into wider media ecologies and social and political structures.
High School Dropouts After They Exit School: Challenges and Directions for Sociological Research
Authors: Campbell Colin 
Published: July 2015

AbstractSociological research on high school dropouts is largely concerned with who drops out of school and why. Research on the consequences of dropping out is less common. There are clear theoretical reasons to expect dropping out to have a direct and negative effect on life outcomes; however, empirically evaluating these theories is difficult because students who drop out are different from high school graduates in meaningful and complex ways. In this article, I first provide a brief review of sociological research on high school dropouts, emphasizing the demographics of dropouts and reasons for dropping out. I then discuss the possible role of human capital differences, signaling theory, and social closure in creating worse outcomes for high school dropouts and outline the empirical challenges to researching the effects of dropping out. I conclude by discussing avenues for future research and important unanswered questions about the consequences of dropping out.
Fragmented to Death: The Study of Violence and the Utility of Criminology
Authors: McGoldrick Stacy K. 
Published: July 2015

AbstractThis essay examines the current state of the field of criminology and argues that by under‐representing corporate violence, over‐representing street crime, and not often addressing political crime, criminology as a field is doing a disservice to our students. Further, the study of group violence and “new wars” could be enriched by the viewpoint of sociologists and criminologists.
A
cfr
-Like Gene from Clostridium difficile Confers Multiple Antibiotic Resistance by the Same Mechanism as the
cfr
Gene
Authors: Hansen Lykke H. , Vester Birte 
Published: July 2015

ABSTRACT

The Cfr RNA methyltransferase causes multiple resistances to peptidyl transferase inhibitors by methylation of A2503 23S rRNA. Many
cfr
-like gene sequences in the databases code for unknown functions. This study confirms that a Cfr-like protein from a
Peptoclostridium difficile
(formerly
Clostridium difficile
) strain does function as a Cfr protein. The enzyme is expressed in
Escherichia coli
and shows elevated MICs for five classes of antibiotics. A primer extension stop indicates a modification at A2503 in 23S rRNA.
Variation in the Microbiota of Ixodes Ticks with Regard to Geography, Species, and Sex
Authors: Van Treuren Will , Ponnusamy Loganathan , Brinkerhoff R. Jory , Gonzalez Antonio , Parobek Christian M. , Juliano Jonathan J. , Andreadis Theodore G. , Falco Richard C. , Ziegler Lorenza Beati , Hathaway Nicholas , Keeler Corinna , Emch Michael , Bailey Jeffrey A. , Roe R. Michael , Apperson Charles S. , Knight Rob , Meshnick Steven R. 
Published: July 2015

ABSTRACT

Ixodes scapularis
is the principal vector of Lyme disease on the East Coast and in the upper Midwest regions of the United States, yet the tick is also present in the Southeast, where Lyme disease is absent or rare. A closely related species,
I. affinis
, also carries the pathogen in the South but does not seem to transmit it to humans. In order to better understand the geographic diversity of the tick, we analyzed the microbiota of 104 adult
I. scapularis
and 13 adult
I. affinis
ticks captured in 19 locations in South Carolina, North Carolina, Virginia, Connecticut, and New York. Initially, ticks from 4 sites were analyzed by 454 pyrosequencing. Subsequently, ticks from these sites plus 15 others were analyzed by sequencing with an Illumina MiSeq machine. By both analyses, the microbiomes of female ticks were significantly less diverse than those of male ticks. The dissimilarity between tick microbiomes increased with distance between sites, and the state in which a tick was collected could be inferred from its microbiota. The genus
Rickettsia
was prominent in all locations.
Borrelia
was also present in most locations and was present at especially high levels in one site in western Virginia. In contrast, members of the family
Enterobacteriaceae
were very common in North Carolina
I. scapularis
ticks but uncommon in
I. scapularis
ticks from other sites and in North Carolina
I. affinis
ticks. These data suggest substantial variations in the
Ixodes
microbiota in association with geography, species, and sex.
Microbial Toluene Removal in Hypoxic Model Constructed Wetlands Occurs Predominantly via the Ring Monooxygenation Pathway
Authors: Martínez-Lavanchy P. M. , Chen Z. , Lünsmann V. , Marin-Cevada V. , Vilchez-Vargas R. , Pieper D. H. , Reiche N. , Kappelmeyer U. , Imparato V. , Junca H. , Nijenhuis I. , Müller J. A. , Kuschk P. , Heipieper H. J. 
Published: July 2015

ABSTRACT

In the present study, microbial toluene degradation in controlled constructed wetland model systems, planted fixed-bed reactors (PFRs), was queried with DNA-based methods in combination with stable isotope fractionation analysis and characterization of toluene-degrading microbial isolates. Two PFR replicates were operated with toluene as the sole external carbon and electron source for 2 years. The bulk redox conditions in these systems were hypoxic to anoxic. The autochthonous bacterial communities, as analyzed by Illumina sequencing of 16S rRNA gene amplicons, were mainly comprised of the families
Xanthomonadaceae
,
Comamonadaceae
, and
Burkholderiaceae
, plus
Rhodospirillaceae
in one of the PFR replicates. DNA microarray analyses of the catabolic potentials for aromatic compound degradation suggested the presence of the ring monooxygenation pathway in both systems, as well as the anaerobic toluene pathway in the PFR replicate with a high abundance of
Rhodospirillaceae
. The presence of catabolic genes encoding the ring monooxygenation pathway was verified by quantitative PCR analysis, utilizing the obtained toluene-degrading isolates as references. Stable isotope fractionation analysis showed low-level of carbon fractionation and only minimal hydrogen fractionation in both PFRs, which matches the fractionation signatures of monooxygenation and dioxygenation. In combination with the results of the DNA-based analyses, this suggests that toluene degradation occurs predominantly via ring monooxygenation in the PFRs.
The Genotoxin Colibactin Is a Determinant of Virulence in Escherichia coli K1 Experimental Neonatal Systemic Infection
Authors: McCarthy Alex J. , Martin Patricia , Cloup Emilie , Stabler Richard A. , Oswald Eric , Taylor Peter W. 
Published: July 2015

ABSTRACT

Escherichia coli
strains expressing the K1 capsule are a major cause of sepsis and meningitis in human neonates. The development of these diseases is dependent on the expression of a range of virulence factors, many of which remain uncharacterized. Here, we show that all but 1 of 34
E. coli
K1 neonatal isolates carried
clbA
and
clbP
, genes contained within the
pks
pathogenicity island and required for the synthesis of colibactin, a polyketide-peptide genotoxin that causes genomic instability in eukaryotic cells by induction of double-strand breaks in DNA. Inactivation of
clbA
and
clbP
in
E. coli
A192PP, a virulent strain of serotype O18:K1 that colonizes the gastrointestinal tract and translocates to the blood compartment with very high frequency in experimental infection of the neonatal rat, significantly reduced the capacity of A192PP to colonize the gut, engender double-strand breaks in DNA, and cause invasive, lethal disease. Mutation of
clbA
, which encodes a pleiotropic enzyme also involved in siderophore synthesis, impacted virulence to a greater extent than mutation of
clbP
, encoding an enzyme specific to colibactin synthesis. Restoration of colibactin gene function by complementation reestablished the fully virulent phenotype. We conclude that colibactin contributes to the capacity of
E. coli
K1 to colonize the neonatal gastrointestinal tract and to cause invasive disease in the susceptible neonate.
Chemorepulsion from the Quorum Signal Autoinducer-2 Promotes Helicobacter pylori Biofilm Dispersal
Authors: Anderson Jeneva K. , Huang Julie Y. , Wreden Christopher , Sweeney Emily Goers , Goers John , Remington S. James , Guillemin Karen 
Published: July 2015

ABSTRACT

The gastric pathogen
Helicobacter pylori
forms biofilms on abiotic and biotic surfaces. We have shown previously that
H. pylori
perceives the quorum signal autoinducer-2 (AI-2) as a chemorepellent. We report here that
H. pylori
chemorepulsion from endogenous AI-2 influences the proportions and spatial organization of cells within biofilms. Strains that fail to produce AI-2 (
∆luxS
strains) or are defective for chemotaxis (
∆cheA
strains) formed more spatially homogenous biofilms with a greater proportion of adherent versus planktonic cells than wild-type biofilms. Reciprocally, a strain that overproduced AI-2 (

luxS
OP

) formed biofilms with proportionally fewer adherent cells. Along with the known AI-2 chemoreceptor, TlpB, we identified AibA and AibB, two novel periplasmic binding proteins that are required for the AI-2 chemorepulsion response. Disruptions in any of the proteins required for AI-2 chemotaxis recapitulated the biofilm adherence and spatial organization phenotype of the
∆luxS
mutant. Furthermore, exogenous administration of AI-2 was sufficient to decrease the proportion of adherent cells in biofilms and promote dispersal of cells from biofilms in a chemotaxis-dependent manner. Finally, we found that disruption of AI-2 production or AI-2 chemotaxis resulted in increased clustering of cells in microcolonies on cultured epithelial cells. We conclude that chemotaxis from AI-2 is a determinant of
H. pylori
biofilm spatial organization and dispersal.

IMPORTANCE
Bacterial biofilms are ubiquitous in nature, but the mechanisms governing their assembly and spatial organization are not fully understood. Bacterial communication through quorum sensing has been shown to influence biofilm growth through the regulation of biofilm genes. Our study revealed a new role for quorum sensing in biofilms through rapid chemotactic responses to quorum signals. Specifically, we studied how chemorepulsion of
Helicobacter pylori
from the universal quorum signal autoinducer-2 (AI-2) shapes the spatial organization of its biofilms. We demonstrate that the chemorepulsive response of
H. pylori
to AI-2 is necessary to promote its dispersal from biofilms grown on both abiotic and biotic surfaces and is sufficient to promote dispersal in a chemotaxis-dependent manner. This work has broad implications for understanding the mechanisms by which endogenously produced microbial compounds shape the assembly and spatial organization of microbial communities in their environments.
Breastfeeding, lung volumes and alveolar size at school-age
Authors: Dogaru Cristian M , Narayanan Manjith , Spycher Ben D , Pescatore Anina M , Owers-Bradley John , Beardsmore Caroline S , Silverman Michael , Kuehni Claudia E 
Published: July 2015

BackgroundPrevious studies found larger lung volumes at school-age in formerly breastfed children, with some studies suggesting an effect modification by maternal asthma. We wanted to explore this further in children who had undergone extensive lung function testing. The current study aimed to assess whether breastfeeding was associated with larger lung volumes and, if so, whether all compartments were affected. We also assessed association of breastfeeding with apparent diffusion coefficient (ADC), which measures freedom of gas diffusion in alveolar-acinar compartments and is a surrogate of alveolar dimensions. Additionally, we assessed whether these effects were modified by maternal asthma.MethodsWe analysed data from 111 children and young adults aged 11–21 years, who had participated in detailed lung function testing, including spirometry, plethysmography and measurement of ADC of3Helium (3He) by MR. Information on breastfeeding came from questionnaires applied in early childhood (age 1–4 years). We determined the association between breastfeeding and these measurements using linear regression, controlling for potential confounders.ResultsWe did not find significant evidence for an association between duration of breastfeeding and lung volumes or alveolar dimensions in the entire sample. In breastfed children of mothers with asthma, we observed larger lung volumes and larger average alveolar size than in non-breastfed children, but the differences did not reach significance levels.ConclusionsConfirmation of effects of breastfeeding on lung volumes would have important implications for public health. Further investigations with larger sample sizes are warranted.
Combining an Aurora Kinase Inhibitor and a Death Receptor Ligand/Agonist Antibody Triggers Apoptosis in Melanoma Cells and Prevents Tumor Growth in Preclinical Mouse Models
Authors: Liu Yan , Hawkins Oriana E. , Vilgelm Anna E. , Pawlikowski Jeffrey S. , Ecsedy Jeffrey A. , Sosman Jeffrey A. , Kelley Mark C. , Richmond Ann 
Published: July 2015

Abstract
Purpose: Preclinical studies show that inhibition of aurora kinases in melanoma tumors induces senescence and reduces tumor growth, but does not cause tumor regression. Additional preclinical models are needed to identify agents that will synergize with aurora kinase inhibitors to induce tumor regression.
Experimental Design: We combined treatment with an aurora kinase A inhibitor, MLN8237, with agents that activate death receptors (Apo2L/TRAIL or death receptor 5 agonists) and monitored the ability of this treatment to induce tumor apoptosis and melanoma tumor regression using human cell lines and patient-derived xenograft (PDX) mouse models.
Results: We found that this combined treatment led to apoptosis and markedly reduced cell viability. Mechanistic analysis showed that the induction of tumor cell senescence in response to the AURKA inhibitor resulted in a decreased display of Apo2L/TRAIL decoy receptors and increased display of one Apo2L/TRAIL receptor (death receptor 5), resulting in enhanced response to death receptor ligand/agonists. When death receptors were activated in senescent tumor cells, both intrinsic and extrinsic apoptotic pathways were induced independent of BRAF, NRAS, or p53 mutation status. Senescent tumor cells exhibited BID-mediated mitochondrial depolarization in response to Apo2L/TRAIL treatment. In addition, senescent tumor cells had a lower apoptotic threshold due to decreased XIAP and survivin expression. Melanoma tumor xenografts of one human cell line and one PDX displayed total blockage of tumor growth when treated with MLN8237 combined with DR5 agonist antibody.
Conclusions: These findings provide a strong rationale for combining senescence-inducing therapeutics with death receptor agonists for improved cancer treatment. Clin Cancer Res; 21(23); 5338–48. ©2015 AACR.
Stool Bacteriomic Profiling in Patients with Metastatic Renal Cell Carcinoma Receiving Vascular Endothelial Growth Factor–Tyrosine Kinase Inhibitors
Authors: Pal Sumanta K. , Li Sierra M. , Wu Xiwei , Qin Hanjun , Kortylewski Marcin , Hsu JoAnn , Carmichael Courtney , Frankel Paul 
Published: July 2015

Abstract
Purpose: Diarrhea occurs in approximately half of patients with metastatic renal cell carcinoma (mRCC) receiving vascular endothelial growth factor–tyrosine kinase inhibitors (VEGF-TKI). We evaluated the relationship between VEGF-TKI–related diarrhea and stool microbiota.
Experimental Design: Stool samples were collected from 20 mRCC patients receiving VEGF-TKIs. 16S rRNA sequencing was used to characterize the stool bacteriomic profiling of patients. Assay validation with Salmonella typhimurium spike-in experiments suggested greatest speciation with use of the V5 region.
Results: Higher levels of Bacteroides spp. and lower levels of Prevotella spp. were found in patients with diarrhea. In addition, patients receiving VEGF-TKIs with mRCC appeared to have less relative abundance of Bifidobacterium spp. as compared with previous reports based on healthy subjects.
Conclusions: We have thus demonstrated interplay between microbiota and VEGF-TKI–induced diarrhea. Further studies are warranted to evaluate the potential causative role of preexisting dysbiosis in VEGF-TKI–related diarrhea. Clin Cancer Res; 21(23); 5286–93. ©2015 AACR.
Moving Beyond “Lumpology”: PET/CT Imaging of Pheochromocytoma and Paraganglioma
Authors: Hofman Michael S. , Hicks Rodney J. 
Published: July 2015

Abstract
High somatostatin receptor expression on the cell membrane of succinate dehydrogenase mutation-related pheochromocytoma and paraganglioma provides a potential target for imaging and therapy. 68Ga-DOTATATE positron emission PET/CT may represent a new gold standard for staging pheochromocytoma/paraganglioma and have future therapeutic implications. Clin Cancer Res; 21(17); 3815–7. ©2015 AACR.
See related article by Janssen et al., p. 3888
High-Sensitivity Cardiac Troponin T and Risk of Hypertension
Authors: McEvoy John W. , Chen Yuan , Nambi Vijay , Ballantyne Christie M. , Sharrett A. Richey , Appel Lawrence J. , Post Wendy S. , Blumenthal Roger S. , Matsushita Kunihiro , Selvin Elizabeth 
Published: July 2015

Background—
The diagnosis of hypertension is often preceded by cardiac structural abnormalities. Thus, we assessed whether high-sensitivity cardiac troponin T (hs-cTnT), a marker of subclinical myocardial damage, can identify individuals at risk for hypertension or left ventricular hypertrophy.

Methods and Results—

We studied 6516 Atherosclerosis Risk in Communities (ARIC) Study participants who were free of prevalent hypertension and cardiovascular disease at baseline (1990–1992). We examined the association of baseline hs-cTnT categories with incident diagnosed hypertension (defined by self-report of a diagnosis or medication use during a maximum of 19.9 years of follow-up) and with incident visit-based hypertension (defined by self-report, medication use, or measured blood pressure >140/90 mm Hg over 6 years). Relative to hs-cTnT <5 ng/L, adjusted hazard ratios for incident diagnosed hypertension were 1.16 (95% confidence interval, 1.08–1.25) for individuals with hs-cTnT of 5 to 8 ng/L, 1.29 (95% confidence interval, 1.14–1.47) for hs-cTnT of 9 to 13 ng/L, and 1.31 (95% confidence interval, 1.07–1.61) for hs-cTnT ≥14ng/L (
P
for trend <0.001). Associations were stronger for incident visit-based hypertension. These associations were driven by higher relative hazard in normotensive people (compared with those with prehypertension;
P
for interaction=0.001). Baseline hs-cTnT was also strongly associated with incident left ventricular hypertrophy by electrocardiography over 6 years (eg, adjusted hazard ratio, 5.19 [95% confidence interval, 1.49–18.08] for hs-cTnT ≥14 versus <5 ng/L). Findings were not appreciably changed after accounting for competing deaths or adjusting for baseline blood pressure levels or N-terminal probrain natriuretic peptide.

Conclusions—
In an ambulatory population with no history of cardiovascular disease, hs-cTnT was associated with incident hypertension and risk of left ventricular hypertrophy. Further research is needed to determine whether hs-cTnT can identify people who may benefit from ambulatory blood pressure monitoring or hypertension prevention lifestyle strategies.
Relationship Between Cancer and Cardiovascular Outcomes Following Percutaneous Coronary Intervention
Authors: Hess Connie N. , Roe Matthew T. , Clare Robert M. , Chiswell Karen , Kelly Joseph , Tcheng James E. , Hagstrom Emil , James Stefan K. , Khouri Michel G. , Hirsch Bradford R. , Kong David F. , Abernethy Amy P. , Krucoff Mitchell W. 
Published: July 2015

Background
Cardiovascular disease and cancer increasingly coexist, yet relationships between cancer and long‐term cardiovascular outcomes post–percutaneous coronary intervention (PCI) are not well studied.

Methods and Results

We examined stented PCI patients at Duke (1996–2010) using linked data from the Duke Information Systems for Cardiovascular Care and the Duke Tumor Registry (a cancer treatment registry). Our primary outcome was cardiovascular mortality. Secondary outcomes included composite cardiovascular mortality, myocardial infarction, or repeat revascularization and all‐cause mortality. We used adjusted cause‐specific hazard models to examine outcomes among cancer patients (cancer treatment pre‐PCI) versus controls (no cancer treatment pre‐PCI). Cardiovascular mortality was explored in a cancer subgroup with recent (within 1 year pre‐PCI) cancer and in post‐PCI cancer patients using post‐PCI cancer as a time‐dependent variable. Among 15 008 patients, 3.3% (n=496) were cancer patients. Observed rates of 14‐year cardiovascular mortality (31.4% versus 27.7%,
P
=0.31) and composite cardiovascular death, myocardial infarction, or revascularization (51.1% versus 55.8%,
P
=0.37) were similar for cancer versus control groups; all‐cause mortality rates were higher (79.7% versus 49.3%,
P
<0.01). Adjusted risk of cardiovascular mortality was similar for cancer patients versus controls (hazard ratio 0.95; 95% CI 0.76 to 1.20) and for patients with versus without recent cancer (hazard ratio 1.46; 95% CI 0.92 to 2.33). Post‐PCI cancer, present in 4.3% (n=647) of patients, was associated with cardiovascular mortality (adjusted hazard ratio 1.51; 95% CI 1.11 to 2.03).

Conclusions
Cancer history was present in a minority of PCI patients but was not associated with worse long‐term cardiovascular outcomes. Further investigation into PCI outcomes in this population is warranted.