Continued Funding:
Sergei Atamas, MD, PhD
Novel Molecular Mechanisms of Pulmonary Fibrosis in Rheumatic Diseases


Megan E. B. Clowse, MD, MPH
Immunologic alterations in lupus pregnancies leading to preterm birth

Loren D. Erickson, PhD
Homeostatic Regulation of Plasma Cell Precursors in Systemic Autoimmunity

John P. Fisher, PhD
IGF-1 Signaling in Engineered Cartilage

Diane Getsy-Palmer, MD, PhD
PTH Receptor Stimulated Osteoblast Mitogenesis

 Uzma Haque, MD
Treatment of vitamin D deficiency in rheumatoid arthritis

Richard J. Loeser, Jr., MD
A Systems Biology Approach for the Discovery of Novel Pathways in OA

 Esi M. Morgan DeWitt, MD
Cost-effectiveness of Biologics for RA in Clinical Practice

Jaspreet Pannu, PhD
Role of IGF-I/IGFBP axis in Scleroderma

Barbara J. Vilen, PhD
The Regulation of DC/MF-mediated Tolerance in Tolerance and Autoimmunity

Paul Weinhold, PhD
Electrical stimulation to improve proprioception in knee osteoarthritis

New Funding:
AnneMarie Brescia, MD
Prognostic Synovial Biomarkers in Juvenile Idiopathic Arthritis

Yvonne M. Golightly, PhD
Quality of a Foot Outcome Measure in a Community-Based Osteoarthritis Study


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Sergei Atamas, MD, PhD
Novel Molecular Mechanisms of Pulmonary Fibrosis in Rheumatic Diseases

University of Maryland-Baltimore
$100,000-Maryland Chapter Institutional Grant
Award Period: July 2008-June 2010

The Division of Rheumatology and Clinical Immunology (DRCI) at the University of Maryland School of Medicine offers advanced diagnostic and therapeutic services to patients with arthritis and other musculoskeletal and rheumatic diseases. The DRCI works closely with the Department of Orthopaedic Surgery and other components of the Center for Musculoskeletal Medicine to offer comprehensive patient management. In addition to providing state-of-the-art clinical care to patients, the DRCI is also a major educational resource on clinical and scientific aspects of arthritis for patients, their families and caregivers, students, practicing physicians, medical investigators, and staff. The Division has established a vigorous biomedical research program aimed at better understanding of the underlying causes and disease processes in patients with arthritis, musculoskeletal and rheumatic diseases. The ultimate goal of this research is to apply new knowledge to the development of better preventive measures and better treatments for patients with arthritis. This research program brings together the combined expertise of faculty members, physicians and scientists, from the DRCI; the Program in Integrative Medicine; and Departments of Microbiology and Immunology, Pathology, Epidemiology and Preventive Medicine, and Orthopaedic Surgery,. Research interests are focused on osteoarthritis, osteoporosis and recovery following hip fracture, and connective tissue diseases including systemic lupus erythematosus and scleroderma. The research proposed in this Institutional grant application focuses on novel mechanisms of excessive tissue scarring, particularly in the lungs (so-called pulmonary fibrosis), in connective tissue diseases. The DRCI is internationally recognized for its leadership in research on pulmonary fibrosis, a major complication in patients with connective tissue diseases. Studies will focus on two molecular mediators by which normally protective cells called T lymphocytes may promote excessive scarring of the lungs. Project 1 will test the hypothesis that a molecule called IL-4delta2 that is produced by T lymphocytes affects the lung in two ways – by promoting scarring directly (by itself) and also by attracting other cells from the blood that also contribute to scarring. Project 2 will examine whether a different molecule produced by T lymphocytes, called TRAIL, is involved in the lung scarring in live experimental animals and, if so, what mechanisms explain this relationship. To test these novel hypotheses, investigators in the DRCI will conduct experiments in laboratory animals (mice) that suffer from excessive scarring of the lungs. Experiments will be also conducted in vitro to look at the molecules within cells that become activated during lung scarring. These studies may form the basis for creating novel therapies and thus directly relate to the mission of Arthritis Foundation to improve the lives of patients with arthritis and related diseases.    
 

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Megan E. B. Clowse, MD, MPH
Immunologic alterations in lupus pregnancies leading to preterm birth
Duke University Medical Center
Sponsor: David S. Pisetsky, MD, PhD
$71,250-Arthritis Investigator Award
Award Period: January 2008-December 2011

A pregnant woman’s immune system must make remarkable changes to protect her fetus from rejection. Any alteration of this maternal tolerance for the fetus may lead to premature birth. Systemic Lupus Erythematosus (SLE) is characterized by a loss of tolerance to self-antigens, leading to inflammation and damage. Pregnancies in women with lupus encounter frequent complications, including a rate of preterm birth over 3 times higher than expected. Preterm birth places an infant at significant risk for long-term disabilities and death. Increased lupus activity has been identified as a major risk factor for preterm birth. The immunologic mechanism that links increased lupus activity and preterm birth, however, is unknown. In this study, I will identify immunologic changes in lupus that lead to preterm birth. I will initiate the Duke Autoimmune Pregnancy Cohort, in which I will collect detailed clinical information throughout each lupus pregnancy. In Specific Aim 1, I will assess the predictive value of previously defined markers for preterm birth at 24 weeks of pregnancy. I will test the predictive value of increased lupus activity on pregnancy outcomes. In non-lupus pregnancies, biomarkers such as C reactive protein, alpha-fetoprotein, ferritin, and fetal fibronectin are predictors for preterm birth. As these laboratory predictors of preterm birth have not been tested in lupus pregnancies, I will measure their clinical usefulness in this high-risk population. In Specific Aims 2 and 3, I will determine the extent to which experimental markers of lupus activity are associated with preterm birth. Samples will be collected and analyzed from several points: 24 weeks gestation, delivery, and from the cord blood. Prior studies show that lupus activity is accompanied by an increase in a unique subset of B cells. Pregnancy, on the other hand, is characterized by a decrease in B cells, though specific subsets have not been explored. Another marker of SLE activity, Interferon (IFN) Signature, is a collection of genes up-regulated by IFN-alpha. Though the IFN Signature has not been measured in pregnancy before, increased levels of IFN-alpha have been shown to harm pregnancy success. I will measure B cell subsets and the IFN signature, with the hypothesis that as each marker changes in pregnancy in response to SLE activity, maternal tolerance is impaired, and preterm birth is encouraged. This study will identify inflammatory and immunologic changes that promote preterm birth in lupus pregnancy and will direct future mechanistic studies in maternal tolerance in lupus. Though I was previously trained in clinical research, it is clear to me that the next advances in lupus pregnancy will be in immunology. This grant will provide me with the education and research training to enable my future work in clinical immunology. In doing so, I will develop a career dedicated to improving the lives, pregnancies, and families of women with lupus.

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Loren D. Erickson, PhD
Homeostatic Regulation of Plasma Cell Precursors in Systemic Autoimmunity
University of Virginia
Sponsor: Timothy Bender, PhD
$85,500–Arthritis Investigator Award
Award Period: July 2006–June 2010

A hallmark of a protective antibody response to pathogens is its longevity, and is the basis for childhood immunizations. One cellular component that contributes to the vast lifespan of this response is the plasma cell (PC). While PC longevity is an asset for protective immunity, it is a morbid liability in PC disorders, such as autoimmune diseases like rheumatoid arthritis that is mediated by the production of antibodies that destroy one's own body. We have identified a novel cell type that is a proximal precursor of PCs that we believe are aberrantly regulated in autoimmunity, leading to the production of self-reactive antibodies. Recently, we have reported that a new molecule, BCMA, is critical for normal PC survival. We are trying to understand the role of BCMA at the precursor level in hopes of targeting it as a novel therapeutic in the treatment of autoimmune disease. 
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John P. Fisher, PhD
IGF-1 Signaling in Engineered Cartilage
University of Maryland-College Park
Sponsor: Raymond A. Adomaitis, PhD
$85,500-Arthritis Investigator Award
Award Period: July 2006–June 2010

As the average age in both the United States and Western Europe begins to rapidly increase, diseases associated with older populations have become more prevalent. Osteoarthritis, or the degradation of joint cartilage, is certainly one of these conditions. The strategy we propose for the treatment of osteoarthritis, as well as other degenerative articular cartilage conditions, is articular cartilage regeneration by cell transplantation. Here, cartilage forming cells would be taken from the patient, encapsulated in a synthetic biomaterial, and then transplanted into the defect site. After implantation, the biomaterial would slowly degrade away while the transplanted cells would synthesize new cartilage, regenerating cartilage tissue in the defect site. While this approach has been proposed by many investigators, we hypothesize that the key factor that must be considered for successful transplantation of cells is the effect of the synthetic biomaterial on the ability of the cells to communicate with one another. Communication, or signaling, among cell populations is a process that has been widely investigated in scientific literature. However, little is known about how cells communicate with one another when they exist within a synthetic material. Clearly, the different environment that the transplanted cells experience must affect their typical processes. Furthermore, the movement of signals from signaling cells to receiving cells will certainly be different in synthetic biomaterials than in normal tissue. Therefore, we propose to examine these processes in biomaterials, so as to direct the development of constructs for successful cell transplantation. To this end, we propose experiments that try to discern the effect of different biomaterial properties on the signaling of cell populations. Using a rational design, we first examine biomaterials characteristics that augment the synthesis of signals. Next we examine properties that control the movement of these signals between cells. Finally, we contrast the effects of signal synthesis and movement to understand their ability to control cell function. The successful completion of the proposed work will be an exciting, new approach for the development of cartilage tissue as well as other tissues

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Diane Getsy-Palmer, MD, PhD
PTH Receptor Stimulated Osteoblast Mitogenesis
Duke University Medical Center
Sponsor: Robert J. Lefkowitz, MD
$85,500-Arthritis Investigator
Award Period: January 2007-December 2010

The overall goal of the proposed research is to increase our understanding of how parathyroid hormone (PTH) mediates anabolic bone formation. Osteoporosis, which is characterized by loss of bone micro-architecture, low bone mass, and fractures, is a significant clinical problem for individuals afflicted with rheumatoid arthritis. Although the causes of osteoporosis are complex, it represents the overall imbalance between osteoblast-mediated bone formation and osteoclast-mediated bone-resorption. Current therapies for the treatment of osteoporosis are aimed primarily at inhibiting the bone resorption process and do not regenerate lost bone architecture that is critical to bone strength. PTH has been shown to be a potent agent capable of stimulating bone accrual. Little is currently known about the mechanistic basis for these effects. Cell surface receptors for PTH have been recognized as important regulators of osteoblast (bone forming cells) proliferation and differentiation. Receptors for PTH interact with key signaling proteins Gq, Gs, beta-arrestin, and epidermal growth factor receptors (EGFRs). We hypothesize that altering the interaction between the PTH receptor and these signaling proteins will result in changes in bone development. This proposal presents a research plan whose goal is to determine the role of four mediators, Gq, Gs, beta-arrestin and EGFR of PTH stimulated cell signaling and their affect on growth and differentiation in osteoblasts. Increasing our understanding of PTH receptor signaling is essential in order to devise novel therapeutics to selectively target anabolic bone formation.

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Uzma Haque, MD
Treatment of vitamin D deficiency in rheumatoid arthritis
Johns Hopkins School of Medicine
$50,000-Maryland Office Grant
Award Period: July 2008-June 2010

Rheumatoid arthritis (RA) is a chronic, destructive arthritis associated with increased morbidity and mortality. It is the most prevalent inflammatory arthritis, with significant disease burden on the individual and on the society.
Vitamin D is a steroid hormone with important skeletal and non-skeletal biologic functions. Its deficiency is prevalent with serious musculoskeletal consequences. There is growing evidence that vitamin D may be important in prevention of diseases, such as cancer and autoimmune disorders. Clinical manifestations of vitamin D deficiency are subtle; thus it frequently is undiagnosed. Once diagnosed, however this deficiency is easily corrected.
Preliminary studies show a high prevalence of vitamin D deficiency in RA. In our RA dataset, 60% of the patients tested were vitamin D deficient (25(OH) D < 30ng/ml). Recent studies suggest that low vitamin D levels may be associated with increased disease activity and disability in RA. However, the effect of correcting vitamin D deficiency in RA is unknown.
In this pilot study, our aims are:
(1) to conduct a cross-sectional analysis and compare quality of life /health status and disease activity in RA patients who are vitamin D deficient with those who are vitamin D sufficient; and (2) to supplement vitamin D in the deficient group in a randomized placebo controlled trial with open label extension to establish the short and long term effect of normalizing vitamin D on quality of life/health status and disease activity in vitamin D deficient RA patients.
Thus, this study will generate preliminary data regarding treatment of vitamin D deficiency and its effect on important patient related quality of life outcomes in RA.

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Richard J. Loeser, Jr., MD
A Systems Biology Approach for the Discovery of Novel Pathways in OA
Wake Forest University Health Sciences
$95,000-Innovative Research Grant
Award Period: August 2008-July 2010

Osteoarthritis (OA) is the most common cause of chronic disability in older adults and new treatments for this condition are desperately needed. OA results from progressive destruction of the articular cartilage which is the tissue present on the ends of the bones that is responsible for normal joint movement. The damage to the cartilage is accompanied by thickening of the bone beneath the cartilage, growth of bony spurs, inflammation in the joint lining, and destruction of other joint tissues, including the menisci (in the knee) and ligaments. The joint destruction is associated with pain and loss of function leading to “joint failure”. There are two major roadblocks in the management of people with OA: 1) lack of therapies proven to stop or even slow progression of the disease; and 2) lack of biomarkers proven to detect early disease, predict which people are more likely to progress, or measure response to therapy. These roadblocks exist in large part because translational research in OA has been limited by: 1) the lack of availability of diseased tissue from humans except at advanced stages (after joint replacement); 2) lack of adequate animal models; and 3) a predominant focus on the study of the disease in a single tissue (most often cartilage) without consideration of the joint as an organ affected by OA.
The long-term goal of this project is to use a novel systems biology approach to provide a better understanding of the basic cellular and molecular mechanisms driving joint tissue destruction during the development of osteoarthritis. Systems biology is a term used to describe a comprehensive research strategy used to better understand complex biological systems by integrating different types of data and analyzing the data with recently developed computational methods. The goal is to develop a map or model of how different components of the system interact to result in a disease process. We propose to use these methods to develop a map of the transcriptional regulatory networks that underlie development of OA in a stage-specific (early, middle, and late stages of the disease), whole organ (the joint), manner. Transcriptional regulatory networks are processes that control activity of the genes within a tissue which are responsible for controlling how the tissue functions or, in the case of arthritis, how the tissue destruction is being regulated. By integrating this transcriptional regulatory network with publicly available information on signaling pathways and protein-protein interaction networks, we propose to: 1) identify key genes and proteins that could serve as novel targets for disease modifying therapy, as well as novel stage-specific biomarkers; and 2) identify pathways that are involved in the disease process, which will enhance our understanding of the mechanism and be useful in developing new therapies to modulate the activity of these pathways.

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Esi M. Morgan DeWitt, MD
Cost-effectiveness of Biologics for RA in Clinical Practice
Duke University Medical Center
$150,000-Engalitcheff Arthritis Outcomes Initiative-Maryland Chapter (moved to Cincinnati Childrens Hospital
Medical Center)
Award Period: July 2006–June 2010


Rheumatoid arthritis (RA) is a chronic disabling disease without cure that afflicts 1% of the population. TNF-alpha inhibitors (adalimumab, etanercept, infliximab, “biologic drugs”) have revitalized RA treatment with the promise of rapid symptom relief and inhibition of disease progression. However, the enthusiasm generated by these biologic drugs is tempered by their substantial acquisition costs of $12,500-$20,000 per patient per year. The climate of rising healthcare costs and increased shifting of the cost burden to patients raises three important questions about the use of biologic drugs for treatment of RA in clinical practice: 1) which patients have access to such therapies, 2) which patients benefit from the therapies, and 3) whether the higher costs are reasonable given the additional health benefits from treatment with biologic drugs (that is, are they “cost-effective”). We will address the questions above by analysis of data from the Arthritis, Rheumatism, and Aging Medical Information System (ARAMIS). ARAMIS is a high quality, large, longitudinal observational dataset with more than 2 decades of information on patient disease status, medication use, health care resource use and patient outcomes. There have been previous cost-effectiveness studies of biologic drugs which were based on data from randomized clinical trials; however, they do not capture the real world use of these drugs. We will address four scientific aims that will identify potential disparities in treatment with biologic drugs in the current practice of rheumatology, examine the effectiveness as well as variability in outcomes of patients treated with biologic drugs, compare medical resource use and costs in patients treated with biologic drugs compared to a matched comparable group of patients who were treated with other medications, and perform head-to-head comparisons of the cost-effectiveness of the different biologic drugs . The long term goal of this study is to enhance the rational use of biologic drugs in treatment of RA. The project will entail collaboration between investigators from the Center for Clinical and Genetic Economics, Duke Clinical Research Institute, the Leonard Davis Institute of Health Economics of the University of Pennsylvania, and Stanford University.

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Jaspreet Pannu, PhD
Role of IGF-I/IGFBP axis in Scleroderma
University of Maryland-Baltimore
$75,000-Maryland Office
Award Period: April 2008-March 2010


Scleroderma, also called systemic sclerosis (SSc) is a severe disease. Scleroderma patients suffer from significant scarring of their skin and internal organs, and joint inflammation (arthritis) because their immune system that normally protects against viruses and bacteria now attacks their own body. The excessive scarring in patients is also called fibrosis. Women, especially African-American women, are afflicted by scleroderma, including fibrosis, most severely. There is no cure for scleroderma and current treatments simply provide symptomatic relief. The proposed research is aimed at better understanding one of the mechanisms contributing to overproduction of collagen. We observed that a molecule called insulin-like growth factor-I (IGF-I) may be involved in scleroderma, particularly in the excessive scarring process. However such involvement appears complex, as IGF-I interacts with a number of other molecules in these patients, contributing to the disease. This study will help better understand mechanism of excessive scarring in patients with arthritis and thus is directed to improving their lives.    

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Barbara J. Vilen, PhD
The Regulation of DC/MF-mediated Tolerance in Tolerance and Autoimmunity
University of North Carolina, Chapel Hill
$95,000-Innovative Research Grant
Award Period: July 2008-June 2010


When our immune system responds to infections (innate immunity) dendritic cell, macrophages and B cells, become activated by bacterial and viral products such as bacterial LPS and viral DNA/RNA. The dendritic cells and macrophages produce cytokines (IL-6 and soluble (s)CD40L) while the B cells produce immunoglobulins (antibodies) of multiple specificities in an effort to clear the pathogen. Most secreted antibodies have a positive outcome for the host because some will bind to the pathogen and facilitate clearance. However, inherent in this process is the ability of self-reactive B cells to become activated and produce antibodies that bind host proteins (autoantibodies). This has a negative outcome because it can lead to autoimmune disease. Thus, it seems that individuals who never develop autoimmune disease (non-autoimmune-prone) have internal mechanisms that repress the production of autoantibody from self-reactive cells while simultaneously allowing antibodies that bind foreign proteins to be produced. Understanding how this “selective” regulation occurs is central to treating autoimmune diseases without the use of non-specific immunosuppressive therapies.
Our studies focus on how autoreactive B cells are regulated during innate immunity. We found that myeloid cells (dendritic cells and macrophages) within the immune system selectively repress the production of autoantibodies by self-reactive B cells without affecting the ability of other B cells to produce beneficial antibodies. This is achieved through the production of IL-6 and soluble CD40L by dendritic cells and macrophages. This is an important finding because it provides a cellular explanation for how the host is allowed to produce antibodies to clear pathogens but simultaneously maintains autoreactive B cells in an unresponsive state. We hypothesize that defects in this mechanism underlie the production of autoantibody and disease in lupus-prone mice. In this application we propose to establish the molecular basis for how the self-reactive B cells repress autoantibody secretion while the B cells that are reactive to foreign antigens are allowed to produce antibody. We propose that lupus-prone mice lose their ability to selectively repress autoreactive B cells allowing these cells to become activated during infection like their naïve counterparts. We have some exciting preliminary data showing that B cells from lupus-prone mice fail to respond to IL-6 and soluble CD40L in a repressive manner; leading us to hypothesize that “lupus-prone” B cells harbor intrinsic defects that preclude their regulation during innate immune responses.

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Paul Weinhold, PhD
Electrical stimulation to improve proprioception in knee osteoarthritis
University of North Carolina at Chapel Hill
$95,000-Innovative Research Grant
Award Period: September 2008-August 2010


Proprioception is the awareness of limb position and movement in space. Poor proprioception is believed to have a role in the progression of knee osteoarthritis (OA) by contributing to detrimental loading of the knee joint. A novel means of improving proprioception may be thru stochastic resonance electrical stimulation (SR). SR has been shown to enhance an individual’s ability to perceive sensory stimuli. This study’s broad objective is to evaluate the potential effectiveness of SR as a novel therapy for knee OA. Three conditions (no stimulation/no sleeve, no stimulation/sleeve, and stimulation/sleeve) will be used in all knee OA patients and compared. The subject’s awareness of the position of the knee joint will be assessed during a seated and standing task to evaluate SR’s influence on knee proprioception. We hypothesize that SR will improve knee proprioception compared to the control and sleeve alone conditions. In addition, knee mechanics and muscle activation patterns will be assessed during walking to evaluate the influence of SR on detrimental loading patterns present with knee OA. We hypothesize that SR will cause increased knee flexion and decreased muscle co-contraction, knee axial loads, and loading rates during walking. Balance performance will also be assessed during a single leg stance test. It is hypothesized that SR will improve balance as indicated by a reduction in the amount of sway the subject displays during the test. Subjects will also complete a WOMAC Osteoarthritis index questionnaire assessing their functional activity and a questionnaire assessing their knee instability. Scores from the questionnaires and the other outcome measures will be related to the results of the proprioception tests to determine which measures are predictive of poor proprioception.    

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NEW Funding:
AnneMarie Brescia, MD
Prognostic Synovial Biomarkers in Juvenile Idiopathic Arthritis
Alfred I. duPont Hospital for Children
Innovative Research Grant – Juvenile Arthritis

Juvenile Idiopathic Arthritis (JIA) is the most common pediatric rheumatic disease, affecting 50,000 children in the US. There are 7 subsets, one of which, oligoarticular form (oligo-JIA), represents 50% of the cases and is the focus of this proposal. Outcome in oligo-JIA is usually benign, but 30% of affected children evolve into another form known as extended oligo-JIA, with more joints involved. Since this evolution may entail disability, early prediction of this course is desirable. Current knowledge does not provide accurate ways of predicting outcome and response to treatment. The aims of this study are to investigate biomarkers to predict disease extension and sustained response to treatment. We hypothesize that fibroblast-like synoviocytes (FLS), cells that reside in the joint, rather than blood cells, are likely to be informative. Our preliminary work showed that levels of certain chemicals (cytokines) in joint fluid predicted a sustained response to joint injection. We have also conducted gene expression microarrays comparing FLS from oligo-JIA and control FLS. There were striking differences in gene expression between control and oligo-JIA FLS, underlining the potential of FLS as source of biomarkers. Gene expression microarray is like a snapshot of what the DNA of a cell is commanding the cell to make at a given time. This snapshot is made by determining the state of activation of about 30,000 genes at the same time. We plan to apply microarray to investigate what is different about the FLS of patients who respond and those who do not respond to joint injection and also between FLS of those with extension vs. those without. In addition, our work could lay the groundwork for further study of disease mechanism of JIA, which is so far unknown. Based on preliminary work, our second hypothesis is that dysregulation of the TGFbeta signaling pathway is central to the pathogenesis of JIA. Bony overgrowth is a feature unique to JIA and is not seen in adult RA. We will investigate whether changes in the expression of TGFbeta-related cytokines seen in our initial data may have a role in this clinical finding in patients. Although significant work has been done on FLS from the joints of adult patients with rheumatoid arthritis (RA), investigations of these critical cells are lacking in children. Much of parental concern surrounding this disease is fear of the unknown: Development of biomarkers allows us to provide families and patients with more complete information regarding prognosis and to make more informed decisions regarding treatment strategies. Addressing juvenile idiopathic arthritis as early as possible to prevent joint damage will in turn significantly improve the long-term functional outcome and life enjoyment of children with arthritis. Demonstrating the role of the TGFbeta signaling pathway in the pathogenesis of JIA has implications for future treatment options.

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Yvonne M. Golightly, PhD
Quality of a Foot Outcome Measure in a Community-Based Osteoarthritis Study
University of North Carolina at Chapel Hill
Postdoctoral Fellowship Award
Supervisor: Joanne Jordan, MD

Foot pain has been shown to be associated with physical disability, especially in older adults. Medical doctors, other health professionals, and researchers need to pay more attention to foot symptoms and problems with the foot in their patients. One way a doctor, other health professional, or researcher can learn about a patient’s foot symptoms and daily physical function is with a questionnaire. One questionnaire that may be useful in both the clinic and in research studies is the Foot and Ankle Outcome Score (FAOS). This questionnaire contains 42 questions that ask about pain, other symptoms, physical function, and quality of life. This questionnaire takes 7-10 minutes to complete, and it can be completed by the patient in the waiting room. This questionnaire has been tested in adults who were 20-60 years old with ankle stability problems. This questionnaire needs to be tested in older adults who have other foot and ankle problems, including arthritis, to see if it can help these patients communicate their symptoms and problems with physical function. In this study, the FAOS will be tested by participants in the Johnston County Osteoarthritis Project. This study includes nearly 1,500 African American and white men and women from a rural North Carolina county, and participants are 45-94 years old. This study will help doctors, other health professionals, and researchers learn whether the FAOS questionnaire would be a useful questionnaire among older adults with a variety of foot problems. The FAOS questionnaire may help identify adults who are having foot symptoms and problems so that doctors and other health professionals can prevent or treat physical disability.

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