bluuebunny/crossref_metadata_2025_split huggingface dataset:
An Experimental Analysis of the Demand for Payday Loans
Authors: Wilson Bart J , Findlay David W. , Meehan James W. , Wellford Charissa , Schurter Karl 
Published: October 2010

Abstract
The payday loan industry is one of the fastest growing segments of the consumer financial services market in the United States. We design an environment similar to the one that payday loan customers face and then conduct a laboratory experiment to examine what effect, if any, the existence of payday loans has on individuals abilities to manage and to survive financial setbacks. Our primary objective is to examine whether access to payday loans improves or worsens the likelihood of financial survival in our experiment. We also test the degree to which peoples use of payday loans affects their ability to survive financially. We find that payday loans help the subjects to absorb expenditure shocks and therefore survive financially. However, subjects whose demand for payday loans exceeds a certain threshold level are at a greater risk than a corresponding subject in the treatment in which payday loans do not exist.
Emerging CAE technologies and their role in Future Ambient Intelligence Environments
Authors: Noor Ahmed 
Published: October 2010

AbstractDramatic improvements are on the horizon in Computer Aided Engineering (CAE) and various simulation technologies. The improvements are due, in part, to the developments in a number of leading-edge technologies and their synergistic combinations/convergence. The technologies include ubiquitous, cloud, and petascale computing; ultra high-bandwidth networks, pervasive wireless communication; knowledge based engineering; networked immersive virtual environments and virtual worlds; novel human-computer interfaces; and powerful game engines and facilities. This paper describes the frontiers and emerging simulation technologies, and their role in the future virtual product creation and learning/training environments. The environments will be ambient intelligence environments, incorporating a synergistic combination of novel agent-supported visual simulations (with cognitive learning and understanding abilities); immersive 3D virtual world facilities; development chain management systems and facilities (incorporating a synergistic combination of intelligent engineering and management tools); nontraditional methods; intelligent, multimodal and human-like interfaces; and mobile wireless devices. The Virtual product creation environment will significantly enhance the productivity and will stimulate creativity and innovation in future global virtual collaborative enterprises. The facilities in the learning/training environment will provide timely, engaging, personalized/collaborative and tailored visual learning.
Microsatellite loci for Paspalum atratum (Poaceae) and cross‐amplification in other species
Authors: Cidade F. W. , de Souza‐Chies T. T. , Souza F. H. D. , Batista L. A. R. , Dall'Agnol M. , Valls J. F. M. , Zucchi M. I. , Souza A. P. 
Published: October 2010

• Premise of the study: Paspalum atratum is a perennial, cespitose, tropical grass native to Central and South America. This species belongs to a polyploid complex (Plicatula group) little known at the genetic level. The characterized microsatellite markers provide new informative tools for further studies of the hybridization, mating systems, and structure of the population.• Methods and Results: Using the microsatellite‐enriched library method, we isolated and characterized 19 microsatellite markers from P. atratum. Eleven of them were polymorphic, showing a variable degree of variation, while eight were monomorphic in the samples analyzed. Additionally, the transferability of these microsatellite markers was tested in other species.• Conclusions: These results suggest that the characterized markers have enough discriminatory potential to be used in genetic characterizations of Paspalum taxa, which are based on an understanding of their mating systems and genetic structure, as well as in understanding the evolutionary processes involved in the evolution of groups of Paspalum.
Quantitative Power Doppler Ultrasonography Is a Sensitive Measure of Metacarpophalangeal Joint Synovial Vascularity in Rheumatoid Arthritis and Declines Significantly Following a 2-week Course of Oral Low-dose Corticosteroids
Authors: LARCHÉ MAGGIE J. , SEYMOUR MATTHEW , LIM ADRIAN , ECKERSLEY ROBERT J. , PÉTAVY FRANK , CHIESA FLAMINIA , RIOJA INMACULADA , LUKEY PAULINE T. , BINKS MICHAEL , McCLINTON CATHERINE , DOLAN KATHLEEN , TAYLOR PETER C. 
Published: October 2010

Objective.To investigate the stability over 2 weeks of ultrasonographic assessments of synovial thickness and vascularity in all 10 metacarpophalangeal joints of subjects with rheumatoid arthritis (RA) with a range of disease activities as measured by the validated Disease Activity Score-28 joint score (DAS28-ESR). And in subjects with severe disease activity, to compare the sensitivity of these measurements, acute-phase markers, and vascular endothelial growth factor to change in response to 2 weeks of oral prednisolone (7.5 mg daily).Methods.A group of 38 subjects with RA were enrolled, 13 (mean DAS28 2.1), 14 (mean DAS28 5.2), and 11 (mean DAS28 5.7) meriting oral corticosteroid treatment. Synovial thickness and vascularity were assessed by ultrasonography at 3 timepoints. Images were ranked by semiquantitative scale. Vascularity was also measured by quantitative determination of the power Doppler area (PDA).Results.In the whole RA cohort, baseline indices of synovial thickness and vascularity correlated with DAS28, as did PDA (r = 0.42, p < 0.05). In the RA groups on stable therapy, synovial thickness and vascularity showed little variation over 2 weeks. In the corticosteroid group, PDA had fold changes of −1.9-fold (p < 0.05) after 1 week and −2.2-fold (p < 0.05) after 2 weeks. These were the largest fold changes of all measured variables.Conclusion.Ultrasonographic measures can differentiate disease severity in RA correlating closely with DAS28. Quantitative power Doppler signal was significantly reduced within 1 week of oral prednisolone, a rapid kinetic suggesting that PDA may have value as a sensitive early marker of therapeutic response.
Systematic Review of MRI, Ultrasound, and Scintigraphy as Outcome Measures for Structural Pathology in Interventional Therapeutic Studies of Knee Arthritis: Focus on Responsiveness
Authors: KEEN HELEN I. , MEASE PHILIP J. , BINGHAM CLIFTON O. , GILES JON T. , KAELEY GURJIT , CONAGHAN PHILIP G. 
Published: October 2010

Objective.Validated imaging outcome tools to assess response to therapies in a single joint are required. Our aim was to review the published literature to ascertain the responsiveness of novel imaging techniques as outcome measures in interventional therapeutic studies of knee arthritis.Methods.An Ovid Medline search was performed for original articles in English that used imaging techniques to assess response at the knee joint to therapy in osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Changes in response to therapy were assessed with regard to both internal and external responsiveness.Results.In the studies that presented appropriate statistical data to allow responsiveness to be assessed, MRI was generally found to be internally responsive to pathologies imaged, and externally responsive, referenced against both other imaging modalities and biochemical biomarkers of arthritis. Ultrasonography was found to demonstrate internal responsiveness with regard to synovial thickness, effusion size, and popliteal cyst size. External responsiveness was demonstrated against several referenced health status measures. Scintigraphy was found to be externally responsive in the majority of studies, with internal responsiveness demonstrated in 1 study.Conclusion.While the imaging techniques appear to be responsive from the data we present, further inspection reveals that interpreting the responsiveness of imaging techniques was difficult, largely because of a lack of standardization of image acquisition, definitions of pathology, and scoring systems. Refined pathological definitions and scoring systems are required to enable the development of valid and responsive tools for interventional clinical trials.
Anticentromere-A and Anticentromere-B Antibodies Show High Concordance and Similar Clinical Associations in Patients with Systemic Sclerosis
Authors: HANKE KATHARINA , BECKER MIKE O. , BRUECKNER CLAUDIA S. , MEYER WOLFGANG , JANSSEN ANTHONINA , SCHLUMBERGER WOLFGANG , HIEPE FALK , BURMESTER GERD-R. , RIEMEKASTEN GABRIELA 
Published: October 2010

Objective.To determine the diagnostic sensitivity and specificity and the clinical usefulness of parallel anticentromere-A and anticentromere-B antibody (anti-CENP-A and anti-CENP-B) testing in patients with systemic sclerosis (SSc).Methods.Sera from 280 consecutive patients with SSc and 259 controls were tested for the presence of anti-CENP-A and anti-CENP-B antibodies by a monospecific line immunoblot assay (LIA) with recombinant human centromere proteins A and B as well as by indirect immunofluorescence (IIF). Crossreactivity and possible associations with clinical manifestations were studied.Results.Both antibodies revealed a diagnostic sensitivity of 36.8% and a specificity of > 97% for SSc, with a high concordance rate of 94.3% despite different amino acid sequences of the antigens and absence of crossreactivity. There was a significant correlation of the antibody levels measured by LIA. Both antibodies were associated with similar clinical manifestations and identified patients with limited disease and rather mild skin sclerosis.Conclusion.Detected by LIA, anti-CENP-A and anti-CENP-B antibodies show high concordance in patients with SSc and share significant associations to clinical manifestations, but are not completely identical. Detection of both antibodies in parallel may slightly increase the diagnostic sensitivity for SSc.
IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection
Authors: Li Wei , Sun Wei , Liu Li , Yang Fang , Li Yongkui , Chen Yanni , Fang Jiali , Zhang Wenjing , Wu Jianguo , Zhu Ying 
Published: October 2010

AbstractOur previous studies with clinical data analysis have shown that the proinflammatory factor IL-32 is activated in response to influenza virus infection. However, little is known about how influenza virus induces IL-32 production, and the role of IL-32 in the host immune responses during viral infection remains unclear. In this study, we show that IL-32 production is stimulated by influenza A virus or dsRNA in human PBMCs from healthy volunteers. We demonstrate that the NF-κB and CREB pathways play key roles in the activation of IL-32 production in response to influenza virus infection in A549 human lung epithelial cells. We then show that aberrant epigenetic modifications in the IL32 promoter are important in the transcriptional regulation of IL-32 expression. Interestingly, one CpG demethylation within the CREB binding site increases the binding of CREB to the promoter, which is followed by IL32 transcriptional activation in influenza A virus-infected cells. Overexpression assays combined with RNA interference show that DNA methyltransferases DNMT1 and DNMT3b are critical for IL32 promoter methylation and gene silencing before viral infection. We have demonstrated the anti-influenza virus function of IL-32. Assays for each of the six IL-32 isoforms (α, β, γ, δ, ε, and ζ) during influenza virus infection indicated that all the isoforms have antiviral activity, with different inhibitory rates, and that the effect of IL-32γ is strongest. Our results indicate that the elevated IL-32 levels triggered by influenza virus infection in turn hamper viral replication.
Hypoxia-Induced Mitogenic Factor (HIMF/FIZZ1/RELMα) Increases Lung Inflammation and Activates Pulmonary Microvascular Endothelial Cells via an IL-4–Dependent Mechanism
Authors: Yamaji-Kegan Kazuyo , Su Qingning , Angelini Daniel J. , Myers Allen C. , Cheadle Chris , Johns Roger A. 
Published: October 2010

Abstract
Hypoxia-induced mitogenic factor (HIMF), also known as found in inflammatory zone 1 and resistin-like molecule α, belongs to a novel class of cysteine-rich secreted proteins. It exhibits mitogenic and chemotactic properties during pulmonary hypertension-associated vascular remodeling, as well as fibrogenic properties during pulmonary fibrosis. HIMF expression in the lung was reported to be regulated by Th2 cytokines (IL-4 and IL-13) via the transcription factor STAT6 pathway in a bleomycin-induced pulmonary fibrosis model. However, in this study, we found that in the hypoxia-induced pulmonary hypertension model, lung HIMF expression is increased in IL-4 and STAT6 knockout (KO) mice to the same degree as in wild-type (WT) mice, suggesting that induction of HIMF expression does not require Th2 regulation in this model. We also found that HIMF-induced proliferative activity, hypertrophy, collagen, and extracellular matrix deposition in the pulmonary arteries are significantly less in IL-4 KO mice than in WT mice. In addition, HIMF-induced production of angiogenic factors/chemokines, such as vascular endothelial growth factor, MCP-1, and stromal-derived factor-1, in the lung resident cells, as well as macrophage infiltration, were significantly suppressed in the lungs of IL-4 KO mice. We also show that IL-4 was significantly increased in the lungs of HIMF-treated WT mice. Our in vitro studies using pulmonary microvascular endothelial cells revealed that HIMF stimulated cell proliferation, vascular endothelial growth factor expression, and MCP-1 production in a manner that is dependent on the IL-4/IL-4Rα system. These findings suggest that IL-4 signaling may play a significant role in HIMF-induced lung inflammation and vascular remodeling.
Cutting Edge: CD4 T Cells Generated from Encounter with Seasonal Influenza Viruses and Vaccines Have Broad Protein Specificity and Can Directly Recognize Naturally Generated Epitopes Derived from the Live Pandemic H1N1 Virus
Authors: Richards Katherine A. , Topham David , Chaves Francisco A. , Sant Andrea J. 
Published: October 2010

Abstract
The unexpected emergence of pandemic H1N1 influenza has generated significant interest in understanding immunological memory to influenza and how previous encounters with seasonal strains influence our ability to respond to novel strains. In this study, we evaluate the memory T cell repertoire in healthy adults to determine the abundance and protein specificity of influenza-reactive CD4 T cells, using an unbiased and empirical approach, and assess the ability of CD4 T cells to recognize epitopes naturally generated by infection with pandemic H1N1 virus. Our studies revealed that most individuals have abundant circulating CD4 T cells that recognize influenza-encoded proteins and that a strikingly large number of CD4 T cells can recognize autologous cells infected with live H1N1 virus. Collectively, our results indicate that a significant fraction of CD4 T cells generated from priming with seasonal virus and vaccines can be immediately mobilized upon infection with pandemic influenza strains derived from antigenic shift.
CXCR7 Protein Is Not Expressed on Human or Mouse Leukocytes
Authors: Berahovich Robert D. , Zabel Brian A. , Penfold Mark E. T. , Lewén Susanna , Wang Yu , Miao Zhenhua , Gan Lin , Pereda Jaime , Dias Jessica , Slukvin Igor I. , McGrath Kathleen E. , Jaen Juan C. , Schall Thomas J. 
Published: October 2010

Abstract
Since the discovery that CXCR7 binds to CXCL12/SDF-1α, the role of CXCR7 in CXCL12-mediated biological processes has been under intensive scrutiny. However, there is no consensus in the literature on the expression of CXCR7 protein by peripheral blood cells. In this study we analyzed human and mouse leukocytes and erythrocytes for CXCR7 protein expression, using a competitive CXCL12 binding assay as well as by flow cytometry and immunohistochemistry using multiple CXCR7 Abs. CXCR7−/− mice were used as negative controls. Together, these methods indicate that CXCR7 protein is not expressed by human peripheral blood T cells, B cells, NK cells, or monocytes, or by mouse peripheral blood leukocytes. CXCR7 protein is, however, expressed on mouse primitive erythroid cells, which supply oxygen to the embryo during early stages of development. These studies therefore suggest that, whereas CXCR7 protein is expressed by primitive RBCs during murine embryonic development, in adult mammals CXCR7 protein is not expressed by normal peripheral blood cells.
A Nonredundant Role for IL-21 Receptor Signaling in Plasma Cell Differentiation and Protective Type 2 Immunity against Gastrointestinal Helminth Infection
Authors: King Irah L. , Mohrs Katja , Mohrs Markus 
Published: October 2010

Abstract
Pathogen-specific Ab production following infection with the gut-dwelling roundworm Heligmosomoides polygyrus is critical for protective immunity against reinfection. However, the factors required for productive T cell–B cell interactions in the context of a type 2-dominated immune response are not well defined. In the present study, we identify IL-21R signaling as a critical factor in driving pathogen-specific plasma cell differentiation and protective immunity against H. polygyrus in mice. We show that B cells require direct IL-21R signals to differentiate into CD138+ plasma cells. In contrast, IL-21R signaling is dispensable for germinal center formation, isotype class switching, and Th2 and T follicular helper cell differentiation. Our studies demonstrate a selective role for IL-21 in plasma cell differentiation in the context of protective antiparasitic type 2 immunity.
Granulysin Production and Anticryptococcal Activity Is Dependent upon a Far Upstream Enhancer That Binds STAT5 in Human Peripheral Blood CD4+ T Cells
Authors: Xing Junji , Wu Fuqing , Wang Shuai , Krensky Alan M. , Mody Christopher H. , Zheng Chunfu 
Published: October 2010

Abstract
Previous studies have demonstrated that STAT5 is critical for expression of granulysin and antimicrobial activity. Because the signaling pathway and the resultant microbicidal activity are defective in HIV-infected patients, the mechanism by which STAT5 leads to granulysin expression is of great interest. In the current study, IL-2–stimulated CRL-2105 CD4+ T cells expressed granulysin and killed Cryptococcus neoformans similar to primary CD4+ T cells. The enhancer activity of the upstream element of the granulysin promoter was analyzed in primary CD4+ T cells and CRL-2105 T cells with a luciferase reporter assay, and a STAT5 binding site, 18,302 to 18,177 bp upstream of the transcription start site, was identified as an enhancer. Additionally, the enhancer functioned in the context of heterologous SV40 promoter irrespective of its transcriptional orientation. Chromatin immunoprecipitation and EMSAs demonstrated that the enhancer element bound STAT5 both in vivo and in vitro, and mutation of the STAT5 binding site abrogated its enhancer activity. Furthermore, overexpression of a dominant negative STAT5a abolished the enhancer activity of the STAT5 binding site and abrogated the anticryptococcal activity of IL-2–stimulated primary CD4+ T cells. Taken together, these data provide details about the complex regulation leading to granulysin expression and anticryptococcal activity in primary CD4+ T cells.
Disruption of Intestinal CD4+ T Cell Homeostasis Is a Key Marker of Systemic CD4+ T Cell Activation in HIV-Infected Individuals
Authors: Gordon Shari N. , Cervasi Barbara , Odorizzi Pamela , Silverman Randee , Aberra Faten , Ginsberg Gregory , Estes Jacob D. , Paiardini Mirko , Frank Ian , Silvestri Guido 
Published: October 2010

Abstract
HIV infection is associated with depletion of intestinal CD4+ T cells, resulting in mucosal immune dysfunction, microbial translocation, chronic immune activation, and progressive immunodeficiency. In this study, we examined HIV-infected individuals with active virus replication (n = 15), treated with antiretroviral therapy (n = 13), and healthy controls (n = 11) and conducted a comparative analysis of T cells derived from blood and four gastrointestinal (GI) sites (terminal ileum, right colon, left colon, and sigmoid colon). As expected, we found that HIV infection is associated with depletion of total CD4+ T cells as well as CD4+CCR5+ T cells in all GI sites, with higher levels of these cells found in ART-treated individuals than in those with active virus replication. While the levels of both CD4+ and CD8+ T cell proliferation were higher in the blood of untreated HIV-infected individuals, only CD4+ T cell proliferation was significantly increased in the gut of the same patients. We also noted that the levels of CD4+ T cells and the percentages of CD4+Ki67+ proliferating T cells are inversely correlated in both blood and intestinal tissues, thus suggesting that CD4+ T cell homeostasis is similarly affected by HIV infection in these distinct anatomic compartments. Importantly, the level of intestinal CD4+ T cells (both total and Th17 cells) was inversely correlated with the percentage of circulating CD4+Ki67+ T cells. Collectively, these data confirm that the GI tract is a key player in the immunopathogenesis of HIV infection, and they reveal a strong association between the destruction of intestinal CD4+ T cell homeostasis in the gut and the level of systemic CD4+ T cell activation.
Cutting Edge: Thymic NK Cells Develop Independently from T Cell Precursors
Authors: Ribeiro Vera S. G. , Hasan Milena , Wilson Anne , Boucontet Laurent , Pereira Pablo , Lesjean-Pottier Sarah , Satoh-Takayama Naoko , Di Santo James P. , Vosshenrich Christian A. J. 
Published: October 2010

Abstract
Although NK cells in the mouse are thought to develop in the bone marrow, a small population of NK cells in the thymus has been shown to derive from a GATA3-dependent pathway. Characteristically, thymic NK cells express CD127 and few Ly49 molecules and lack CD11b. Because these NK cells develop in the thymus, the question of their relationship to the T cell lineage has been raised. Using several different mouse models, we find that unlike T cells, thymic NK cells are not the progeny of Rorc-expressing progenitors and do not express Rag2 or rearrange the TCRγ locus. We further demonstrate that thymic NK cells develop independently of the Notch signaling pathway, supporting the idea that thymic NK cells represent bona fide NK cells that can develop independently of all T cell precursors.