Exploring the role of wearable technology in sport kinematics and kinetics: a systematic review

The aim of this review was to understand the use of wearable technology in sport in order to enhance performance and prevent injury. Understanding sports biomechanics is important for injury prevention and performance enhancement and is traditionally assessed using optical motion capture. However, such approaches are limited by capture volume restricting assessment to a laboratory environment, a factor that can be overcome by wearable technology. A systematic search was carried out across seven databases where wearable technology was employed to assess kinetic and kinematic variables in sport. Articles were excluded if they focused on sensor design and did not measure kinetic or kinematic variables or apply the technology on targeted participants. A total of 33 articles were included for full-text analysis where participants took part in a sport and performed dynamic movements relating to performance monitored by wearable technologies. Inertial measurement units, flex sensors and magnetic field and angular rate sensors were among the devices used in over 15 sports to quantify motion. Wearable technology usage is still in an exploratory phase, but there is potential for this technology to positively influence coaching practice and athletes’ technique

Human Mesenchymal Stem Cells Protect Human Islets from Pro-Inflammatory Cytokines

Transplantation of human islets is an attractive alternative to daily insulin injections for patients with type 1 diabetes. However, the majority of islet recipients lose graft function within five years. Inflammation is a primary contributor to graft loss, and inhibiting pro-inflammatory cytokine activity can reverse inflammation mediated dysfunction of islet grafts. As mesenchymal stem cells (MSCs) possess numerous immunoregulatory properties, we hypothesized that MSCs could protect human islets from pro-inflammatory cytokines. Five hundred human islets were co-cultured with 0.5 or 1.0×106 human MSCs derived from bone marrow or pancreas for 24 hours followed by 48 hour exposure to interferon-γ, tumor necrosis factor-α and interleukin 1β. Controls include islets cultured alone (± cytokines) and with human dermal fibroblasts (± cytokines). For all conditions, glucose stimulated insulin secretion (GSIS), total islet cellular insulin content, islet β cell apoptosis, and potential cytoprotective factors secreted in the culture media were determined. Cytokine exposure disrupted human islet GSIS based on stimulation index and percentage insulin secretion. Conversely, culture with 1.0×106 bMSCs preserved GSIS from cytokine treated islets. Protective effects were not observed with fibroblasts, indicating that preservation of human islet GSIS after exposure to pro-inflammatory cytokines is MSC dependent. Islet β cell apoptosis was observed in the presence of cytokines; however, culture of bMSCs with islets prevented β cell apoptosis after cytokine treatment. Hepatocyte growth factor (HGF) as well as matrix metalloproteinases 2 and 9 were also identified as putative secreted cytoprotective factors; however, other secreted factors likely play a role in protection. This study, therefore, demonstrates that MSCs may be beneficial for islet engraftment by promoting cell survival and reduced inflammation

Fibroblast Growth Factor-2 Primes Human Mesenchymal Stem Cells for Enhanced Chondrogenesis

Human mesenchymal stem cells (hMSCs) are multipotent cells capable of differentiating into a variety of mature cell types, including osteoblasts, adipocytes and chondrocytes. It has previously been shown that, when expanded in medium supplemented with fibroblast growth factor-2 (FGF-2), hMSCs show enhanced chondrogenesis (CG). Previous work concluded that the enhancement of CG could be attributed to the selection of a cell subpopulation with inherent chondrogenic potential. In this study, we show that FGF-2 pretreatment actually primed hMSCs to undergo enhanced CG by increasing basal Sox9 protein levels. Our results show that Sox9 protein levels were elevated within 30 minutes of exposure to FGF-2 and progressively increased with longer exposures. Further, we show using flow cytometry that FGF-2 increased Sox9 protein levels per cell in proliferating and non-proliferating hMSCs, strongly suggesting that FGF-2 primes hMSCs for subsequent CG by regulating Sox9. Indeed, when hMSCs were exposed to FGF-2 for 2 hours and subsequently differentiated into the chondrogenic lineage using pellet culture, phosphorylated-Sox9 (pSox9) protein levels became elevated and ultimately resulted in an enhancement of CG. However, small interfering RNA (siRNA)-mediated knockdown of Sox9 during hMSC expansion was unable to negate the prochondrogenic effects of FGF-2, suggesting that the FGF-2-mediated enhancement of hMSC CG is only partly regulated through Sox9. Our findings provide new insights into the mechanism by which FGF-2 regulates predifferentiation hMSCs to undergo enhanced CG

Secretion of growth factors and cytokines from human islet and bone marrow MSC co-cultures.

<p>Levels of cytoprotective factors were also measured from conditioned media from islets cultured alone, with cytokines and with bone marrow MSCs with and without cytokines. Values obtained from cell cultures were subtracted from background levels (<0.5% of measured values for IL-6, HGF, VEGF, MMP2 and 1–10% of measured values for IL-10, MMP9) measured in culture media alone. All values are normalized to the DNA contents of each culture condition. Values are expressed as mean ± SEM (n = 5).</p>*<p>p<0.05 for islet + cytokine vs. all conditions.</p

Effect of hepatocyte growth factor (HGF) on human islet total cellular insulin content and insulin secretory capacity after exposure to pro-inflammatory cytokines.

<p>Results are reported as % recovery of total cellular insulin relative to untreated controls (islets alone). Islet function is assessed by a static glucose stimulated insulin release assay. The stimulation index (SI) is calculated as a ratio of insulin release at high glucose versus low glucose. Insulin release (% insulin content) is reported as insulin secreted at 2.8 mM glucose or 20.0 mM glucose divided by insulin content for corresponding islets. Values are expressed as mean ± SEM.</p>*<p>p<0.05 for islet vs. islet + cytokine.</p>†<p>p<0.05 for islet vs. islet + HGF (10 ng/mL) + cytokine.</p>‡<p>p<0.05 for islet + cytokines vs. islet + HGF (10 ng/mL) + cytokine.</p

Protection of human islets from cytokine induced apoptosis by bone marrow derived MSCs.

<p>A-C) 500 Islets, D-F) 500 Islets + cytokines, G-I) 500 Islets +1.0×10⁶ bMSCs, + cytokines. Tissues were stained for insulin (A,D,G) in red and TUNEL (B,E,H) in green. The merge of the red and green images are presented in panels C, F, and I. Islets cultured without cytokines demonstrated minimal TUNEL positive cells. After cytokine exposure, the number of TUNEL positive cells increased; TUNEL and insulin co-expression was also increased with cytokine treatment. Alteration of native islet organization was observed. After cytokine exposure, co-expression of insulin and TUNEL did not increase in the islets + bMSCs group; cytokines – cocktail of IFNγ, TNFα and IL-1β described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0038189#s2" target="_blank">materials and methods</a>. Scale bar represents 100 µm.</p