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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.jshoulderelbow.org/?rss=yes"><title>Journal of Shoulder and Elbow Surgery</title><description>Journal of Shoulder and Elbow Surgery RSS feed: Current Issue.    The official publication for eight leading specialty organizations, this authoritative journal is the only publication to focus exclusively 
on medical, surgical, and physical techniques for treating injury/disease of the upper extremity, including the shoulder girdle, arm, 
and elbow. Clinically oriented and peer-reviewed, the Journal provides an international forum for the exchange of information on new 
techniques, instruments, and materials.  Journal of Shoulder and Elbow Surgery  features vivid photos, professional illustrations, 
and explicit diagrams that demonstrate surgical approaches and depict implant devices. Topics covered include fractures, dislocations, 
diseases and injuries of the rotator cuff, imaging techniques, arthritis, arthroscopy, arthroplasty, and rehabilitation.   </description><link>http://www.jshoulderelbow.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc.  </dc:rights><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:issn>1058-2746</prism:issn><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc.  </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005775/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005210/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005738/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611004757/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005763/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611004824/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005192/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005179/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611004800/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS105827461100468X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005611/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS105827461100560X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005180/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611004812/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005751/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS105827461100574X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611002679/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611002734/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611002771/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611004356/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005933/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005945/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jshoulderelbow.org/article/PIIS1058274611005957/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005775/abstract?rss=yes"><title>Editor’s note</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005775/abstract?rss=yes</link><description>It is well established that secure healing between the rotator cuff tendon and bone after repair is often unpredictable and challenging to achieve. The normal tendon–bone insertion site is a highly specialized tissue, and the structure and composition of this native insertion site is not re-established after rotator cuff repair. This is likely due to deficiencies in both the biologic and biomechanical environment. The cellular and molecular signals that lead to formation of the native insertion site during embryogenesis and development are not recapitulated during tendon healing. This has led to the recent, intense interest in approaches to augment the biologic events that occur during tendon healing.</description><dc:title>Editor’s note</dc:title><dc:creator>Leesa M. Galatz, Scott A. Rodeo</dc:creator><dc:identifier>10.1016/j.jse.2011.11.018</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>147</prism:startingPage><prism:endingPage>148</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005210/abstract?rss=yes"><title>Measurement of in vivo tendon function</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005210/abstract?rss=yes</link><description>Chronic tendon pathologies (eg, rotator cuff tears, Achilles tendon ruptures) are common, painful, debilitating, and a significant source of medical expense. Treatment strategies for managing tendon pathologies vary widely in invasiveness and cost, with little scientific basis on which to base treatment selection. Conventional techniques for assessing the outcomes of physical therapy or surgical repair typically rely on patient-based assessments of pain and function, physical measures (eg, strength, range of motion, or stability), and qualitative assessments using magnetic resonance imaging or ultrasound. Unfortunately, these conventional techniques provide only an indirect assessment of tendon function. The inability to make a direct quantitative assessment of the tendon’s mechanical capabilities may help to explain the relatively high rate of failed tendon repairs and has led to an interest in the development of tools for directly assessing in vivo tendon function. The purpose of this article is to review methods for assessing tendon function (ie, mechanical properties and capabilities) during in vivo activities. This review will describe the general principles behind the experimental techniques and provide examples of previous applications of these techniques. In addition, this review will characterize the advantages and limitations of each technique, along with its potential clinical utility. Future efforts should focus on developing broadly translatable technologies for quantitatively assessing in vivo tendon function. The ability to accurately characterize the in vivo mechanical properties of tendons would improve patient care by allowing for the systematic development and assessment of new techniques for treating tendon pathologies.</description><dc:title>Measurement of in vivo tendon function</dc:title><dc:creator>Michael J. Bey, Kathleen A. Derwin</dc:creator><dc:identifier>10.1016/j.jse.2011.10.023</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>149</prism:startingPage><prism:endingPage>157</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005738/abstract?rss=yes"><title>Basic mechanisms of tendon fatigue damage</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005738/abstract?rss=yes</link><description>Pathologic processes intrinsic and extrinsic to the tendons have been proposed as the underlying cause of rotator cuff disease, but the precise etiology is not known. Tear formation is, in part, attributable to the accumulation of subrupture tendon fatigue damage. We review the molecular, mechanical, and structural changes induced in tendons subjected to controlled amounts of fatigue loading in an animal model of early tendinopathy. The distinct tendon responses to low and moderate levels of loading, as opposed to high levels, provide insight into the potential mechanisms for the therapeutic benefits of exercise in the treatment of rotator cuff tendinopathy. The progression of damage accumulation leading to fiber rupture and eventual tendon tearing seen with higher loading illustrates the progression from tendinopathy to full-thickness tearing. We hope that this more realistic animal model of tendon fatigue damage will allow better assessment of biologic, mechanical, tissue-engineering, and rehabilitation strategies to improve repair success.</description><dc:title>Basic mechanisms of tendon fatigue damage</dc:title><dc:creator>Andrew Neviaser, Nelly Andarawis-Puri, Evan Flatow</dc:creator><dc:identifier>10.1016/j.jse.2011.11.014</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>158</prism:startingPage><prism:endingPage>163</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611004757/abstract?rss=yes"><title>Muscle degeneration in rotator cuff tears</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611004757/abstract?rss=yes</link><description>Rotator cuff tears are among the most common injuries seen by orthopedic surgeons. Although small- and medium-sized tears do well after arthroscopic and open repair, large and massive tears have been shown to develop marked muscle atrophy and fatty infiltration within the rotator cuff muscles. These pathologic changes have been found to be independent predictors of failed surgical repair with poor functional outcomes. To understand the pathophysiology of rotator cuff disease, we must first develop an understanding of the changes that occur within the cuff muscles themselves. The purpose of this review is to summarize the molecular pathways behind muscular degeneration and emphasize new findings related to the clinical relevance of muscle atrophy and fatty infiltration seen with rotator cuff tears. Understanding these molecular pathways will help guide further research and treatment options that can aim to alter expression of these pathways and improve outcomes after surgical repair of massive rotator cuff tears.</description><dc:title>Muscle degeneration in rotator cuff tears</dc:title><dc:creator>Dominique Laron, Sanjum P. Samagh, Xuhui Liu, Hubert T. Kim, Brian T. Feeley</dc:creator><dc:identifier>10.1016/j.jse.2011.09.027</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>164</prism:startingPage><prism:endingPage>174</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005763/abstract?rss=yes"><title>Mechanisms of fatty degeneration in massive rotator cuff tears</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005763/abstract?rss=yes</link><description>Fatty degeneration of chronically injured muscle is a commonly recognized consequence of massive rotator cuff tears. Current surgical treatments are unable to alter or reverse the progression of fatty degeneration and are associated with poor functional outcomes in these patients. Therefore, a better understanding of the pathophysiology of fatty degeneration is required. As such, recent discoveries in stem cell biology and new animal models have significantly advanced our understanding of the cellular and molecular basis of fatty degeneration. Future studies will facilitate development of novel treatments to prevent the progression of fatty degeneration and improve muscle regeneration in patients with massive rotator cuff tears.</description><dc:title>Mechanisms of fatty degeneration in massive rotator cuff tears</dc:title><dc:creator>Jason R. Kang, Ranjan Gupta</dc:creator><dc:identifier>10.1016/j.jse.2011.11.017</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>175</prism:startingPage><prism:endingPage>180</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611004824/abstract?rss=yes"><title>Biologic approaches to enhance rotator cuff healing after injury</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611004824/abstract?rss=yes</link><description>Background: Despite the advances in surgical procedures to repair the rotator cuff, there is a high incidence of failure. Biologic approaches, such as growth factor delivery and stem cell and gene therapy, are potential targets for optimization to improve the outcome of rotator cuff therapies and reduce rates of reinjury. This article outlines the current evidence for growth factor and stem cell therapy in tendon healing and the augmentation of rotator cuff repair.Methods: Literature on the PubMed–National Center for Biotechnology Information database was searched using the keywords growth factor, factor, gene therapy, stem cell, mesenchymal, or bone marrow in combination with rotator cuff, supraspinatus, or infraspinatus. Articles that studied growth factors or stem cells alone in rotator cuff repair were selected. Only 3 records showed use of stem cells in rotator cuff repair; thus, we expanded our search to include selected studies on stem cells and Achilles or patellar tendon repairs. Bibliographies and proceedings of meetings were searched to include additional applicable studies. We also included hitherto unpublished data by our group on the use of stem cell transplantation for rotator cuff therapy.Results: More than 70 articles are summarized, with focus on recent original research papers and significant reviews that summarized earlier records.Conclusions: Use of growth factors, stem cell therapy, and other tissue-engineering means serve to augment classical surgical rotator cuff repair procedures. The combination of stem cells and growth factors resulted in enhanced repair that emulated uninjured tissue, but the literature search reflected paucity of research in this field. Preclinical evidence from gene therapy and stem cell studies can be used as a start to move therapy from the experimental phase to clinical translation in patients.Level of evidence: Review Article.</description><dc:title>Biologic approaches to enhance rotator cuff healing after injury</dc:title><dc:creator>Christian Isaac, Burhan Gharaibeh, Michelle Witt, Vonda J. Wright, Johnny Huard</dc:creator><dc:identifier>10.1016/j.jse.2011.10.004</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>181</prism:startingPage><prism:endingPage>190</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005192/abstract?rss=yes"><title>Lessons we can learn from gene expression patterns in rotator cuff tears and tendinopathies</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005192/abstract?rss=yes</link><description>Persistently high failure rates that are reported after rotator cuff repairs have encouraged greater understanding of the pathophysiology that underlies rotator cuff tears. Biologic changes that contribute to the pathogenesis of rotator cuff tears and tendinopathies, as well as adaptation after these changes, have been well described. A subset of patients with a genetic predisposition to early onset of rotator cuff tears and earlier symptom and disease progression have been identified. Many biologic changes occurring at the gene level have been identified. Pathways that are believed to contribute to rotator cuff tendinopathies include extracellular matrix remodeling, angiogenesis, changes in metabolism, apoptosis, and stress-related genes. Metaplasia of rotator cuff cells is contributed to by changes in gene expression. Modification of these gene changes may be possible through mechanical loading, drugs, or cellular manipulation. Gene changes may offer greater insight into why certain tears fail to heal and help to identify therapeutic targets.</description><dc:title>Lessons we can learn from gene expression patterns in rotator cuff tears and tendinopathies</dc:title><dc:creator>Salma Chaudhury, Andrew J. Carr</dc:creator><dc:identifier>10.1016/j.jse.2011.10.022</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>191</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005179/abstract?rss=yes"><title>Metalloproteases and rotator cuff disease</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005179/abstract?rss=yes</link><description>The molecular changes occurring in rotator cuff tears are still unknown, but much attention has been paid to better understand the role of matrix metalloproteinases (MMP) in the development of tendinopathy. These are potent enzymes that, once activated, can completely degrade all components of the connective tissue, modify the extracellular matrix (ECM), and mediatethe development of painful tendinopathy and tendon rupture. To control the local activity of activated proteinases, the same cells produce tissue inhibitors of metalloproteinases (TIMP) that bind to the enzymes and prevent degradation. The balance between the activities of MMPs and TIMPs regulates tendon remodeling, whereas an imbalance produces a collagen dis-regulation and disturbances intendons. ADAMs (a disintegrin and metalloproteinase) are cell membrane-linked enzymes with proteolytic and cell signaling functions. ADAMTSs (ADAM with thrombospondin motifs) are secreted into the circulation, and constitute a heterogenous family of proteases with both anabolic and catabolic functions. Biologic modulation of endogenous MMP activity to basal levels may reduce pathologic tissue degradation and favorably influence healing after rotator cuff repair. Further studies are needed to better define the mechanism of action, and whether these new strategies are safe and effective in larger models.</description><dc:title>Metalloproteases and rotator cuff disease</dc:title><dc:creator>Angelo Del Buono, Francesco Oliva, Umile Giuseppe Longo, Scott A. Rodeo, John Orchard, Vincenzo Denaro, Nicola Maffulli</dc:creator><dc:identifier>10.1016/j.jse.2011.10.020</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>200</prism:startingPage><prism:endingPage>208</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611004800/abstract?rss=yes"><title>Potential of collagen cross-linking therapies to mediate tendon mechanical properties</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611004800/abstract?rss=yes</link><description>Collagen cross-links are fundamental to the mechanical integrity of tendon, with orderly and progressive enzymatic cross-linking being central to healthy development and injury repair. However, the nonenzymatic cross-links that form as we age are associated with increased tendon brittleness, diminished mechanical resistance to injury, and impaired matrix remodeling. Collagen cross-linking thus sits at the center of tendon structure and function, with important implications to age, disease, injury, and therapy. The current review touches on these aspects from the perspective of their potential relevance to the shoulder surgeon. We first introduce the most well-characterized endogenous collagen cross-linkers that enable fibrillogenesis in development and healing. We also discuss the glycation-mediated cross-links that are implicated in age- and diabetes-related tendon frailty and summarize work toward therapies against these disadvantageous cross-links. Conversely, we discuss the introduction of exogenous collagen cross-links to augment the mechanical properties of collagen-based implants or native tendon tissue. We conclude with a summary of our early results using exogenous collagen cross-linkers to prevent tendon tear enlargement and eventual failure in an in vitro model of partial tendon tear.</description><dc:title>Potential of collagen cross-linking therapies to mediate tendon mechanical properties</dc:title><dc:creator>Gion Fessel, Christian Gerber, Jess G. Snedeker</dc:creator><dc:identifier>10.1016/j.jse.2011.10.002</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>209</prism:startingPage><prism:endingPage>217</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS105827461100468X/abstract?rss=yes"><title>Cytokines in rotator cuff degeneration and repair</title><link>http://www.jshoulderelbow.org/article/PIIS105827461100468X/abstract?rss=yes</link><description>The pathogenesis of rotator cuff degeneration remains poorly defined, and the incidence of degenerative tears is increasing in the aging population. Rates of recurrent tear and incomplete tendon-to-bone healing after repair remain significant for large and massive tears. Previous studies have documented a disorganized, fibrous junction at the tendon-to-bone interface after rotator cuff healing that does not recapitulate the organization of the native enthesis. Many biologic factors have been implicated in coordinating tendon-to-bone healing and maintenance of the enthesis after rotator cuff repair, including the expression and activation of transforming growth factor-β, basic fibroblast growth factor, platelet-derived growth factor-β, matrix metalloproteinases, and tissue inhibitors of metalloproteinases. Future techniques to treat tendinopathy and enhance tendon-to-bone healing will be driven by our understanding of the biology of this healing process after rotator cuff repair surgery. The use of cytokines to provide important signals for tissue formation and differentiation, the use of gene therapy techniques to provide sustained cytokine delivery, the use of stem cells, and the use of transcription factors to modulate endogenous gene expression represent some of these possibilities.</description><dc:title>Cytokines in rotator cuff degeneration and repair</dc:title><dc:creator>Asheesh Bedi, Travis Maak, Christopher Walsh, Scott A. Rodeo, Dan Grande, David M. Dines, Joshua S. Dines</dc:creator><dc:identifier>10.1016/j.jse.2011.09.020</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>218</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005611/abstract?rss=yes"><title>The role of mechanobiology in tendon healing</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005611/abstract?rss=yes</link><description>Mechanical cues affect tendon healing, homeostasis, and development in a variety of settings. Alterations in the mechanical environment are known to result in changes in the expression of extracellular matrix proteins, growth factors, transcription factors, and cytokines that can alter tendon structure and cell viability. Loss of muscle force in utero or in the immediate postnatal period delays tendon and enthesis development. The response of healing tendons to mechanical load varies depending on anatomic location. Flexor tendons require motion to prevent adhesion formation, yet excessive force results in gap formation and subsequent weakening of the repair. Excessive motion in the setting of anterior cruciate ligament reconstruction causes accumulation of macrophages, which are detrimental to tendon graft healing. Complete removal of load is detrimental to rotator cuff healing; yet, large forces are also harmful. Controlled loading can enhance healing in most settings; however, a fine balance must be reached between loads that are too low (leading to a catabolic state) and too high (leading to microdamage). This review will summarize existing knowledge of the mechanobiology of tendon development, homeostasis, and healing.</description><dc:title>The role of mechanobiology in tendon healing</dc:title><dc:creator>Megan L. Killian, Leonardo Cavinatto, Leesa M. Galatz, Stavros Thomopoulos</dc:creator><dc:identifier>10.1016/j.jse.2011.11.002</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>228</prism:startingPage><prism:endingPage>237</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS105827461100560X/abstract?rss=yes"><title>The role of nitric oxide in tendon healing</title><link>http://www.jshoulderelbow.org/article/PIIS105827461100560X/abstract?rss=yes</link><description>Nitric oxide (NO) is a small free radical that is generated by a family of enzymes called the nitric oxide synthases (NOS). There are 3 isoforms of NOS: endothelial NOS (eNOS), brain or neuronal NOS (bNOS), and inducible NOS (iNOS). In experiments performed during the last 20 years, we have shown that NO is induced by all 3 isoforms of NOS after tendon injury and that NOS activity is upregulated in tendinopathy. In normal uninjured tendons, there is very little NOS activity. In injured rat and human tendons, NOS activity was found in healing fibroblasts in a temporal fashion. In animal models, competitive inhibition of NOS resulted in reduced tendon healing, whereas the addition of NO resulted in enhanced tendon healing. In cultured human cells, the addition of NO via chemical means and adenovirus transfection resulted in enhanced collagen synthesis. We performed 3 randomized, double-blinded clinical trials that demonstrated a significant positive beneficial effect of NO treatment on clinical symptoms and function in patients with Achilles tendinopathy, tennis elbow, and supraspinatus tendonitis. NO was delivered via glyceryl trinitrate (GTN) patches. We also conducted a 3-year prospective follow-up that demonstrated significant long-term efficacy of GTN patches in treating noninsertional Achilles tendinopathy. In a 5-year prospective comparison treating lateral epicondylitis, we found no additional benefits of GTN vs placebo at 5 years. The use of a new GTN patch, OrthoDerm, demonstrated no evidence for efficacy in treating chronic lateral epicondylitis.</description><dc:title>The role of nitric oxide in tendon healing</dc:title><dc:creator>Ali R. Bokhari, George A.C. Murrell</dc:creator><dc:identifier>10.1016/j.jse.2011.11.001</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>238</prism:startingPage><prism:endingPage>244</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005180/abstract?rss=yes"><title>Fiber-aligned polymer scaffolds for rotator cuff repair in a rat model</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005180/abstract?rss=yes</link><description>Background: Repair techniques of rotator cuff tendon tears have improved in recent years; nonetheless, the failure rate remains high. Despite the availability of various graft materials for repair augmentation, there has yet to be a biomechanical study using fiber-aligned scaffolds in vivo. The objective of this study was to evaluate the efficacy of fiber-aligned nanofibrous polymer scaffolds as a potential treatment-delivery vehicle in a rat rotator cuff injury model.Materials and methods: Scaffolds with and without sacrificial fibers were fabricated via electrospinning and implanted to augment supraspinatus repair in rats. Repairs without scaffold augmentation were also performed to serve as controls. Rats were sacrificed at 4 and 8 weeks postoperatively, and repairs were evaluated histologically and biomechanically.Results: Both scaffold formulations remained in place, with more noticeable cellular infiltration and colonization at 4 and 8 weeks after injury and repair for scaffolds lacking sacrificial fibers. Specimens with scaffolds were larger in cross-sectional area compared with controls. Biomechanical testing revealed no significant differences in structural properties between the groups. Some apparent material properties were significantly reduced in the scaffold groups. These reductions were due to increases in cross-sectional area, most likely caused by the extra thickness of the implanted scaffold material. No differences were observed between the 2 scaffold groups.Conclusions: No adverse effect of surgical implantation of overlaid fiber-aligned scaffolds on structural properties of supraspinatus tendons in rat rotator cuff repair was demonstrated, validating this model as a platform for targeted delivery.</description><dc:title>Fiber-aligned polymer scaffolds for rotator cuff repair in a rat model</dc:title><dc:creator>David P. Beason, Brianne K. Connizzo, LeAnn M. Dourte, Robert L. Mauck, Louis J. Soslowsky, David R. Steinberg, Joseph Bernstein</dc:creator><dc:identifier>10.1016/j.jse.2011.10.021</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>245</prism:startingPage><prism:endingPage>250</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611004812/abstract?rss=yes"><title>Scaffold devices for rotator cuff repair</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611004812/abstract?rss=yes</link><description>Rotator cuff tears affect 40% or more of those aged older than 60 years, and repair failure rates of 20% to 70% remain a significant clinical challenge. Hence, there is a need for repair strategies that can augment the repair by mechanically reinforcing it, while at the same time biologically enhancing the intrinsic healing potential of the tendon. Tissue engineering strategies to improve rotator cuff repair healing include the use of scaffolds, growth factors, and cell seeding, or a combination of these approaches. Currently, scaffolds derived from mammalian extracellular matrix, synthetic polymers, and a combination thereof, have been cleared by the U.S. Food and Drug Administration and are marketed as medical devices for rotator cuff repair in humans. Despite the growing clinical use of scaffold devices for rotator cuff repair, there are numerous questions related to their indication, surgical application, safety, mechanism of action, and efficacy that remain to be clarified or addressed. This article reviews the current basic science and clinical understanding of commercially available synthetic and extracellular matrix scaffolds for rotator cuff repair. Our review will emphasize the host response and scaffold remodeling, mechanical and suture-retention properties, and preclinical and clinical studies on the use of these scaffolds for rotator cuff repair. We will discuss the implications of these data on the future directions for use of these scaffolds in tendon repair procedures.</description><dc:title>Scaffold devices for rotator cuff repair</dc:title><dc:creator>Eric T. Ricchetti, Amit Aurora, Joseph P. Iannotti, Kathleen A. Derwin</dc:creator><dc:identifier>10.1016/j.jse.2011.10.003</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>251</prism:startingPage><prism:endingPage>265</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005751/abstract?rss=yes"><title>Biomimetic scaffold design for functional and integrative tendon repair</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005751/abstract?rss=yes</link><description>Rotator cuff tears represent the most common shoulder injuries in the United States. The debilitating effect of this degenerative condition coupled with the high incidence of failure associated with existing graft choices underscores the clinical need for alternative grafting solutions. The 2 critical design criteria for the ideal tendon graft would require the graft to not only exhibit physiologically relevant mechanical properties but also be able to facilitate functional graft integration by promoting the regeneration of the native tendon-to-bone interface. Centered on these design goals, this review will highlight current approaches to functional and integrative tendon repair. In particular, the application of biomimetic design principles through the use of nanofiber- and nanocomposite-based scaffolds for tendon tissue engineering will be discussed. This review will begin with nanofiber-based approaches to functional tendon repair, followed by a section highlighting the exciting research on tendon-to-bone interface regeneration, with an emphasis on implementation of strategic biomimicry in nanofiber scaffold design and the concomitant formation of graded multi-tissue systems for integrative soft-tissue repair. This review will conclude with a summary and discussion of future directions.</description><dc:title>Biomimetic scaffold design for functional and integrative tendon repair</dc:title><dc:creator>Xinzhi Zhang, Danielle Bogdanowicz, Cevat Erisken, Nancy M. Lee, Helen H. Lu</dc:creator><dc:identifier>10.1016/j.jse.2011.11.016</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>266</prism:startingPage><prism:endingPage>277</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS105827461100574X/abstract?rss=yes"><title>Cell- and gene-based approaches to tendon regeneration</title><link>http://www.jshoulderelbow.org/article/PIIS105827461100574X/abstract?rss=yes</link><description>Repair of rotator cuff tears in experimental models has been significantly improved by the use of enhanced biologic approaches, including platelet-rich plasma, bone marrow aspirate, growth factor supplements, and cell- and gene-modified cell therapy. Despite added complexity, cell-based therapies form an important part of enhanced repair, and combinations of carrier vehicles, growth factors, and implanted cells provide the best opportunity for robust repair. Bone marrow–derived mesenchymal stem cells provide a stimulus for repair in flexor tendons, but application in rotator cuff repair has not shown universally positive results. The use of scaffolds such as platelet-rich plasma, fibrin, and synthetic vehicles and the use of gene priming for stem cell differentiation and local anabolic and anti-inflammatory impact have both provided essential components for enhanced tendon and tendon-to-bone repair in rotator cuff disruption. Application of these research techniques in human rotator cuff injury has generally been limited to autologous platelet-rich plasma, bone marrow concentrate, or bone marrow aspirates combined with scaffold materials. Cultured mesenchymal progenitor therapy and gene-enhanced function have not yet reached clinical trials in humans. Research in several animal species indicates that the concept of gene-primed stem cells, particularly embryonic stem cells, combined with effective culture conditions, transduction with long-term integrating vectors carrying anabolic growth factors, and development of cells conditioned by use of RNA interference gene therapy to resist matrix metalloproteinase degradation, may constitute potential advances in rotator cuff repair. This review summarizes cell- and gene-enhanced cell research for tendon repair and provides future directions for rotator cuff repair using biologic composites.</description><dc:title>Cell- and gene-based approaches to tendon regeneration</dc:title><dc:creator>Alan J. Nixon, Ashlee E. Watts, Lauren V. Schnabel</dc:creator><dc:identifier>10.1016/j.jse.2011.11.015</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Special Issue on Rotator Cuff Biology and Healing</prism:section><prism:startingPage>278</prism:startingPage><prism:endingPage>294</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611002679/abstract?rss=yes"><title>High-resolution 3-Tesla magnetic resonance neurography of musculocutaneous neuropathy</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611002679/abstract?rss=yes</link><description>The musculocutaneous nerve originates from the lateral cord of the brachial plexus, with contributions from the C5, C6, and C7 nerve roots. Once the musculocutaneous nerve leaves the lateral cord, it pierces the coracobrachialis muscle and then travels along the lateral aspect of the arm, coursing between the biceps brachii and brachialis muscles, and finally continuing in the forearm as the lateral antebrachial cutaneous nerve. It supplies the biceps brachii, brachialis, and coracobrachialis muscles and provides cutaneous innervations to the lateral forearm and lateral cubital region.</description><dc:title>High-resolution 3-Tesla magnetic resonance neurography of musculocutaneous neuropathy</dc:title><dc:creator>Avneesh Chhabra, Pearlene P. Lee, Cary Bizzell, Neda Faridian-Aragh, Shar Hashemi, Alan J. Belzberg, John A. Carrino</dc:creator><dc:identifier>10.1016/j.jse.2011.06.008</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2011-09-02</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2011-09-02</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e6</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611002734/abstract?rss=yes"><title>Extremely rare synovial chondrosarcoma arising from the elbow joint: case report and review of the literature</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611002734/abstract?rss=yes</link><description>Primary synovial chondromatosis is benign disease of the mucosal membrane in the joint. This disease often affects the knee joint but rarely the elbow joint. Chondrosarcoma, however, is a common malignant bone tumor that usually arises from cartilaginous tissue but which can also arise de novo in extraskeletal tissues. Synovial chondrosarcoma arising from chondromatosis is one of the rarest types of chondrosarcoma. To our knowledge, only 31 patients with a malignant transformation of synovial chondromatosis have been reported ().</description><dc:title>Extremely rare synovial chondrosarcoma arising from the elbow joint: case report and review of the literature</dc:title><dc:creator>Keiichi Muramatsu, Tomoyuki Miyoshi, Atsushi Moriya, Hiroshi Onaka, Mitsunori Shigetomi, Daisuke Nakashima, Toshihiko Taguchi</dc:creator><dc:identifier>10.1016/j.jse.2011.06.014</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>e7</prism:startingPage><prism:endingPage>e11</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611002771/abstract?rss=yes"><title>Triceps avulsion, radial head fracture, and medial collateral ligament rupture about the elbow: a report of 4 cases</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611002771/abstract?rss=yes</link><description>Triceps tendon rupture is a rare but well-reported entity. Three of these reports have documented the occurrence of a triceps avulsion with a radial head fracture. There have also been reports of triceps rupture with medial collateral ligament (MCL) avulsion or insufficiency. These reports did not describe a triceps avulsion with a radial head fracture and concomitant rupture of the MCL.</description><dc:title>Triceps avulsion, radial head fracture, and medial collateral ligament rupture about the elbow: a report of 4 cases</dc:title><dc:creator>Michele Y. Yoon, Mark J. Koris, Jose A. Ortiz, Rick F. Papandrea</dc:creator><dc:identifier>10.1016/j.jse.2011.06.017</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2011-10-17</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2011-10-17</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>e12</prism:startingPage><prism:endingPage>e17</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611004356/abstract?rss=yes"><title>Sequential ipsilateral glenohumeral arthrodesis and scapulothoracic fusion: a case report</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611004356/abstract?rss=yes</link><description>Glenohumeral arthrodesis is a well-established surgical procedure with a variety of indications, which include brachial plexus palsies and other paralytic disorders. Disorders requiring scapulothoracic fusion, however, are much less frequent, and scapulothoracic fusion is usually indicated for paralysis of the muscles controlling the scapulothoracic articulation, often the result of facioscapulohumeral dystrophy or occasional damage to the long thoracic nerve, the spinal accessory nerve, or the dorsal scapular nerve.</description><dc:title>Sequential ipsilateral glenohumeral arthrodesis and scapulothoracic fusion: a case report</dc:title><dc:creator>Syed A. Faisal, Peter T. Campbell, Allan P. Skirving</dc:creator><dc:identifier>10.1016/j.jse.2011.08.064</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Case Reports</prism:section><prism:startingPage>e18</prism:startingPage><prism:endingPage>e20</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005933/abstract?rss=yes"><title>Contents</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005933/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1058-2746(11)00593-3</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A3</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005945/abstract?rss=yes"><title>Sponsoring Societies</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005945/abstract?rss=yes</link><description></description><dc:title>Sponsoring Societies</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1058-2746(11)00594-5</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A4</prism:startingPage><prism:endingPage>A4</prism:endingPage></item><item rdf:about="http://www.jshoulderelbow.org/article/PIIS1058274611005957/abstract?rss=yes"><title>Editorial Board</title><link>http://www.jshoulderelbow.org/article/PIIS1058274611005957/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1058-2746(11)00595-7</dc:identifier><dc:source>Journal of Shoulder and Elbow Surgery 21, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Journal of Shoulder and Elbow Surgery</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>21</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1058-2746(11)X0009-5</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A5</prism:startingPage><prism:endingPage>A5</prism:endingPage></item></rdf:RDF>
