15-Epi-LXA4 and MaR1 counter inflammation in stromal cells from patients with Achilles tendinopathy and rupture.

Resolution of inflammation is poorly understood in Achilles tendon disorders. Herein, we investigated the bioactive lipid mediator profiles of tendon-derived stromal cells isolated from patients with Achilles tendinopathy (AT) or Achilles rupture (AR) under baseline and IL-1ß-stimulated conditions. We also determined whether incubating these cells with 2 of the mediators produced by tendon-derived stromal cells, 15-epi-Lipoxin A4 (15-epi-LXA4) or maresin (MaR)-1, moderated their proinflammatory phenotype. Under baseline conditions, AT cells showed concurrent increased levels of proinflammatory eicosanoids and proresolving mediators compared with AR cells. IL-1ß treatment induced profound prostaglandin E2 release in AR compared with AT cells. Incubation of IL-1ß treated AT and AR tendon-derived stromal cells in 15-epi-LXA4 or MaR1 reduced proinflammatory eicosanoids and potentiated the release of proresolving mediators. These mediators also induced specialized proresolving mediator (SPM) biosynthetic enzymes arachidonate lipoxygenase (ALOX) 12 and ALOX15 and up-regulated the proresolving receptor ALX compared with vehicle-treated cells. Incubation in 15-epi-LXA4 or MaR1 also moderated the proinflammatory phenotype of AT and AR cells, regulating podoplanin, CD90, signal transducer and activator of transcription (STAT)-1, IL-6, IFN regulatory factor (IRF) 5, and TLR4 and suppressed c-Jun N-terminal kinase 1/2/3, Lyn, STAT-3, and STAT-6 phosphokinase signaling. In summary, we identify proresolving mediators that are active in AT and AR and propose SPMs, including 15-epi-LXA4 or MaR1, as a potential strategy to counterregulate inflammatory processes in these cells.-Dakin, S. G., Colas, R. A., Newton, J., Gwilym, S., Jones, N., Reid, H. A. B., Wood, S., Appleton, L., Wheway, K., Watkins, B., Dalli, J., Carr, A. J. 15-Epi-LXA4 and MaR1 counter inflammation in stromal cells from patients with Achilles tendinopathy and rupture.

What works to promote walking at the population level? A systematic review.

OBJECTIVE: Interventions to promote walking have focused on individual or group-based approaches, often via the randomised controlled trial design. Walking can also be promoted using population health approaches. We systematically reviewed the effectiveness of population approaches to promote walking among individuals and populations. DESIGN: A systematic review. DATA SOURCES: 10 electronic databases searched from January 1990 to March 2017. ELIGIBILITY CRITERIA: Eligibility criteria include pre-experimental and postexperimental studies of the effects of population interventions to change walking, and the effects must have been compared with a 'no intervention', or comparison group/area/population, or variation in exposure; duration of ≥12 months of follow up; participants in free-living populations; and English-language articles. RESULTS: 12 studies were identified from mostly urban high-income countries (one focusing on using tax, incentivising the loss of parking spaces; and one using policy only, permitting off-leash dogs in city parks). Five studies used mass media with either environment (n=2) or community (n=3) approaches. Four studies used environmental changes that were combined with policies. One study had scaled up school-based approaches to promote safe routes to schools. We found mass media, community initiatives and environmental change approaches increased walking (range from 9 to 75 min/week).

Chronic inflammation is a feature of Achilles tendinopathy and rupture.

BACKGROUND: Recent investigation of human tissue and cells from positional tendons such as the rotator cuff has clarified the importance of inflammation in the development and progression of tendon disease. These mechanisms remain poorly understood in disease of energy-storing tendons such as the Achilles. Using tissue biopsies from patients, we investigated if inflammation is a feature of Achilles tendinopathy and rupture. METHODS: We studied Achilles tendon biopsies from symptomatic patients with either mid-portion tendinopathy or rupture for evidence of abnormal inflammatory signatures. Tendon-derived stromal cells from healthy hamstring and diseased Achilles were cultured to determine the effects of cytokine treatment on expression of inflammatory markers. RESULTS: Tendinopathic and ruptured Achilles highly expressed CD14+ and CD68+ cells and showed a complex inflammation signature, involving NF-κB, interferon and STAT-6 activation pathways. Interferon markers IRF1 and IRF5 were highly expressed in tendinopathic samples. Achilles ruptures showed increased PTGS2 and interleukin-8 expression. Tendinopathic and ruptured Achilles tissues expressed stromal fibroblast activation markers podoplanin and CD106. Tendon cells isolated from diseased Achilles showed increased expression of pro-inflammatory and stromal fibroblast activation markers after cytokine stimulation compared with healthy hamstring tendon cells. CONCLUSIONS: Tissue and cells derived from tendinopathic and ruptured Achilles tendons show evidence of chronic (non-resolving) inflammation. The energy-storing Achilles shares common cellular and molecular inflammatory mechanisms with functionally distinct rotator cuff positional tendons. Differences seen in the profile of ruptured Achilles are likely to be attributable to a superimposed phase of acute inflammation and neo-vascularisation. Strategies that target chronic inflammation are of potential therapeutic benefit for patients with Achilles tendon disease.

Starvation Resulting From Inadequate Dietary Planning for a 50-Day Rowing Expedition.

Meeting the energy demands of prolonged arduous expeditions and endurance sport may be a significant barrier to success. Expedition rowing is associated with high levels of body-mass loss, reflecting the challenge of meeting energy expenditure in this exacting environment. PURPOSE: To use the doubly labeled water (DLW) technique to calculate the total energy expenditure (TEE) and body-composition changes of two 28-y-old healthy male athletes during a 50-d continuous and unsupported row around Great Britain. METHODS: A measured dose of DLW was taken at the start of 2 separate study periods (days 5-19 and 34-48) followed by sequential urine collection, which was analyzed on return to land. RESULTS: Mean TEE was 15.3 MJ/d: athlete 1, 16.4 MJ/d; athlete 2, 14.9 MJ/d. Athlete 1 lost 11.2 kg and athlete 2 lost 14.9 kg of body mass during the row. Average energy provision was 19.1 MJ per 24-h ration pack. CONCLUSIONS: These results highlight the difficulty of maintaining energy balance during expedition rowing. A starvation state was observed despite dietary provision in excess of estimated energy expenditure, indicating that nutritional strategy rather than caloric availability was at fault. The authors recommend that future expeditions prioritize thorough testing and the individualization of rations to ensure that they are both palatable and practical during the weeks to months at sea.