bluuebunny/crossref_metadata_2025_split huggingface dataset:
Circulating Endothelial Progenitor Cells in Periodontitis
Authors: Jönsson Daniel , Spinell Thomas , Vrettos Anastasios , Stoecklin‐Wasmer Christin , Celenti Romanita , Demmer Ryan T. , Kebschull Moritz , Papapanou Panos N. 
Published: August 2014

Background: Several biologically plausible mechanisms have been proposed to mediate the association between periodontitis and atherosclerotic vascular disease (AVD), including adverse effects on vascular endothelial function. Circulating endothelial progenitor cells (cEPCs) are known to contribute to vascular repair, but limited data are available regarding the relationship between cEPC levels and periodontitis. The aims of this cross‐sectional study are to investigate the levels of hemangioblastic and monocytic cEPCs in patients with periodontitis and periodontally healthy controls and to associate cEPC levels with the extent and severity of periodontitis.Methods: A total of 112 individuals (56 patients with periodontitis and 56 periodontally healthy controls, aged 26 to 65 years; mean age: 43 years) were enrolled. All participants underwent a full‐mouth periodontal examination and provided a blood sample. Hemangioblastic cEPCs were assessed using flow cytometry, and monocytic cEPCs were identified using immunohistochemistry in cultured peripheral blood mononuclear cells. cEPC levels were analyzed in the entire sample, as well as in a subset of 50 pairs of patients with periodontitis/periodontally healthy controls, matched with respect to age, sex, and menstrual cycle.Results: Levels of hemangioblastic cEPCs were approximately 2.3‐fold higher in patients with periodontitis than periodontally healthy controls, after adjustments for age, sex, physical activity, systolic blood pressure, and body mass index (P = 0.001). A non‐significant trend for higher levels of monocytic cEPCs in periodontitis was also observed. The levels of hemangioblastic cEPCs were positively associated with the extent of bleeding on probing, probing depth, and clinical attachment loss. Hemangioblastic and monocytic cEPC levels were not correlated (Spearman correlation coefficient 0.03, P = 0.77), suggesting that they represent independent populations of progenitor cells.Conclusion: These findings further support the notion that oral infections have extraoral effects and document that periodontitis is associated with a mobilization of EPCs from the bone marrow, apparently in response to systemic inflammation and endothelial injury.
Periodontitis in Rats Induces Systemic Oxidative Stress That Is Controlled by Bone‐Targeted Antiresorptives
Authors: Oktay Sehkar , Chukkapalli Sasanka S. , Rivera‐Kweh Mercedes F. , Velsko Irina M. , Holliday L. Shannon , Kesavalu Lakshmyya 
Published: August 2014

Background: Periodontitis is a chronic, polymicrobial inflammatory disease that degrades connective tissue and alveolar bone and results in tooth loss. Oxidative stress has been linked to the onset of periodontal tissue breakdown and systemic inflammation, and the success of antiresorptive treatments will rely on how effectively they can ameliorate periodontal disease–induced oxidative stress during oral infection.Methods: Rats were infected with polybacterial inoculum consisting of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, as an oral lavage every other week for 12 weeks. Daily subcutaneous injections of enoxacin, bis‐enoxacin, alendronate, or doxycycline were administered for 6 weeks after 6 weeks of polybacterial infection in rats. The serum levels of oxidative stress parameters and antioxidant enzymes, including glutathione peroxidase, superoxide dismutase, and catalase, were evaluated in each of the infected, treated, and sham‐infected rats.Results: Rats infected with the periodontal pathogens displayed a five‐fold increase in the oxidative stress index compared with controls as a result of increased levels of serum oxidants and decreases in total antioxidant activity. The overall decrease in antioxidant activity occurred despite increases in three important antioxidant enzymes, suggesting an imbalance between antioxidant macromolecules/small molecules production and antioxidant enzyme levels. Surprisingly, the bone‐targeted antiresorptives bis‐enoxacin and alendronate inhibited increases in oxidative stress caused by periodontitis. Bis‐enoxacin, which has both antiresorptive and antibiotic activities, was more effective than alendronate, which acts only as an antiresorptive.Conclusion: To the best of the authors’ knowledge, this is the first study to demonstrate that the increased oxidative stress induced by periodontal infection in rats can be ameliorated by bone‐targeted antiresorptives.
Decreased alveolar bone turnover is related to the occurrence of root resorption during experimental tooth movement in dogs
Authors: Deguchi Toru , Seiryu Masahiro , Daimaruya Takayoshi , Garetto Lawrence P. , Takano-Yamamoto Teruko , Roberts W. Eugene 
Published: August 2014

ABSTRACT

Objective:
To investigate the relationship between root resorption (RR) and bone turnover in two different types of tooth movement in dogs.

Materials and Methods:
A total of 16 dogs in two different groups were used. Tooth movement of dog premolars resulted from approximately 200 g of force. Histomorphometric analysis of premolar roots was assessed after 4 and 12 weeks of tooth movement by comparing nonresorptive to resorptive surfaces.

Results:
Histomorphometric analysis indicated a significant decrease in the bone formation rate in the root resorptive areas, which resulted in decreased bone volume after 12 weeks. The threshold to detect RR in periapical radiographs was about 1.0 mm2.

Conclusions:
A sustained mechanical load, due to the prolonged stress and strain of continuous mechanics, induces elevated bone metabolic activity, such as the bone turnover (remodeling) and change in bone volume (modeling). Therefore, our data support the hypothesis that increased RR is related to decreased bone formation (turnover) in high stress areas exposed to prolonged orthodontic tooth movement.
The Use of Manual Therapy Post–Hip Arthroscopy When an Exercise-Based Therapy Approach Has Failed: A Case Report
Authors: LeBeau Robert T. , Nho Shane J. 
Published: August 2014

Study Design Case report. Background Although there is a growing body of literature on both surgical intervention and postsurgical rehabilitation of acetabular labral repairs and femoroacetabular impingement, there is a paucity of information on how to manage individuals who show a lack of progress postsurgery. Case Description A 30-year-old woman underwent surgical labral repair with femoroacetabular impingement osteochondroplasty. Postsurgery, she was initially treated with an exercise-based approach, but experienced an increase in hip pain and further decline in function. Her primary functional deficits were difficulty standing and pain (6/10) with ambulation. A combination of soft tissue mobilization and trigger point dry needling was used to address perceived muscle dysfunction, and nonthrust manipulation was used to address perceived hip joint hypomobility. Outcomes Following 12 therapy sessions over 120 days, the patient returned to her demanding occupation with minimal residual symptoms. By the end of the period of care, the patient's Harris hip score had improved from 56 to 96 and her Lower Extremity Functional Scale score had improved from 26 to 70. Discussion This case describes a multimodal manual therapy approach and the health outcomes of a patient following labral repair with femoroacetabular impingement decompression who did not respond to an initial exercise-based postsurgical rehabilitation approach. Level of Evidence Therapy, level 4. J Orthop Sports Phys Ther 2014;44(9):712–721. Epub 6 August 2014. doi:10.2519/jospt.2014.5047
The STarT Back Screening Tool for Prediction of 6-Month Clinical Outcomes: Relevance of Change Patterns in Outpatient Physical Therapy Settings
Authors: Beneciuk Jason M. , Fritz Julie M. , George Steven Z. 
Published: August 2014

Study Design Observational cohort. Objectives To describe changes in STarT Back Tool (SBT) categorization following 4 weeks of outpatient physical therapy and to evaluate predictive capabilities of SBT categorization when administered at multiple time points. Background Initial assessment information is commonly used to predict long-term outcomes but does not account for changes that occur following initiation of treatment. Changes in SBT categorization during the course of treatment have potential to provide additional prognostic information that could positively impact management of low back pain. Methods Patients (n = 123) receiving nonstandardized physical therapy care for low back pain were administered the SBT at intake and 4 weeks later to evaluate SBT changes, which were described as improved (SBT categorization changed from medium to low, high to low, or high to medium risk), stable (SBT categorization remained low or medium risk), or worsened (SBT categorization changed from low to medium, low to high, medium to high, or remained high risk). Clinical outcomes consisted of pain intensity and self-reported disability. Relative contributions of SBT categorization (at intake and 4 weeks) and SBT change patterns as predictors of 6-month clinical outcomes were assessed using separate multiple-regression models, while controlling for other prognostic variables. Results Most patients (81.8%) initially categorized as SBT high risk were categorized differently by the SBT at 4 weeks. Eleven percent of patients were described as worsened, based on SBT-category change patterns at 4 weeks. Prediction of 6-month disability scores was improved when considering intake, 4-week, or 4-week change for SBT categorization, with SBT high risk consistently providing unique contributions. Conclusion Repeated SBT assessment during the episode of physical therapy has potential to provide additional information for prediction of disability at 6 months. Future studies should investigate optimal management strategies for patients who have worsened SBT risk following physical therapy intervention. Level of Evidence Prognosis, level 2b. J Orthop Sports Phys Ther 2014;44(9):656–664. Epub 6 August 2014. doi:10.2519/jospt.2014.5178
Early Ankle Movement Versus Immobilization in the Postoperative Management of Ankle Fracture in Adults: A Systematic Review and Meta-analysis
Authors: Keene David J. , Williamson Esther , Bruce Julie , Willett Keith , Lamb Sarah E. 
Published: August 2014

Study Design Systematic review and meta-analysis. Objectives To compare early ankle movement versus ankle immobilization after surgery for ankle fracture on clinical and patient-reported outcomes. Background A significant proportion of patients undergoing surgery for ankle fracture experience postoperative complications and delayed return to function. The risks and benefits of movement of the ankle in the first 6 weeks after surgery are not known, and clinical practice varies widely. Methods We searched bibliographic databases and reference lists to identify eligible trials. Two independent reviewers conducted data extraction and risk-of-bias assessments. Results Fourteen trials (705 participants) were included in the review, 11 of which were included in the meta-analysis. The quality of the trials was universally poor. The pooled effect of early ankle movement on function at 9 to 12 weeks after surgery compared to immobilization was inconclusive (standardized mean difference, 0.46; 95% confidence interval: −0.02, 0.93; P = .06; I2 = 72%), and no differences were observed between groups at 1 year. The odds of venous thromboembolism were significantly lower with early ankle movement compared to immobilization (Peto odds ratio = 0.12; 95% confidence interval: 0.02, 0.71; P = .02; I2 = 0%). Deep surgical site infection (Peto odds ratio = 7.08; 95% confidence interval: 1.39, 35.99; P = .02; I2 = 0%), superficial surgical site infection, fixation failure, and reoperation to remove metalwork were more common after early ankle movement compared to immobilization. Conclusion The quality of evidence is poor. The effects of early movement after ankle surgery on short-term functional outcomes are unclear, but there is no observable difference in the longer term. There is a small reduction in risk of postoperative thromboembolism with early ankle movement. Current evidence suggests that deep and superficial surgical site infections, fixation failure, and the need to remove metalwork are more common after early ankle movement. Level of Evidence Therapy, level 1a-. J Orthop Sports Phys Ther 2014;44(9):690–701. Epub 6 August 2014. doi:10.2519/jospt.2014.5294
The Inward Turn: American Opera Revisits America’s Past
Authors: Hutcheon Linda , Hutcheon Michael 
Published: August 2014

Abstract:Many modern American operas revisit canonical American literature (e.g., The Great Gatsby, A Streetcar Named Desire, Of Mice and Men, An American Tragedy, A View from a Bridge, Moby-Dick, McTeague, Margaret Garner) or base themselves on historical events, especially recent ones (e.g., X: The Life and Times of Malcolm X, Nixon in China, Dr. Atomic). However, what is striking is that the focus of the latter is most often on the remarkable or heroic individual—as, indeed, it is in what could be called recent “celebrity opera” as well (as in Marilyn or Jackie O)—thus revealing the enduring power of American exceptionalism to this day.
Doing the Lady Gaga Dance: Postmodern Transaesthetics and the Art of Spectacle in Don DeLillo’s The Body Artist
Authors: Radia Pavlina 
Published: August 2014

Abstract: Performances by Lady Gaga, particularly her music video “Bad Romance,” exemplify postmodern America’s preoccupation with spectacle. They expose how the gaze, as a public-driven or self-imposed zone of terror and destruction, inscribes potentialities of renewal, wherein the subject’s authenticity is reasserted through the very process of commodification, or a kind of singeing of the image. Such a notion also lies at the heart of Don DeLillo’s novel, The Body Artist. Through the lens of the grieving body artist, Lauren Hartke, DeLillo interrogates body art as a productive, yet potentially commodifying means of renewal whereby corporeal suffering is reduced to a plethora of aestheticized crossings. Examining DeLillo’s novel in combination with Gaga’s performance art, I argue that such crossings constitute what Jean Baudrillard calls, in his essay “Transaesthetics,” “a [postmodern] materialization of aesthetics where … art mime[s] its own disappearance,” but also expose the complex dystopias underpinning America’s bad romance with its own renewal.
“I Love Working for Uncle Sam, Lets Me Know Just Who I Am”: Culture, the Human Terrain System, and the Inquiry of World War I
Authors: Foster Brian 
Published: August 2014

Abstract:In 2006, twenty-five teams of cultural anthropologists were deployed by the US military as part of the Human Terrain System (HTS). The backlash against the use of academics and the “militarization of culture” was immediate. The American Anthropology Association published a series of works admonishing HTS participants and, in a related move, lifted an almost century-old censure of Franz Boas’s 1919 work, “Scientists as Spies.” Boas’s once-marginalized argument—that the “scientist who uses his research as a cover for political spying forfeits the right to be classified as a scientist”—was now recast as an accepted professional principle. This paper explores these two interrelated instances of the contestation of culture in geopolitical military strategies. Placing Boas within a larger history of the use of and conflict over the definition of culture during World War I, I argue that anthropologist-spies were only the tip of the iceberg in his time, just as HTS is in ours. The Paris Peace Talks (1917–9), for example, saw social scientists working with the state on a massive scale to literally redraw the world map. This article focuses on one secretive American organization, the Inquiry, which worked closely with military and state apparatuses, gathering ethnographic/cultural data that helped carve out official state positions and war aims. By situating the HTS as part of this larger historical narrative, we see how the “ethnographic” culture concept came to occupy such a dominant (albeit contested) place in thought.
Les libéraux et les problèmes bruxellois 1945-1962
Authors: Brassinne Jacques 
Published: August 2014

La synthèse de ce Courrier hebdomadaire a été présentée lors du colloque Het probleem Brussel sinds Hertoginnedal (1963) qui s’est tenu à la Vrije Universiteit Brussel (VUB) les 20 et 21 octobre 1988 et qui était organisé par le professeur Els Witte (VUB) et le CRISP.
The Fli-1 Transcription Factor Regulates the Expression of CCL5/RANTES
Authors: Lennard Richard Mara L. , Sato Shuzo , Suzuki Eiji , Williams Sarah , Nowling Tamara K. , Zhang Xian K. 
Published: August 2014

Abstract
The friend leukemia insertion site 1 (Fli-1) transcription factor, an Ets family member, is implicated in the pathogenesis of systemic lupus erythematosus in human patients and murine models of lupus. Lupus-prone mice with reduced Fli-1 expression have significantly less nephritis, prolonged survival, and decreased infiltrating inflammatory cells into the kidney. Inflammatory chemokines, including CCL5, are critical for attracting inflammatory cells. In this study, decreased CCL5 mRNA expression was observed in kidneys of lupus-prone NZM2410 mice with reduced Fli-1 expression. CCL5 protein expression was significantly decreased in endothelial cells transfected with Fli-1–specific small interfering RNA compared with controls. Fli-1 binds to endogenous Ets binding sites in the distal region of the CCL5 promoter. Transient transfection assays demonstrate that Fli-1 drives transcription from the CCL5 promoter in a dose-dependent manner. Both Ets1, another Ets family member, and Fli-1 drive transcription from the CCL5 promoter, although Fli-1 transactivation was significantly stronger. Ets1 acts as a dominant-negative transcription factor for Fli-1, indicating that they may have at least one DNA binding site in common. Systematic deletion of DNA binding sites demonstrates the importance of the sites located within a 225-bp region of the promoter. Mutation of the Fli-1 DNA binding domain significantly reduces transactivation of the CCL5 promoter by Fli-1. We identified a novel regulator of transcription for CCL5. These results suggest that Fli-1 is a novel and critical regulator of proinflammatory chemokines and affects the pathogenesis of disease through the regulation of factors that recruit inflammatory cells to sites of inflammation.
The MHC Class II Cofactor HLA-DM Interacts with Ig in B Cells
Authors: Macmillan Henriette , Strohman Michael J. , Ayyangar Sashi , Jiang Wei , Rajasekaran Narendiran , Spura Armin , Hessell Ann J. , Madec Anne-Marie , Mellins Elizabeth D. 
Published: August 2014

AbstractB cells internalize extracellular Ag into endosomes using the Ig component of the BCR. In endosomes, Ag-derived peptides are loaded onto MHC class II proteins. How these pathways intersect remains unclear. We find that HLA-DM (DM), a catalyst for MHC class II peptide loading, coprecipitates with Ig in lysates from human tonsillar B cells and B cell lines. The molecules in the Ig/DM complexes have mature glycans, and the complexes colocalize with endosomal markers in intact cells. A larger fraction of Ig precipitates with DM after BCR crosslinking, implying that complexes can form when DM meets endocytosed Ig. In vitro, in the endosomal pH range, soluble DM directly binds the Ig Fab domain and increases levels of free Ag released from immune complexes. Taken together, these results argue that DM and Ig intersect in the endocytic pathway of B cells with potential functional consequences.
Activated CD8+ T Cells Induce Expansion of Vβ5+ Regulatory T Cells via TNFR2 Signaling
Authors: Joedicke Jara J. , Myers Lara , Carmody Aaron B. , Messer Ronald J. , Wajant Harald , Lang Karl S. , Lang Philipp A. , Mak Tak W. , Hasenkrug Kim J. , Dittmer Ulf 
Published: August 2014

Abstract
Vβ5+ regulatory T cells (Tregs), which are specific for a mouse endogenous retroviral superantigen, become activated and proliferate in response to Friend virus (FV) infection. We previously reported that FV-induced expansion of this Treg subset was dependent on CD8+ T cells and TNF-α, but independent of IL-2. We now show that the inflammatory milieu associated with FV infection is not necessary for induction of Vβ5+ Treg expansion. Rather, it is the presence of activated CD8+ T cells that is critical for their expansion. The data indicate that the mechanism involves signaling between the membrane-bound form of TNF-α on activated CD8+ T cells and TNFR2 on Tregs. CD8+ T cells expressing membrane-bound TNF-α but no soluble TNF-α remained competent to induce strong Vβ5+ Treg expansion in vivo. In addition, Vβ5+ Tregs expressing only TNFR2 but no TNFR1 were still responsive to expansion. Finally, treatment of naive mice with soluble TNF-α did not induce Vβ5+ Treg expansion, but treatment with a TNFR2-specific agonist did. These results reveal a new mechanism of intercellular communication between activated CD8+ T cell effectors and Tregs that results in the activation and expansion of a Treg subset that subsequently suppresses CD8+ T cell functions.
Selective Phosphorylation of the Dlg1AB Variant Is Critical for TCR-Induced p38 Activation and Induction of Proinflammatory Cytokines in CD8+ T Cells
Authors: Crocetti Jillian , Silva Oscar , Humphries Lisa A. , Tibbs Michelle D. , Miceli M. Carrie 
Published: August 2014

Abstract
CD8+ T cells respond to TCR stimulation by producing proinflammatory cytokines, and destroying infected or malignant cells through the production and release of cytotoxic granules. Scaffold protein Discs large homolog 1 (Dlg1) specifies TCR-dependent functions by channeling proximal signals toward the activation of p38-dependent proinflammatory cytokine gene expression and/or p38-independent cytotoxic granule release. Two Dlg1 variants are expressed in CD8+ T cells via alternative splicing, Dlg1AB and Dlg1B, which have differing abilities coordinate TCR-dependent functions. Although both variants facilitate p38-independent cytotoxicity, only Dlg1AB coordinates p38-dependent proinflammatory cytokine expression. In this study, we identify TCR-induced Dlg1 tyrosine phosphorylation as a key regulatory step required for Dlg1AB-mediated p38-dependent functions, including proinflammatory cytokine expression. We find that Dlg1AB but not Dlg1B is tyrosine phosphorylated by proximal tyrosine kinase Lck in response to TCR stimulation. Furthermore, we identify Dlg1 tyrosine 222 (Y222) as a major site of Dlg1 phosphorylation required for TCR-triggered p38 activation and NFAT-dependent expression of proinflammatory cytokines, but not for p38-independent cytotoxicity. Taken together, our data support a model where TCR-induced phosphorylation of Dlg1 Y222 is a key point of control that endows Dlg1AB with the ability to coordinate p38 activation and proinflammatory cytokine production. We propose blocking Dlg1AB phosphorylation as a novel therapeutic target to specifically block proinflammatory cytokine production but not cytotoxicity.