bluuebunny/crossref_metadata_2025_split huggingface dataset:
Are Quantitative Bacterial Wound Cultures Useful?
Authors: Kallstrom George 
Published: March 2014

ABSTRACT
Determining if a nonhealing wound is infected can be difficult. The surface of a wound is not sterile and can be colonized with numerous commensal, environmental, and potentially pathogenic microorganisms. Different types of wounds have various clinical presentations, with some signs and symptoms more likely to be present than others depending on the type and location of the wound. Clinicians often order microbiology wound cultures to assist in determining if a nonhealing wound is infected. This minireview briefly summarizes the clinical microbiology of wound cultures, with an emphasis on the history and utility (or lack thereof) of the quantitative wound culture.
Point-Counterpoint: The Automated Clinical Microbiology Laboratory: Fact or Fantasy?
Authors: Ledeboer Nathan A. , Dallas Steven D. 
Published: March 2014

ABSTRACT
Automated chemistry laboratories dependent on robotic processes are the standard in both academic and large community hospital settings. Diagnostic microbiology manufacturers are betting that robotics will be used for specimen processing, plate reading, and organism identification in the near future. These systems are highly complex and have large footprints and hefty price tags. However, they are touted as being more efficient, rapid, and accurate than standard processes. Certain features, such as image collection, are highly innovative. Hospital administrators may be swayed to institute these new systems because of the promise of the need for fewer skilled workers, higher throughput, and greater efficiency. They also may be swayed by the fact that workers with the requisite clinical microbiology skills are becoming more difficult to find, and this technology should allow fewer skilled workers to handle larger numbers of cultures. In this Point-Counterpoint, Nate Ledeboer, Medical Director, Clinical Microbiology and Molecular Diagnostics, Dynacare Laboratories, and Froedtert Hospital, Milwaukee, WI, will explain why he believes that this approach will become widespread, while Steve Dallas of the University of Texas Health Science Center San Antonio explains why he thinks that this automation may not become widely used.
Improved Detection Limit in Rapid Detection of Human Enterovirus 71 and Coxsackievirus A16 by a Novel Reverse Transcription–Isothermal Multiple-Self-Matching-Initiated Amplification Assay
Authors: Ding Xiong , Nie Kai , Shi Lei , Zhang Yong , Guan Li , Zhang Dan , Qi Shunxiang , Ma Xuejun 
Published: March 2014

ABSTRACT

Rapid detection of human enterovirus 71 (EV71) and coxsackievirus A16 (CVA16) is important in the early phase of hand-foot-and-mouth disease (HFMD). In this study, we developed and evaluated a novel reverse transcription–isothermal multiple-self-matching-initiated amplification (RT-IMSA) assay for the rapid detection of EV71 and CVA16 by use of reverse transcriptase, together with a strand displacement DNA polymerase. Real-time RT-IMSA assays using a turbidimeter and visual RT-IMSA assays to detect EV71 and CVA16 were established and completed in 1 h, and the reported corresponding real-time reverse transcription–loop-mediated isothermal amplification (RT-LAMP) assays targeting the same regions of the VP1 gene were adopted as parallel tests. Through testing VP1 RNAs transcribed
in vitro
, the real-time RT-IMSA assays exhibited better linearity of quantification, with
R
2
values of 0.952 (for EV71) and 0.967 (for CVA16), than the real-time RT-LAMP assays, which had
R
2
values of 0.803 (for EV71) and 0.904 (for CVA16). Additionally, the detection limits of the real-time RT-IMSA assays (approximately 937 for EV71 and 67 for CVA16 copies/reaction) were higher than those of real-time RT-LAMP assays (approximately 3,266 for EV71 and 430 for CVA16 copies/reaction), and similar results were observed in the visual RT-IMSA assays. The new approaches also possess high specificities for the corresponding targets, with no cross-reactivity observed. In clinical assessment, compared to commercial reverse transcription-quantitative PCR (qRT-PCR) kits, the diagnostic sensitivities of the real-time RT-IMSA assays (96.4% for EV71 and 94.6% for CVA16) were higher than those of the real-time RT-LAMP assays (91.1% for EV71 and 90.8% for CVA16). The visual RT-IMSA assays also exhibited the same results. In conclusion, this proof-of-concept study suggests that the novel RT-IMSA assay is superior to the RT-LAMP assay in terms of detection limit and has the potential to rapidly detect EV71 and CVA16 viruses.
Trichosporon mycotoxinivorans Infection in Patients with Cystic Fibrosis
Authors: Shah Avani V. , McColley Susanna A. , Weil Diane , Zheng Xiaotian 
Published: March 2014

ABSTRACT

We describe the clinical course of four patients who had
Trichosporon mycotoxinivorans
recovered from multiple sputum cultures over time with various clinical consequences but no fatalities. We also report successful rapid identification of this organism using matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry.
Systematic Evaluation of Commercial Susceptibility Testing Methods for Determining the
In Vitro
Activity of Daptomycin versus Staphylococcus aureus and Enterococci
Authors: Kirn Thomas J. , Onyeaso Elizabeth , Syed Madiha , Weinstein Melvin P. 
Published: March 2014

ABSTRACT

We systematically evaluated 5 methods for testing daptomycin versus 48
Enterococcus faecalis
, 51
Enterococcus faecium
, and 50
Staphylococcus aureus
isolates using (i and ii) broth microdilution (BMD) with 50-mg/liter calcium medium supplementation (reference method) and 30-mg/liter calcium medium supplementation (BMD30 method), (iii) Etest, and (iv and v) MicroScan panel 33 using 2 methods to prepare the bacterial inoculum (MicroScan turbidity and MicroScan Prompt). Isolates were categorized as susceptible (S) or nonsusceptible (NS) based on measured MICs. Essential (±1 dilution) agreement (EA) and categorical (S/NS) agreement (CA) for each method were compared to the reference method. For
E. faecium
, categorical agreement was poor between the reference method and BMD30 as well as with the three commercial methods, with frequent false-NS results (30 for BMD30, 18 for Etest, 22 for MicroScan Prompt, and 25 for MicroScan turbidity). All
E. faecalis
isolates were judged to be S by the reference method; two of these isolates were categorized as NS using the BMD30 method, and one was categorized as NS by all three commercial methods. All
S. aureus
isolates were judged to be S using all five methods. MIC values determined by the comparator methods tended to be higher than those for the reference method, especially for
E. faecium
isolates. EAs between the reference BMD and BMD30, Etest, MicroScan Prompt, and MicroScan turbidity were 63%, 63%, 63%, and 56%, respectively, for
E. faecium
, 87%, 83%, 98%, and 80%, respectively, for
E. faecalis
, and all 100% for
S. aureus
.
Alpha/Beta Interferon Receptor Signaling Amplifies Early Proinflammatory Cytokine Production in the Lung during Respiratory Syncytial Virus Infection
Authors: Goritzka Michelle , Durant Lydia R. , Pereira Catherine , Salek-Ardakani Samira , Openshaw Peter J. M. , Johansson Cecilia 
Published: March 2014

ABSTRACT

Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-α/β) receptor (IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. To investigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined their importance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1
−/−
) mice displayed increased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedly reduced in the lungs of IFNAR1
−/−
mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokines in the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels of proinflammatory cytokines were also detected in the lungs of IFNAR1
−/−
mice challenged with noninfectious innate immune stimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN-α was sufficient to potentiate the production of inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to its well-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responses in the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterized by enhanced inflammatory cytokine production.

IMPORTANCE
The initial response to viral infection is characterized by the production of interferons (IFNs). One group of IFNs, the type I IFNs, are produced early upon virus infection and signal through the IFN-α/β receptor (IFNAR) to induce proteins important for limiting viral replication and directing immune responses. Here we examined the importance of type I IFNs in early responses to respiratory syncytial virus (RSV). Our data suggest that type I IFN production and IFNAR receptor signaling not only induce an antiviral state but also serve to amplify proinflammatory responses in the respiratory tract. We also confirm this conclusion in another model of acute inflammation induced by noninfectious stimuli. Our findings are of relevance to human disease, as RSV is a major cause of infant bronchiolitis and polymorphisms in the IFN system are known to impact disease severity.
Synthesis of time-stratigraphic relationships and their impact on hydrocarbon reservoir distribution and performance, Bridport Sand Formation, Wessex Basin, UK
Authors: Hampson Gary J. , Morris Jenny E. , Johnson Howard D. 
Published: March 2014

Abstract
The Lower Jurassic Bridport Sand Formation records net deposition in the Wessex Basin, southern UK of a low-energy, siliciclastic shoreface that was dominated by storm-event beds reworked by bioturbation. Shoreface sandstones dip at 2–3° to define (subaerial?) clinoforms that pass distally into a near-horizontal platform, and then steepen again to form steep (2–3°) subaqueous clinoforms in the underlying Down Cliff Clay Member. The overall morphology indicates mud-dominated clinoforms of compound geometry. Compound clinoforms are grouped into progradational sets whose stacking reflects tectonic subsidence and sediment dispersal patterns, and also controls basin-scale reservoir distribution and diachroneity of the formation.
Each shoreface clinoform set consists of an upward-shallowing succession that is several tens of metres thick with a laterally continuous mudstone interval at its base. The successions are punctuated by calcite-cemented concretionary layers of varying lateral continuity, which formed along bioclastic lags at the base of storm-event beds. Concretionary layers thus represent short periods of rapid sediment accumulation, while their distribution likely results from variations in storm-wave climate, relative sea-level, and/or sediment availability. The distribution of impermeable mudstone intervals that bound each clinoform set and concretionary layers along clinoform surfaces controls oil drainage in the Bridport Sand Formation reservoir.
CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells
Authors: Jia Jinping , Bosley Allen D. , Thompson Abbey , Hoskins Jason W. , Cheuk Adam , Collins Irene , Parikh Hemang , Xiao Zhen , Ylaya Kris , Dzyadyk Marta , Cozen Wendy , Hernandez Brenda Y. , Lynch Charles F. , Loncarek Jadranka , Altekruse Sean F. , Zhang Lizhi , Westlake Christopher J. , Factor Valentina M. , Thorgeirsson Snorri , Bamlet William R. , Hewitt Stephen M. , Petersen Gloria M. , Andresson Thorkell , Amundadottir Laufey T. 
Published: March 2014

Abstract
Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3–1.5–fold; PDAY7 &lt; 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10−4). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33. Cancer Res; 74(10); 2785–95. ©2014 AACR.
Anti-VEGF Antibodies Mitigate the Development of Radiation Necrosis in Mouse Brain
Authors: Jiang Xiaoyu , Engelbach John A. , Yuan Liya , Cates Jeremy , Gao Feng , Drzymala Robert E. , Hallahan Dennis E. , Rich Keith M. , Schmidt Robert E. , Ackerman Joseph J.H. , Garbow Joel R. 
Published: March 2014

AbstractPurpose: To quantify the effectiveness of anti-VEGF antibodies (bevacizumab and B20-4.1.1) as mitigators of radiation-induced, central nervous system (brain) necrosis in a mouse model.Experimental Design: Cohorts of mice were irradiated with single-fraction 50- or 60-Gy doses of radiation targeted to the left hemisphere (brain) using the Leksell Perfexion Gamma Knife. The onset and progression of radiation necrosis were monitored longitudinally by in vivo, small-animal MRI, beginning 4 weeks after irradiation. MRI-derived necrotic volumes for antibody (Ab)-treated and untreated mice were compared. MRI results were supported by correlative histology.Results: Hematoxylin and eosin–stained sections of brains from irradiated, non–Ab-treated mice confirmed profound tissue damage, including regions of fibrinoid vascular necrosis, vascular telangiectasia, hemorrhage, loss of neurons, and edema. Treatment with the murine anti-VEGF antibody B20-4.1.1 mitigated radiation-induced changes in an extraordinary, highly statistically significant manner. The development of radiation necrosis in mice under treatment with bevacizumab (a humanized anti-VEGF antibody) was intermediate between that for B20-4.1.1–treated and non–Ab-treated animals. MRI findings were validated by histologic assessment, which confirmed that anti-VEGF antibody treatment dramatically reduced late-onset necrosis in irradiated brain.Conclusions: The single-hemispheric irradiation mouse model, with longitudinal MRI monitoring, provides a powerful platform for studying the onset and progression of radiation necrosis and for developing and testing new therapies. The observation that anti-VEGF antibodies are effective mitigants of necrosis in our mouse model will enable a wide variety of studies aimed at dose optimization and timing and mechanism of action with direct relevance to ongoing clinical trials of bevacizumab as a treatment for radiation necrosis. Clin Cancer Res; 20(10); 2695–702. ©2014 AACR.
Human Melanoma Metastases Demonstrate Nonstochastic Site-Specific Antigen Heterogeneity That Correlates with T-cell Infiltration
Authors: Bartlett Edmund K. , Fetsch Patricia A. , Filie Armando C. , Abati Andrea , Steinberg Seth M. , Wunderlich John R. , White Donald E. , Stephens Daniel J. , Marincola Francesco M. , Rosenberg Steven A. , Kammula Udai S. 
Published: March 2014

Abstract
Purpose: Metastasis heterogeneity presents a significant obstacle to the development of targeted cancer therapeutics. In this study, we sought to establish from a large series of human melanoma metastases whether there exists a determined pattern in tumor cellular heterogeneity that may guide the development of future targeted immunotherapies.
Experimental Design: From a cohort of 1,514 patients with metastatic melanoma, biopsies were procured over a 17-year period from 3,086 metastatic tumors involving various anatomic sites. To allow specific tumor cell profiling, we used established immunohistochemical methods to perform semiquantitative assessment for a panel of prototypic melanocyte differentiation antigens (MDA), including gp100, MART-1, and tyrosinase. To gain insight into the endogenous host immune response against these tumors, we further characterized tumor cell expression of MHC I and MHC II and, also, the concomitant CD4+ and CD8+ T-cell infiltrate.
Results: Tumor cell profiling for MDA expression demonstrated an anatomic site-specific pattern of antigen expression that was highest in brain, intermediate in soft tissues/lymph nodes, and lowest in visceral metastases. Hierarchical clustering analysis supported that melanoma metastases have a phylogenetically determined, rather than a stochastic, pattern of antigen expression that varies by anatomic site. Furthermore, tyrosinase expression was more frequently lost in metastatic sites outside of the brain and was uniquely correlated with both endogenous CD8+ and CD4+ T-cell infiltrates.
Conclusion: Site-specific antigen heterogeneity represents a novel attribute for human melanoma metastases that should be considered in future therapy development and when assessing the responsiveness to antigen-specific immunotherapies. Clin Cancer Res; 20(10); 2607–16. ©2014 AACR.
Postmortem Cardiovascular Magnetic Resonance Imaging in Fetuses and Children
Authors: Taylor Andrew M. , Sebire Neil J. , Ashworth Michael T. , Schievano Silvia , Scott Rosemary J. , Wade Angie , Chitty Lyn S. , Robertson Nikki , Thayyil Sudhin 
Published: March 2014

Background—
Perinatal and pediatric autopsies have declined worldwide in the past decade. We compared the diagnostic accuracy of postmortem, cardiovascular magnetic resonance (CMR) imaging with conventional autopsy and histopathology assessment in fetuses and children.

Methods and Results—
We performed postmortem magnetic resonance imaging in 400 fetuses and children, using a 1.5-T Siemens Avanto magnetic resonance scanner before conventional autopsy. A pediatric CMR imager reported the CMR images, masked to autopsy information. The pathologists were masked to the information from CMR images. The institutional research ethics committee approved the study, and parental consent was obtained. Assuming a diagnostic accuracy of 50%, 400 cases were required for a 5% precision of estimate. Three cases were excluded from analysis, 2 with no conventional autopsy performed and 1 with insufficient CMR sequences performed. Thirty-eight CMR data sets were nondiagnostic (37 in fetuses ≤24 weeks; 1 in a fetus >24 weeks). In the remaining 359 cases, 44 cardiac abnormalities were noted at autopsy. Overall sensitivity and specificity (95% confidence interval) of CMR was 72.7% (58.2–83.7%) and 96.2% (93.5–97.8%) for detecting any cardiac pathology, with positive and negative predictive values of 72.7% (58.2–83.7%) and 96.2% (93.5–97.8%), respectively. Higher sensitivity of 92.6% (76.6–97.9%), specificity of 99.1% (97.4–99.7%), positive predictive value of 89.3% (72.8–96.3%), and negative predictive value of 99.4% (97.8–99.8%) were seen for major structural heart disease.

Conclusions—
Postmortem CMR imaging may be a useful alternative to conventional cardiac autopsy in fetuses and children for detecting cardiac abnormalities.

Clinical Trial Registration—

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT01417962.
Encountering Extraordinary Worlds: The Rules of Ethnographic Engagement and the Limits of Anthropological Knowing
Authors: Kahn Joel S. 
Published: March 2014

AbstractThis article explores the ways anthropology might both draw on and contribute to current debates on religion by asking how the ethnographic encounter provides a perspective from which to address “bigger” questions about the place of religion in modern lifeworlds. In particular, the article addresses situations in which the gap between anthropological “construals” of the world and those of its research subjects becomes impossible to ignore. I begin by the phenomenological strategy of “suspending disbelief.” This turns out to be problematic in the light of the postmodern/poststructuralist critique of phenomenology, which suggests that “experience,” being so tightly bound up in context, cannot be shared across cultural, linguistic, and ontological boundaries. However, to refuse to take our respondents’ claims about extraordinary experience seriously is hardly the democratizing move that anthropologists and others claim it to be. How, then, is the experiential dimension to be incorporated into ethnographic practice? Acknowledging the multiple ways in which anthropologists are bound up in an already constituted world of encounters challenges many of the received understandings of ethnography. It allows us to bring experience back into the anthropological frame by allowing us to see that experiences deemed extraordinary — “ours” as well as “theirs” — are a valid and crucial component of human existence. If “we” are part of “their” world and they are part of ours, can we really not share experiences across the ontological divide?
A Novel Financial Market for Mitigating Hurricane Risk. Part I: Market Structure and Model Results
Authors: Wilks Daniel S. , Horowitz Kenneth A. 
Published: March 2014

Abstract
A novel financial market for hedging the effects of landfalling hurricanes is described and illustrated. The structure of the market is one sided and parimutuel, so that participants buy contracts pertaining to hurricane landfall locations from an exchange rather than from other market participants, and settlements for contracts associated with the landfall location are funded by purchases in all other outcomes. Contract prices are updated automatically and objectively using a recently developed adaptive control algorithm that responds to inferred aggregate probability assessments of the market participants. The market is intended to supplement insurance by providing a mechanism to shift risk for costs not covered under existing windstorm insurance. Operation of the market mechanism is illustrated in an idealized setting and in a spatially explicit historical simulation for Hurricane Charley (2004). A companion paper in this issue describes empirical validation of this market mechanism in an experimental market setting.