bluuebunny/crossref_metadata_2025_split huggingface dataset:
Harmonic analysis for the characterization and correction of geometric distortion in MRI
Authors: Tadic Tony , Jaffray David A. , Stanescu Teodor 
Published: October 2014

Purpose:Magnetic resonance imaging (MRI) is gaining widespread use in radiation therapy planning, patient setup verification, and real‐time guidance of radiation delivery. Successful implementation of these technologies relies on the development of simple and efficient methods to characterize and monitor the geometric distortions arising due to system imperfections and gradient nonlinearities. To this end, the authors present the theory and validation of a novel harmonic approach to the quantification of system‐related distortions in MRI.Methods:The theory of spatial encoding in MRI is applied to demonstrate that the 3D distortion vector field (DVF) is given by the solution of a second‐order boundary value problem (BVP). This BVP is comprised of Laplace's equation and a limited measurement of the distortion on the boundary of a specified region of interest (ROI). An analytical series expansion solving this BVP within a spherical ROI is obtained, and a statistical uncertainty analysis is performed to determine how random errors in the boundary measurements propagate to the ROI interior. This series expansion is then evaluated to obtain volumetric DVF mappings that are compared to reference data obtained on a 3 T full‐body scanner. This validation is performed within two spheres of 20 cm diameter (one centered at the scanner origin and the other offset +3 cm along each of the transverse directions). Initially, a high‐order mapping requiring measurements at 5810 boundary points is used. Then, after exploring the impact of the boundary sampling density and the effect of series truncation, a reduced‐order mapping requiring measurements at 302 boundary points is evaluated.Results:The volumetric DVF mappings obtained from the harmonic analysis are in good agreement with the reference data. Following distortion correction using the high‐order mapping, the authors estimate a reduction in the mean distortion magnitude from 0.86 to 0.42 mm and from 0.93 to 0.39 mm within the central and offset ROIs, respectively. In addition, the fraction of points with a distortion magnitude greater than 1 mm is reduced from 35.6% to 2.8% and from 40.4% to 1.5%, respectively. Similarly, following correction using the reduced‐order mapping, the mean distortion magnitude reduces to 0.45–0.42 mm within the central and offset ROIs, and the fraction of points with a distortion magnitude greater than 1 mm is reduced to 2.8% and 1.5%, respectively.Conclusions:A novel harmonic approach to the characterization of system‐related distortions in MRI is presented. This method permits a complete and accurate mapping of the DVF within a specified ROI using a limited measurement of the distortion on the ROI boundary. This technique eliminates the requirement to exhaustively sample the DVF at a dense 3D array of points, thereby permitting the design of simple, inexpensive phantoms that may incorporate additional modules for auxiliary quality assurance objectives.
Genome Assembly of Shigella flexneri ATCC 12022, a Quality Control Reference Strain
Authors: Daligault H. E. , Davenport K. W. , Minogue T. D. , Bishop-Lilly K. A. , Broomall S. M. , Bruce D. C. , Chain P. S. , Coyne S. R. , Freitas T. , Frey K. G. , Gibbons H. S. , Jaissle J. , Lo C.-C. , Meincke L. , Munk A. C. , Redden C. L. , Rosenzweig C. N. , Johnson S. L. 
Published: October 2014

ABSTRACT

Shigella flexneri
causes shigellosis, severe and potentially life-threatening diarrhea, and accounts for 18% of shigellosis cases in the United States. Here, we present the 4.51-Mbp genome assembly of
S. flexneri
ATCC 12022, a quality control and reference strain, in 10 scaffolds.
Draft Genome Sequence of the Plant-Pathogenic Soil Fungus Rhizoctonia solani Anastomosis Group 3 Strain Rhs1AP
Authors: Cubeta Marc A. , Thomas Elizabeth , Dean Ralph A. , Jabaji Suha , Neate Stephen M. , Tavantzis Stellos , Toda Takeshi , Vilgalys Rytas , Bharathan Narayanaswamy , Fedorova-Abrams Natalie , Pakala Suman B. , Pakala Suchitra M. , Zafar Nikhat , Joardar Vinita , Losada Liliana , Nierman William C. 
Published: October 2014

ABSTRACT

The soil fungus
Rhizoctonia solani
is a pathogen of agricultural crops. Here, we report on the 51,705,945 bp draft consensus genome sequence of
R. solani
strain Rhs1AP. A comprehensive understanding of the heterokaryotic genome complexity and organization of
R. solani
may provide insight into the plant disease ecology and adaptive behavior of the fungus.
Whole-Genome Shotgun Sequence of Bacillus mojavensis Strain RRC101, an Endophytic Bacterium Antagonistic to the Mycotoxigenic Endophytic Fungus
Fusarium verticillioides
Authors: Gold S. E. , Blacutt A. A. , Meinersmann R. J. , Bacon C. W. 
Published: October 2014

ABSTRACT

Here, we report the whole-genome shotgun sequence of
Bacillus mojavensis
strain RRC101, isolated from a maize kernel. This strain is antagonistic to the mycotoxigenic plant pathogen
Fusarium verticillioides
and grows within maize tissue, suggesting potential as an endophytic biocontrol agent.
Draft Genome Sequence of Colistin-Only-Susceptible Pseudomonas aeruginosa Strain ST235, a Hypervirulent High-Risk Clone in Spain
Authors: Viedma Esther , Villa Jenifer , Juan Carlos , Oliver Antonio , Chaves Fernando 
Published: October 2014

ABSTRACT

We report the genome of colistin-only-susceptible
Pseudomonas aeruginosa
strain ST235 (PA_ST235). This isolate was obtained in the setting of an outbreak in a tertiary hospital in Spain. This clone was apparently associated with a significantly higher mortality rate. The ST235 clone also appears to be associated with greater virulence.
Understanding the impacts of care farms on health and well-being of disadvantaged populations: a protocol of the Evaluating Community Orders (ECO) pilot study
Authors: Elsey H , Bragg R , Elings M , Cade J E , Brennan C , Farragher T , Tubeuf S , Gold R , Shickle D , Wickramasekera N , Richardson Z , Murray J 
Published: October 2014

IntroductionCare farms, where all or part of the farm is used for therapeutic purposes, show much potential for improving the health and well-being of a range of disadvantaged groups. Studies to date have been qualitative or observational, with limited empirical evidence of the effectiveness of care farms in improving health and well-being. Understanding the underlying mechanisms that lead to improvements for different disadvantaged groups is a further gap in the evidence. Participants in this study are offenders serving community orders. Their low socioeconomic status and poor health outcomes relative to the general population exemplifies disadvantage.Methods and analysisThis paper describes the protocol of a study to understand the impacts of care farms and to pilot the design and tools for a study to assess cost-effectiveness of care farms in improving the quality of life of offenders. As a pilot study, no power calculation has been conducted. However, 150 offenders serving community sentences on care farms and 150 on other probation locations (eg, litter picking, painting) will be recruited over a 1-year period. Changes in quality of life, measured by Clinical Outcome in Routine Evaluation–Outcome Measure, health and reconvictions of offenders at care farms compared to other probation locations will be analysed to inform the sample size calculation for the follow on study. The feasibility of recruitment, retention, collecting cost data and modelling cost-effectiveness will also be assessed. The study will use qualitative methods to explore the experiences of offenders attending care farms and perceptions of probation and care farm staff on the processes and impacts of the intervention.Ethics and disseminationFindings will be published and inform development of a natural experiment and will be disseminated to probation services, care farms and academics. University of Leeds Ethical Review Board approved: SoMREC/13/014. National Offender Management Service (NOMS) approved: 2013-257.
The influence of aortoseptal angulation on provocable left ventricular outflow tract obstruction in hypertrophic cardiomyopathy
Authors: Critoph Christopher Howell , Pantazis Antonios , Tome Esteban Maria Teresa , Salazar-Mendiguchía Joel , Pagourelias Efstathios D , Moon James C , Elliott Perry Mark 
Published: October 2014

ObjectivesAortoseptal angulation (AoSA) can predict provocable left ventricular outflow tract obstruction (LVOTO) in patients with symptomatic hypertrophic cardiomyopathy (HCM). Lack of a standardised measurement technique in HCM without the need for complex three-dimensional (3D) imaging limits its usefulness in routine clinical practice. This study aimed to validate a simple measurement of AoSA using 2D echocardiography and cardiac MR (CMR) imaging as a predictor of LVOTO.MethodsWe retrospectively assessed 160 patients with non-obstructive HCM, referred for exercise stress echocardiography. AoSA was measured using resting 2D echocardiography in all patients, and CMR in 29. Twenty-five controls with normal echocardiograms were used for comparison.ResultsPatients with HCM had a reduced AoSA compared with controls (113°±12 vs 126°±6), p<0.0001. Sixty (38%) patients had provocable LVOTO, with smaller angles than non-obstructive patients (108°±12 vs 116°±12, p<0.0001). AoSA, degree of mitral valvular regurgitation and incomplete systolic anterior motion (SAM) were associated with peak left ventricular outflow tract gradient (r=0.508, p<0.0001). An angle ≤100° had 27% sensitivity, 91% specificity and 59% positive predictive value for predicting provocable LVOTO. When combined with SAM, specificity was 99% and positive predictive value 88%. Intraclass correlation coefficient of AoSA measured by two observers was 0.901 (p<0.0001). Bland-Altman analysis of echocardiographic AoSA showed good agreement with the CMR-derived angle.ConclusionsMeasurement of AoSA using echocardiography in HCM is easy, reproducible and comparable to CMR. Patients with provocable LVOTO have reduced angles compared with non-obstructive patients. AoSA is highly specific for provocable LVOTO and should prompt further evaluation in symptomatic patients without resting obstruction.
Type I Cytokines Synergize with Oncogene Inhibition to Induce Tumor Growth Arrest
Authors: Acquavella Nicolas , Clever David , Yu Zhiya , Roelke-Parker Melody , Palmer Douglas C. , Xi Liqiang , Pflicke Holger , Ji Yun , Gros Alena , Hanada Ken-ichi , Goldlust Ian S. , Mehta Gautam U. , Klebanoff Christopher A. , Crompton Joseph G. , Sukumar Madhusudhanan , Morrow James J. , Franco Zulmarie , Gattinoni Luca , Liu Hui , Wang Ena , Marincola Francesco , Stroncek David F. , Lee Chyi-Chia R. , Raffeld Mark , Bosenberg Marcus W. , Roychoudhuri Rahul , Restifo Nicholas P. 
Published: October 2014

Abstract
Both targeted inhibition of oncogenic driver mutations and immune-based therapies show efficacy in treatment of patients with metastatic cancer, but responses can be either short lived or incompletely effective. Oncogene inhibition can augment the efficacy of immune-based therapy, but mechanisms by which these two interventions might cooperate are incompletely resolved. Using a novel transplantable BRAFV600E-mutant murine melanoma model (SB-3123), we explored potential mechanisms of synergy between the selective BRAFV600E inhibitor vemurafenib and adoptive cell transfer (ACT)–based immunotherapy. We found that vemurafenib cooperated with ACT to delay melanoma progression without significantly affecting tumor infiltration or effector function of endogenous or adoptively transferred CD8+ T cells, as previously observed. Instead, we found that the T-cell cytokines IFNγ and TNFα synergized with vemurafenib to induce cell-cycle arrest of tumor cells in vitro. This combinatorial effect was recapitulated in human melanoma–derived cell lines and was restricted to cancers bearing a BRAFV600E mutation. Molecular profiling of treated SB-3123 indicated that the provision of vemurafenib promoted the sensitization of SB-3123 to the antiproliferative effects of T-cell effector cytokines. The unexpected finding that immune cytokines synergize with oncogene inhibitors to induce growth arrest has major implications for understanding cancer biology at the intersection of oncogenic and immune signaling and provides a basis for design of combinatorial therapeutic approaches for patients with metastatic cancer. Cancer Immunol Res; 3(1); 37–47. ©2014 AACR.
See related commentary by Riddell, p. 23
High Plasma Levels of Heparin-Binding Epidermal Growth Factor Are Associated With a More Stable Plaque Phenotype and Reduced Incidence of Coronary Events
Authors: Rattik Sara , Wigren Maria , Björkbacka Harry , Fredrikson Gunilla Nordin , Hedblad Bo , Siegbahn Agneta , Bengtsson Eva , Schiopu Alexandru , Edsfeldt Andreas , Dunér Pontus , Grufman Helena , Gonçalves Isabel , Nilsson Jan 
Published: October 2014

Objective—
Rupture of atherosclerotic plaques is the major cause of acute coronary events (CEs). Plaque destabilization is the consequence of an imbalance between inflammatory-driven degradation of fibrous tissue and smooth muscle cell–dependent tissue repair. Proinflammatory factors have been documented extensively as biomarkers of cardiovascular risk but factors that contribute to stabilization of atherosclerotic plaques have received less attention. The present study aimed to investigate whether plasma levels of the smooth muscle cell growth factor epidermal growth factor (EGF), heparin-binding-EGF (HB-EGF), and platelet-derived growth factor correlate with plaque phenotype and incidence of CEs.

Approach and Results—

HB-EGF, EGF and platelet-derived growth factor were measured in plasma from 202 patients undergoing carotid endarterectomy and in 384 incident CE cases and 409 matched controls recruited from the Malmö Diet and Cancer cohort. Significant positive associations were found between the plasma levels of all 3 growth factors and the collagen and elastin contents of the removed plaques. CE cases in the Malmö Diet and Cancer cohort had lower levels of HB-EGF in plasma, whereas no significant differences were found for EGF and platelet-derived growth factor. After adjusting for cardiovascular risk factors in a Cox proportional hazard model, the hazard ratio for the highest HB-EGF tertile was 0.61 (95% confidence interval, 0.47–0.82;
P
<0.001).

Conclusions—
The associations between high levels of smooth muscle cell growth factors in plasma and a more fibrous plaque phenotype as well as the association between low levels of HB-EGF and incident CEs point to a potential clinically important role for factors that contribute to plaque stabilization by stimulating smooth muscle cells.
Protein Kinase C δ Deficiency Enhances Megakaryopoiesis and Recovery From Thrombocytopenia
Authors: Kostyak John C. , Bhavanasi Dheeraj , Liverani Elisabeta , McKenzie Steven E. , Kunapuli Satya P. 
Published: October 2014

Objective—
We previously determined that protein kinase C δ (PKCδ) regulates platelet function. However, the function of PKCδ in megakaryopoiesis is unknown.

Approach and Results—

Using PKCδ
-/-
and wild-type littermate mice, we found that deficiency of PKCδ caused an increase in white blood cells and platelet counts, as well as in bone marrow and splenic megakaryocytes (
P
<0.05). Additionally, the megakaryocyte number and DNA content were enhanced in PKCδ
-/-
mouse bone marrow after culturing with exogenous thrombopoietin compared with wild-type (
P
<0.05). Importantly, thrombopoietin-induced signaling was also altered with PKCδ deletion because both extracellular signal-regulated kinase and Akt308 phosphorylation were heightened in PKCδ
-/-
megakaryocytes compared with wild-type. Finally, PKCδ
-/-
mice recovered faster and had a heightened rebound thrombocytosis after thrombocytopenic challenge.

Conclusions—
These data suggest that PKCδ is an important megakaryopoietic protein, which regulates signaling induced by thrombopoietin and represents a potential therapeutic target.
Transdifferentiation of Human Fibroblasts to Endothelial Cells
Authors: Sayed Nazish , Wong Wing Tak , Ospino Frank , Meng Shu , Lee Jieun , Jha Arshi , Dexheimer Phillip , Aronow Bruce J. , Cooke John P. 
Published: October 2014

Background—
Cell fate is fluid and may be altered experimentally by the forced expression of master regulators mediating cell lineage. Such reprogramming has been achieved with the use of viral vectors encoding transcription factors. We recently discovered that the viral vectors are more than passive vehicles for transcription factors because they participate actively in the process of nuclear reprogramming to pluripotency by increasing epigenetic plasticity. On the basis of this recognition, we hypothesized that small-molecule activators of toll-like receptor 3, together with external microenvironmental cues that drive endothelial cell (EC) specification, might be sufficient to induce transdifferentiation of fibroblasts into ECs (induced ECs).

Methods and Results—
We show that toll-like receptor 3 agonist Poly I:C, combined with exogenous EC growth factors, transdifferentiated human fibroblasts into ECs. These induced ECs were comparable to human dermal microvascular ECs in immunohistochemical, genetic, and functional assays, including the ability to form capillary-like structures and to incorporate acetylated low-density lipoprotein. Furthermore, induced ECs significantly improved limb perfusion and neovascularization in the murine ischemic hindlimb. Finally, using genetic knockdown studies, we found that the effective transdifferentiation of human fibroblasts to ECs requires innate immune activation.

Conclusions—
This study suggests that manipulation of innate immune signaling may be generally used to modify cell fate. Because similar signaling pathways are activated by damage-associated molecular patterns, epigenetic plasticity induced by innate immunity may play a fundamental role in transdifferentiation during wound healing and regeneration. Finally, this study is a first step toward development of a small-molecule strategy for therapeutic transdifferentiation for vascular disease.
L-Kynurenine/Aryl Hydrocarbon Receptor Pathway Mediates Brain Damage After Experimental Stroke
Authors: Cuartero María I. , Ballesteros Iván , de la Parra Juan , Harkin Andrew L. , Abautret-Daly Aine , Sherwin Eoin , Fernández-Salguero Pedro , Corbí Ángel L. , Lizasoain Ignacio , Moro María A. 
Published: October 2014

Background—
Aryl hydrocarbon receptor (AhR) is a transcription factor that belongs to the basic helix-loop-helix PAS (Per-Arnt-Sim homology domain) family known to mediate the toxic and carcinogenic effects of xenobiotics. Interestingly, AhR is widely expressed in the central nervous system, but its physiological and pathological roles are still unclear.

Methods and Results—
To define the role of AhR in stroke, we used middle cerebral artery occlusion in mice and oxygen-glucose deprivation in rat cortical neurons. The results presented here show that the ischemic insult increases total and nuclear AhR levels and AhR transcriptional activity in neurons in vivo and in vitro. We also show that AhR has a causal role in acute ischemic damage because pharmacological or genetic loss-of-function approaches result in neuroprotection. Inhibition of cAMP response element-binding protein–dependent signaling may participate in the deleterious actions of AhR. Finally, we have also found that L-kynurenine, a tryptophan metabolite with AhR agonistic properties, is an endogenous ligand that mediates AhR activation in the brain after middle cerebral artery occlusion.

Conclusions—
Our data demonstrate that an L-kynurenine/AhR pathway mediates acute brain damage after stroke and open new possibilities for the diagnosis and treatment of this pathology.
Varying Definitions for Periprocedural Myocardial Infarction Alter Event Rates and Prognostic Implications
Authors: Idris Hanan , Lo Sidney , Shugman Ibrahim M. , Saad Yousef , Hopkins Andrew P. , Mussap Christian , Leung Dominic , Thomas Liza , Juergens Craig P. , French John K. 
Published: October 2014

Background

Periprocedural myocardial infarction (
PMI
) has had several definitions in the last decade, including the Society for Cardiovascular Angiography and Interventions (
SCAI
) definition, that requires marked biomarker elevations congruent with surgical
PMI
criteria.

Methods and Results

The aim of this study was to examine the definition‐based frequencies of
PMI
and whether they influenced the reported association between
PMI
and increased rates of late death/ myocardial infarction (
MI
). We studied 742 patients; 492 (66%) had normal troponin T (TnT) levels and 250 (34%) had elevated, but stable or falling, TnT levels.
PMI
, using the 2007 and the 2012 universal definition, occurred in 172 (23.2%) and in 99 (13.3%) patients, respectively, whereas 19 (2.6%) met the
SCAI PMI
definition (
P
<0.0001). Among patients with
PMI
using the 2012 definition, occlusion of a side branch ≤1 mm occurred in 48 patients (48.5%) and was the most common angiographic finding for
PMI
. The rates of death/
MI
at 2 years in patients with, compared to those without,
PMI
was 14.7% versus 10.1% (
P
=0.087) based on the 2007 definition, 16.9% versus 10.3% (
P
=0.059) based on the 2012 definition, and 29.4% versus 10.7% (
P
=0.015) based on the
SCAI
definition.

Conclusion

In this study,
PMI
, according to the
SCAI
definition, was associated with more‐frequent late death/
MI
, with ≈20% of all patients, who had
PMI
using the 2007 universal
MI
definition, not having
SCAI
‐defined
PMI
. Categorizing these latter patients as
SCAI
‐defined no
PMI
did not alter the rate of death/
MI
among no‐
PMI
patients.
Local SST Impacts on the Summertime Mascarene High Variability
Authors: Morioka Yushi , Takaya Koutarou , Behera Swadhin K. , Masumoto Yukio 
Published: October 2014

Abstract
The interannual variations in the summertime Mascarene high have great impacts on the southern African climate as well as the sea surface temperature (SST) in the southern Indian Ocean. A set of coupled general circulation model (CGCM) experiments are performed to examine a role of the interannual SST variability in the southern Indian Ocean on the summertime Mascarene high variability. The dominant interannual variability in the summertime Mascarene high shows the strengthening (weakening) in its southern part throughout the austral summer (December–February). However, in the experiment where the interannual SST variability in the southern Indian Ocean is suppressed, the strengthening (weakening) of the Mascarene high in its southern part does not persist until February. Also, the Mascarene high variability and its associated SST anomalies in December and January are found to increase (decrease) the southern African rainfall via more (less) moisture supply from the southern Indian Ocean. The Mascarene high variability is actually associated with a meridional dipole of positive and negative SST anomalies, which in turn produces that of the meridional SST gradient anomaly. This causes a southward (northward) shift of the storm tracks and hence the westerly jet, favoring the strengthening (weakening) of the Mascarene high in its southern part. This local ocean–atmosphere feedback effectively operates in February, when the meridional dipole of the SST anomalies reaches the maximum. These results provide new insight into the important role of the local SST variability in the summertime Mascarene high variability and hence the southern African climate.