Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy

No abstract available

How does surgery compare to sham surgery or physiotherapy as a treatment for tendinopathy? A systematic review of randomised trials

Purpose: To assess the effectiveness of surgery on all tendinopathies by comparing it to no treatment, sham surgery and exercise-based therapies for both mid-term (12 months) and long-term (> 12 months) outcomes. Methods: Our literature search included EMBASE, Medline, CINAHL and Scopus. A combined assessment of internal validity, external validity and precision of each eligible study yielded its overall study quality. Results were considered significant if they were based on strong (Level 1) or moderate (Level 2) evidence. Results: 12 studies were eligible. Participants had the following types of tendinopathy: shoulder in seven studies, lateral elbow in three, patellar in one and Achilles in one. Two studies were of good, four of moderate and six of poor overall quality. Surgery was superior to no treatment or placebo, for the outcomes of pain, function, range of movement (ROM) and treatment success in the short and midterm. Surgery had similar effects to sham surgery on pain, function and range of motion in the midterm. Physiotherapy was as effective as surgery both in the midterm and long term for pain, function, ROM and tendon force, and pain, treatment success and quality of life, respectively. Conclusion: We recommend that healthcare professionals who treat tendinopathy encourage patients to comply with loading exercise treatment for at least 12 months before the option of surgery is seriously entertained

A New Operation on Sequences: the Boustrouphedon Transform

A generalization of the Seidel-Entringer-Arnold method for calculating the alternating permutation numbers (or secant-tangent numbers) leads to a new operation on integer sequences, the Boustrophedon transform.Comment: very minor change: corrected typo in author list. June 24 2002: correction to a proof; additional reference

Risk of bias in systematic reviews of tendinopathy management: are we comparing apples with oranges?

We aimed to provide an overview of the use of risk of bias (RoB) assessment tools in systematic reviews (SRs) in tendinopathy management given increased scrutiny of the SR literature in clinical decision making. A search was conducted in Medline from inception to June 2020 for all SRs of randomized controlled trials (RCTs) assessing the effectiveness of any intervention(s) on any location(s) of tendinopathy. Included SRs had to use one of (a) Cochrane Collaboration tool, (b) PEDro scale, or (c) revised Cochrane Collaboration tool (RoB 2) for their RoB assessment. A total of 46 SRs were included. Around half of SRs (46%) did not use an RoB assessment in data synthesis, and only 30% used it to grade the certainty of evidence. The RoB 2 tool was the most likely to determine “overall high RoB” (52%) followed by the Cochrane Collaboration tool (34.6%) and the PEDro scale (18.6%) as determined by the authors of the SRs. We have demonstrated substantial problems associated with the use of RoB assessments in tendinopathy SRs. The universal use of a single RoB assessment tool should be promoted by journals and SR guidance documents

Review: emerging concepts in the pathogenesis of tendinopathy

Tendinopathy is a common clinical problem and has a significant disease burden attached, not only in terms of health care costs, but also for patients directly in terms of time off work and impact upon quality of life. Controversy surrounds the pathogenesis of tendinopathy, however the recent systematic analysis of the evidence has demonstrated that many of the claims of an absence of inflammation in tendinopathy were more based around belief than robust scientific data. This review is a summary of the emerging research in this topical area, with a particular focus on the role of neuronal regulation and inflammation in tendinopathy

The Circular Economy: Swings and Roundabouts?

In the last few decades the Circular Economy has increasingly been advertised as an economic model that can replace the current “linear” economy whilst addressing the issues of environmental deterioration, social equity and long-term economic growth with the explicit suggestion that it can serve as a tool for Sustainable Development. However, despite the individual prominence of the Circular Economy and Sustainable Development in the academic and wider literature, the exact relationship between the two concepts has neither been thoroughly defined nor explored. The consequent result is various inconsistencies occurring across the literature regarding how the Circular Economy can serve as a tool for Sustainable Development and an incomplete understanding of how its long-term effects differ from those of the “linear” economy. A literature review was conducted to interpret the current conceptual relationship between the Circular Economy and Sustainable Development. The review highlights numerous challenges concerning conceptual definition, economic growth and implementation that inhibit the use of the Circular Economy as a tool for Sustainable Development in its current form. The review concludes by providing suggestions for how research concerning the Circular Economy should proceed if it is to provide a potential approach for achieving Sustainable Development

The role of inflammation and cytokines in the pathogenesis of tendinopathy

Tendon disorders - tendinopathies - are the primary reason form musculoskeletal consultation in primary care in the UK and the US. The molecular pathophysiology of tendinopathy remains difficult to interpret while inflammation and its role in tendinopathy have been historically ignored due to its absence in human surgical specimens. This thesis explores the role of inflammation in human tendinopathy and dissects potential molecular pathways involved in its initiation and perpetuation. Firstly I characterize inflammatory cell subtypes within a model of human tendinopathy highlighting a distinct inflammatory infiltrate particularly of mast cells and macrophages. Hypoxia and hypoxic cell death have been a long considered aetiology of tendon degeneration. In this thesis I demonstrate that hypoxia related proteins are present in early tendinopathy biopsies and thereafter in mechanistic studies demonstrate that hypoxia regulates inflammatory and apoptotic mediators in tendon cells associated with a significant shift in collagen matrix synthesis. The cytokines, interleukins 17 and 33 are emerging inflammatory mediators known to play key roles in fibroblast biology. I explored the cellular sources of IL- 17A in human tendinopathy with experiments revealing the majority of IL17A colocalised to mast cells. Moreover IL-17A induced proinflammatory cytokines and apoptosis in vitro and again resulted in a significant switch in collagen extracellular matrix production. IL 33 is a new member of the IL-1 superfamily that signals through the ST2 receptor. Herein I demonstrate that IL-33 expression is up regulated in human tendinopathic biopsies whilst rhIL-33 promotes proinflammatory cytokine release and significantly shifts matrix production toward a collagen III phenotype. WT mice undergoing a tendon injury model showed significant up regulation of IL-33 and ST2 while ST2-/- mice exhibit a reduced collagen response and biomechanical tendon strength at early time points post injury Addition of rh-IL33 increased type III collagen production and reduced the biomechanical strength of WT tendons. Furthermore mechanistic investigations has highlighted a key role for the microRNA 29 family in the modulation of collagen regulation in tendinopathy but also in controlling IL-33 induced changes as a direct target of sST2. Based on these experiments I propose IL-33 as an important and influential alarmin in early tendon injury and tendinopathy, which may be influential in the balance between reparation and degeneration in tendon disease.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Europe rules on harm from fluoroquinolone antibiotics

No abstract available

Why did IL-23p19 inhibition fail in AS: a tale of tissues, trials or translation?

No abstract available