To the critical GHRH (1-29) review of ML-264 results: HEW NIS RG MMS SJ GH. Critically reviewed and approved the manuscript: HEW NIS RG MMS SJ GH. Takes responsibility for the paper as a whole: HEW.
Tendinopathy of the human Achilles and the functionally equivalent equine superficial digital flexor tendon (SDFT) are significant causes of morbidity in athletic individuals [1,2]. Repetitive mechanical loading during exercise is cited as a major causative factor [3,4] with high risk of re-injury [5] due to the inferior mechanical properties of the poorly organised fibrous tissue following healing [6]. The importance of inflammation in tendinopathy is highly debated with the aetiology often cited as a degenerative mechanism [7,8]. However, this inference is influenced by analyses of injured human tendons that are often only available for 23115181 examination at surgery, usually some time after the initial injury, by which time acute phase events are lost and chronic disease is well established. The horse presents an attractive large animal model for the study of the equivalent human injury due to the sharedcharacteristics of aging phenotypes [9,10] and elastic energy storing function common to the weight-bearing tendons of both species [11,12]. Equine tendons present a more readily attainable source than the human counterpart, permitting targeted investigation of disease throughout the injury phases as well as normal (uninjured) tendons of a wide age range for comparison. Furthermore, similar to the human injuries, tendon repair processes are frequently clinically classified into three phases in naturally occurring equine injury; the acute phase occurs immediately after the initial trauma lasting only a few days, followed by sub-acute (3? weeks) and chronic injury phases (.3 months after injury) [13].The tensile region of the equine SDFT is most susceptible to overstrain injury [14,15]. Injured tendons are enlarged compared to normal and exhibit a haemorrhagic granular central core during early stage injury. The histological appearance of injured equine SDFTs are shown in Fig. 1, illustrating increased cellularity soon after injury compared toProstaglandins and Lipoxins in Tendinopathynormal tendons. During healing, the damaged tissue is remodelled and a fibrogenic scar repair forms and the highly organised arrangement of collagen fascicles are not restored (Fig. 1c) and [16], predisposing 15857111 to re-injury due to diminished mechanical strength. The effects of age, exercise and mechanical loading are inextricably linked and are potentially synergistic factors in the development of tendinopathy. The frequency of tendon injury in sprint horses has been shown to increase with age from 6 in 2 year olds to 16 in horses aged 5 years and over [17]. Similarly, an increased incidence of Achilles tendon rupture has also been reported in middle aged athletes or aged non-athletic persons [18,19]. Hence the effects of ageing and cumulative microdamage can further exacerbate the risk of re-injury in diseased tendons. The contribution of inflammation to the development of tendinopathy is not fully elucidated and there is a paucity of data reporting inflammatory processes, particularly during the early stages of injury. However, several studies support the involvement of prostaglandins such as prostaglandin E2 (PGE2) in the development of tendinopathy via inflammatory processes [20?22]. Indeed, prostaglandin lipid mediators are synthesised in response to tissue insult or injury and contr.To the critical review of results: HEW NIS RG MMS SJ GH. Critically reviewed and approved the manuscript: HEW NIS RG MMS SJ GH. Takes responsibility for the paper as a whole: HEW.
Tendinopathy of the human Achilles and the functionally equivalent equine superficial digital flexor tendon (SDFT) are significant causes of morbidity in athletic individuals [1,2]. Repetitive mechanical loading during exercise is cited as a major causative factor [3,4] with high risk of re-injury [5] due to the inferior mechanical properties of the poorly organised fibrous tissue following healing [6]. The importance of inflammation in tendinopathy is highly debated with the aetiology often cited as a degenerative mechanism [7,8]. However, this inference is influenced by analyses of injured human tendons that are often only available for 23115181 examination at surgery, usually some time after the initial injury, by which time acute phase events are lost and chronic disease is well established. The horse presents an attractive large animal model for the study of the equivalent human injury due to the sharedcharacteristics of aging phenotypes [9,10] and elastic energy storing function common to the weight-bearing tendons of both species [11,12]. Equine tendons present a more readily attainable source than the human counterpart, permitting targeted investigation of disease throughout the injury phases as well as normal (uninjured) tendons of a wide age range for comparison. Furthermore, similar to the human injuries, tendon repair processes are frequently clinically classified into three phases in naturally occurring equine injury; the acute phase occurs immediately after the initial trauma lasting only a few days, followed by sub-acute (3? weeks) and chronic injury phases (.3 months after injury) [13].The tensile region of the equine SDFT is most susceptible to overstrain injury [14,15]. Injured tendons are enlarged compared to normal and exhibit a haemorrhagic granular central core during early stage injury. The histological appearance of injured equine SDFTs are shown in Fig. 1, illustrating increased cellularity soon after injury compared toProstaglandins and Lipoxins in Tendinopathynormal tendons. During healing, the damaged tissue is remodelled and a fibrogenic scar repair forms and the highly organised arrangement of collagen fascicles are not restored (Fig. 1c) and [16], predisposing 15857111 to re-injury due to diminished mechanical strength. The effects of age, exercise and mechanical loading are inextricably linked and are potentially synergistic factors in the development of tendinopathy. The frequency of tendon injury in sprint horses has been shown to increase with age from 6 in 2 year olds to 16 in horses aged 5 years and over [17]. Similarly, an increased incidence of Achilles tendon rupture has also been reported in middle aged athletes or aged non-athletic persons [18,19]. Hence the effects of ageing and cumulative microdamage can further exacerbate the risk of re-injury in diseased tendons. The contribution of inflammation to the development of tendinopathy is not fully elucidated and there is a paucity of data reporting inflammatory processes, particularly during the early stages of injury. However, several studies support the involvement of prostaglandins such as prostaglandin E2 (PGE2) in the development of tendinopathy via inflammatory processes [20?22]. Indeed, prostaglandin lipid mediators are synthesised in response to tissue insult or injury and contr.
