tendinopathy/protease

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Protease-activated receptors in the Achilles tendon-a potential explanation for the excessive pain signalling in tendinopathy.

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OBJECTIVE Tendinopathies are pathological conditions of tissue remodelling occurring in the major tendons of the body, accompanied by excessive nociceptive signalling. Tendinopathies have been shown to exhibit an increase in the number of mast cells, which are capable of releasing histamine,

Mini-Review: Toxic Tendinopathy.

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Toxic tendinopathy is a rare but reproducible complication in humans, given agents of four drug classes: aromatase inhibitors, fluoroquinolone antibiotics, glucocorticoids (long-term regimens), and statins. Toxic tendinopathy in humans has been linked less consistently to treatment with anabolic

Achilles tendinopathy following Kaletra (lopinavir/ritonavir) use.

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A multitude of rheumatologic manifestations have been associated with HIV infection and protease inhibitors use. We describe two cases that display a temporal relationship between initiating Kaletra and developing Achilles tendinopathy. Immediate and dramatic resolution of symptoms occurred on

Cathepsins in Rotator Cuff Tendinopathy: Identification in Human Chronic Tears and Temporal Induction in a Rat Model.

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While overuse of the supraspinatus tendon is a leading factor in rotator cuff injury, the underlying biochemical changes have not been fully elucidated. In this study, torn human rotator cuff (supraspinatus) tendon tissue was analyzed for the presence of active cathepsin proteases with multiplex

Metalloproteases and tendinopathy.

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Matrix metalloproteinases (MMP) are involved in the development of tendinopathy. These potent enzymes completely degrade all components of the connective tissue, modify the extracellular matrix (ECM), and mediate the development of painful tendinopathy. To control the local activity of activated

Rheumatological complications associated with the use of indinavir and other protease inhibitors.

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Several cases are reported of rheumatological pathology (temporomandibular dysfunction, frozen shoulder, Dupuytren's disease, and tendinitis) most probably related to the intake of indinavir in HIV positive patients. A survey using an anonymous questionnaire of 878 people with HIV infection treated

Injectable treatments for noninsertional achilles tendinosis: a systematic review.

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BACKGROUND Although there has been a recent increase in interest regarding injectable therapy for noninsertional Achilles tendinosis, there are currently no clear treatment guidelines for managing patients with this condition. The objective of this study was (1) to conduct a systematic review of

Relative contributions of mechanical degradation, enzymatic degradation, and repair of the extracellular matrix on the response of tendons when subjected to under- and over- mechanical stimulations in vitro.

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Tendon response to mechanical loading results in either homeostasis, improvement, or degeneration of tissue condition. In an effort to better understand the development of tendinopathies, this study investigated the mechanical and structural responses of tendons subjected to under- and

Cyclical strain modulates metalloprotease and matrix gene expression in human tenocytes via activation of TGFβ.

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Tendinopathies are a range of diseases characterised by degeneration and chronic tendon pain and represent a significant cause of morbidity. Relatively little is known about the underlying mechanisms; however onset is often associated with physical activity. A number of molecular changes have been

[Rheumatic disorders observed in HIV infected patients undergoing highly active antiretroviral therapy (HAART): a 366 case prospective study in Burkina Faso].

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OBJECTIVE The purpose of this report is to describe epidemiological aspects of rheumatic disorders observed in HIV-infected patients undergoing highly active antiretroviral therapy (HAART). Patients and methods. This cross-sectional study was conducted from January 1 to June 30, 2008 in the HIV unit

Tendon response to matrix unloading is determined by the patho-physiological niche.

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Although the molecular mechanisms behind tendon disease remain obscure, aberrant stromal matrix turnover and tissue hypervascularity are known hallmarks of advanced tendinopathy. We harness a tendon explant model to unwind complex cross-talk between the stromal and vascular tissue compartments. We

Sequential, but not Concurrent, Incubation of Cathepsin K and L with Type I Collagen Results in Extended Proteolysis.

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Degradation of extracellular matrix (ECM) during tendinopathy is, in part, mediated by the collagenolytic cathepsin K (catK) and cathepsin L (catL), with a temporal component to their activity. The objective of this study was to determine how catK and catL act in concert or in conflict to degrade

The effect of ciprofloxacin on tendon, paratenon, and capsular fibroblast metabolism.

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The pathologic mechanisms underlying fluoroquinolone-induced tendinopathy are poorly understood. The observed incidence of tendinitis and tendon rupture in patients treated with ciprofloxacin hydrochloride suggests that the fluoroquinolone antibiotics alter tendon fibroblast metabolism. The purpose

Metalloproteases and rotator cuff disease.

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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

Differential expression and cellular localization of novel isoforms of the tendon biomarker tenomodulin.

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Tenomodulin (Tnmd, also called Tendin) is classified as a type II transmembrane glycoprotein and is highly expressed in developing as well as in mature tendons. Along with scleraxis (scx), Tnmd is a candidate marker gene for tenocytes. Its function is unknown, but it has been reported to have

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