11ß-Hydroxysteroid dehydrogenase type 1 within muscle protects against the adverse effects of local inflammation.

Muscle wasting is a common feature of inflammatory myopathies. Glucocorticoids (GCs), although effective at suppressing inflammation and inflammatory muscle loss, also cause myopathy with prolonged administration. 11ß-Hydroxysteroid dehydrogenase type 1 (11ß-HSD1) is a bidirectional GC-activating enzyme that is potently upregulated by inflammation within mesenchymal-derived tissues. We assessed the regulation of this enzyme with inflammation in muscle, and examined its functional impact on muscle. The expression of 11ß-HSD1 in response to proinflammatory stimuli was determined in a transgenic murine model of chronic inflammation (TNF-Tg) driven by overexpression of tumour necrosis factor (TNF)-α within tissues, including muscle. The inflammatory regulation and functional consequences of 11ß-HSD1 expression were examined in primary cultures of human and murine myotubes and human and murine muscle biopsies ex vivo. The contributions of 11ß-HSD1 to muscle inflammation and wasting were assessed in vivo with the TNF-Tg mouse on an 11ß-HSD1 null background. 11ß-HSD1 was significantly upregulated within the tibialis anterior and quadriceps muscles from TNF-Tg mice. In human and murine primary myotubes, 11ß-HSD1 expression and activity were significantly increased in response to the proinflammatory cytokine TNF-α (mRNA, 7.6-fold, p < 0.005; activity, 4.1-fold, p < 0.005). Physiologically relevant levels of endogenous GCs activated by 11ß-HSD1 suppressed proinflammatory cytokine output (interkeukin-6, TNF-α, and interferon-γ), but had little impact on markers of muscle wasting in human myotube cultures. TNF-Tg mice on an 11ß-11ß-HSD1 knockout background developed greater muscle wasting than their TNF-Tg counterparts (27.4% less; p < 0.005), with smaller compacted muscle fibres and increased proinflammatory gene expression relative to TNF-Tg mice with normal 11ß-HSD1 activity. This study demonstrates that inflammatory stimuli upregulate 11ß-HSD1 expression and GC activation within muscle. Although concerns have been raised that excess levels of GCs may be detrimental to muscle, in this inflammatory TNF-α-driven model, local endogenous GC activation appears to be an important anti-inflammatory response that protects against inflammatory muscle wasting in vivo. © 2016 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

11ß-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess.

The adverse metabolic effects of prescribed and endogenous glucocorticoid (GC) excess, Cushing syndrome, create a significant health burden. We found that tissue regeneration of GCs by 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1), rather than circulating delivery, is critical to developing the phenotype of GC excess; 11ß-HSD1 KO mice with circulating GC excess are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis, adiposity, hypertension, myopathy, and dermal atrophy of Cushing syndrome. Whereas liver-specific 11ß-HSD1 KO mice developed a full Cushingoid phenotype, adipose-specific 11ß-HSD1 KO mice were protected from hepatic steatosis and circulating fatty acid excess. These data challenge our current view of GC action, demonstrating 11ß-HSD1, particularly in adipose tissue, is key to the development of the adverse metabolic profile associated with circulating GC excess, offering 11ß-HSD1 inhibition as a previously unidentified approach to treat Cushing syndrome.

Discovering frequently recurring movement sequences in team-sport athlete spatiotemporal data.

Athlete external load is typically analysed from predetermined movement thresholds. The combination of movement sequences and differences in these movements between playing positions is also currently unknown. This study developed a method to discover the frequently recurring movement sequences across playing position during matches. The external load of 12 international female netball athletes was collected by a local positioning system during four national-level matches. Velocity, acceleration and angular velocity were calculated from positional (X, Y) data, clustered via one-dimensional k-means and assigned a unique alphabetic label. Combinations of velocity, acceleration and angular velocity movement were compared using the Levenshtein distance and similarities computed by the longest common substring problem. The contribution of each movement sequence, according to playing position and relative to the wider data set, was then calculated via the Minkowski distance. A total of 10 frequently recurring combinations of movement were discovered, regardless of playing position. Only the wing attack, goal attack and goal defence playing positions are closely related. We developed a technique to discover the movement sequences, according to playing position, performed by elite netballers. This methodology can be extended to discover the frequently recurring movements within other team sports and across levels of competition.

Quantifying the High-Speed Running and Sprinting Profiles of Elite Female Soccer Players During Competitive Matches Using an Optical Player Tracking System.

The aim of this study was to determine the high-speed running and sprinting profiles of elite female soccer players during competitive matches using a new Optical Player Tracking system. Eight stationary video cameras were positioned at vantage points surrounding the soccer field so that when each camera view was combined, the entire field could be viewed simultaneously. After each match, an optical player tracking system detected the coordinates (x, y) of each player for every video frame. Algorithms applied to the x and y coordinates were used to determine activity variables for 12 elite female players across 7 competitive matches. Players covered 9,220-10,581 m of total distance, 1,772-2,917 m of high-speed running (3.4-5.3 m·s) distance, and 417-850 m of sprinting (>5.4 m·s) distance, with variations between positional groups (p < 0.001; partial η = 0.444-0.488). Similarly, the number of high-speed runs differed between positional groups (p = 0.002; partial η = 0.342), and a large proportion of high-speed runs (81-84%) and sprints (71-78%) were performed over distances less than 10 m. Mean time between high-speed runs (13.9 ± 4.4 seconds) and sprints (86.5 ± 38.0 seconds) varied according to playing position (p < 0.001; partial η = 0.409) and time of the match (p < 0.001; partial η = 0.113-0.310). The results of this study can be used to design match-specific conditioning drills and shows that coaches should take an individualized approach to training load monitoring according to position.

Matchplay characteristics of Grand Slam tennis: implications for training and conditioning.

The purpose of this study was to probe the sex-based differences in the stroke and movement dynamics of Grand Slam hard-court tennis. Player and ball tracking data were collated for 102 male and 95 female players during the 2012-2014 Australian Open tournaments. Serve, serve return, groundstroke and movement data were compared between sexes. Serve statistics were the subject of the largest differences, with males achieving significantly faster speeds, aces and unreturned serves while also winning a greater percentage of service points. When returning serve, women contacted the ball closer to the net, lower to the ground and achieved flatter ball trajectories than males. Groundstroke frequencies were similar between sexes, although males hit with greater speed, flatter trajectories and impacted more shots inside the baseline. Distance covered per set or during points won or lost was not sex dependent, yet men exhibited faster average movement speeds. These findings highlight the need for sex-specific training and practice designs that cater to the different stroke dynamics, particularly in relation to the first serve and serve-return, as well as movement speeds.

Grazing dairy cows had decreased interferon-γ, tumor necrosis factor, and interleukin-17, and increased expression of interleukin-10 during the first week after calving.

Peripartum, and especially during the transition period, dairy cows undergo dramatic physiological changes. These coincide with an increased risk of disease during the first 2 wk after calving and have been linked to dairy cows failing to achieve production as well as reproductive targets. Previous evidence suggests that these physiological changes affect the immune system and that transition dairy cows experience some form of reduced immunocompetence. However, almost all of these studies were undertaken in high-production, housed dairy cows. Grazing cows have much lower levels of production and this study aimed to provide clarity whether or not the dysfunctional attributes of the peripartum immune system reported in high production housed cows are evident in these animals. Therefore, cell culture techniques, flow cytometry, and quantitative PCR were applied to analyze the cellular composition of peripheral blood mononuclear cells from transition dairy cows as well as the performance of these cells in an in vitro assay. First, a combination of in vitro stimulation and quantitative PCR for cytokines was validated as a quantifiable immunocompetence assay in 29 cattle and a correlation of quantitative PCR and ELISA demonstrated. Second, the relative number of T helper cells, cytotoxic T cells, B cells, γδ T cells, natural killer cells, and monocytes in peripheral blood was measured, of which B cells and natural killer cells increased in number postcalving (n=29) compared with precalving. Third, following in vitro stimulation cytokine profiles indicated decreased expression of IFNγ, tumor necrosis factor, and IL-17 and increased expression of IL-10 wk 1 after calving, which later all returned to precalving values (n=39). Additionally, treatment of transition cows with a nonsteroidal anti-inflammatory drug (i.e., carprofen) administered on d 1, 3, and 5 postcalving (n=19; untreated control n=20) did not affect the cytokine expression at any time point. In conclusion, an immunocompetence assay has been developed that highlights a characteristic expression pattern for IFNγ, tumor necrosis factor, IL-17, and IL-10 that reflects a state of reduced immunocompetence in moderate-yielding pasture-based transition cows after calving, which is similar to that described for higher-yielding housed cows.

Has player development in men's tennis really changed? An historical rankings perspective.

Tennis federations are regularly faced with decisions regarding which athletes should be supported in financial terms, and for how long. The financial investments can be considerable, given the cost of competing on tour has been estimated at a minimum $121,000 per year and only the top 130 professionally ranked athletes earned enough prize money to cover this cost in 2012. This study investigates key points of progression in tennis players' careers, to determine how these have changed over time and how that evolution may inform talent development. Approximately 400,000 weekly rankings for 273 male professional tennis players between 1985 and 2010 were compiled, and historical trends in the time taken to reach career milestones were investigated by least-squares regression. The time between earning a first professional ranking point and entry into the Top 100 significantly increased over time for all considered athletes. This was at the detriment of time spent within the Top 100 for some athletes. Career peak Top 50-100 athletes have shown an increase in longevity. These results assist tennis federations in assessing the progress of developing athletes and highlight the evolving nature of the competition for top players.

Rankings in professional men's tennis: a rich but underutilized source of information.

Success in professional tennis is measured, at least in part, by rankings. However, there is little quantitative evidence to inform stakeholders regarding what represents the typical ranking progress of top-ranked players. The objective of this study was therefore to compare the ranking trajectories of male players whom achieved peak professional rankings in the Top 250, 175, 100, 50, 20 and 10. The 11,396 birthdates and weekly professional rankings of all players between 27 August 1973 and 31 October 2011 were collated. The peak ranks for each athlete according to their both chronological age and number of years on tour were identified and athletes were categorised into one of six career-peak ranking bands. One-way analysis of variance tests confirmed distinctive ranking trajectories, which were most pronounced among Top 10 players. The rankings of these players were statistically distinguishable following players' second year on tour or by 17 years of age. The ranking signature of all Top 100 players emerged as significantly different to players that failed to enter the Top 100 by their fourth year on the tour. Indeed, the representation of ranking as a function of years on tour should be considered for use by tennis policy-makers in the future.

Impaired oxidoreduction by 11ß-hydroxysteroid dehydrogenase 1 results in the accumulation of 7-oxolithocholic acid.

11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) mediates glucocorticoid activation and is currently considered as therapeutic target to treat metabolic diseases; however, biomarkers to assess its activity in vivo are still lacking. Recent in vitro experiments suggested that human 11ß-HSD1 metabolizes the secondary bile acid 7-oxolithocholic acid (7-oxoLCA) to chenodeoxycholic acid (CDCA) and minor amounts of ursodeoxycholic acid (UDCA). Here, we provide evidence from in vitro and in vivo studies for a major role of 11ß-HSD1 in the oxidoreduction of 7-oxoLCA and compare its level and metabolism in several species. Hepatic microsomes from liver-specific 11ß-HSD1-deficient mice were devoid of 7-oxoLCA oxidoreductase activity. Importantly, circulating and intrahepatic levels of 7-oxoLCA and its taurine conjugate were significantly elevated in mouse models of 11ß-HSD1 deficiency. Moreover, comparative enzymology of 11ß-HSD1-dependent oxidoreduction of 7-oxoLCA revealed that the guinea-pig enzyme is devoid of 7-oxoLCA oxidoreductase activity. Unlike in other species, 7-oxoLCA and its glycine conjugate are major bile acids in guinea-pigs. In conclusion, the oxidoreduction of 7-oxoLCA and its conjugated metabolites are catalyzed by 11ß-HSD1, and the lack of this activity leads to the accumulation of these bile acids in guinea-pigs and 11ß-HSD1-deficient mice. Thus, 7-oxoLCA and its conjugates may serve as biomarkers of impaired 11ß-HSD1 activity.

Inflammatory regulation of glucocorticoid metabolism in mesenchymal stromal cells.

OBJECTIVE: Tissue glucocorticoid (GC) levels are regulated by the GC-activating enzyme 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1). This enzyme is expressed in cells and tissues arising from mesenchymal stromal cells. Proinflammatory cytokines dramatically increase expression of 11ß-HSD1 in stromal cells, an effect that has been implicated in inflammatory arthritis, osteoporosis, obesity, and myopathy. Additionally, GCs act synergistically with proinflammatory cytokines to further increase enzyme expression. The present study was undertaken to investigate the mechanisms underlying this regulation. METHODS: Gene reporter analysis, rapid amplification of complementary DNA ends (RACE), chemical inhibition experiments, and genetic disruption of intracellular signaling pathways in mouse embryonic fibroblasts (MEFs) were used to define the molecular mechanisms underlying the regulation of 11ß-HSD1 expression. RESULTS: Gene reporter, RACE, and chemical inhibitor studies demonstrated that the increase in 11ß-HSD1 expression with tumor necrosis factor α (TNFα)/interleukin-1ß (IL-1ß) occurred via the proximal HSD11B1 gene promoter and depended on NF-κB signaling. These findings were confirmed using MEFs with targeted disruption of NF-κB signaling, in which RelA (p65) deletion prevented TNFα/IL-1ß induction of 11ß-HSD1. GC treatment did not prevent TNFα-induced NF-κB nuclear translocation. The synergistic enhancement of TNFα-induced 11ß-HSD1 expression with GCs was reproduced by specific inhibitors of p38 MAPK. Inhibitor and gene deletion studies indicated that the effects of GCs on p38 MAPK activity occurred primarily through induction of dual-specificity phosphatase 1 expression. CONCLUSION: The mechanism by which stromal cell expression of 11ß-HSD1 is regulated is novel and distinct from that in other tissues. These findings open new opportunities for development of therapeutic interventions aimed at inhibiting or stimulating local GC levels in cells of mesenchymal stromal lineage during inflammation.

Applying decision tree induction for identification of important attributes in one-versus-one player interactions: a hockey exemplar.

Decision tree induction is a novel approach to exploring attacker-defender interactions in many sports. In this study hockey was chosen as an example to illustrate the potential use of decision tree inductions for the purpose of identifying and communicating characteristics that drive the outcome. Elite female players performed one-versus-one contests (n = 75) over two sessions. Each contest outcome was classified as either a win or loss. Position data were acquired using radio-tracking devices, and movement-based derivatives were calculated for two time epochs (5 to 2.5 seconds, and 2.5 to zero seconds before the outcome occurred). A decision tree model was trained using these attributes from the first session data, which predicted that when the attacker was moving at ≥ 0.5 m · s(-1) faster than the defender during the early epoch, the probability of an attacker's win was 1.00. Conversely, when the speed difference at that time was below this threshold the probability of a loss was 0.78. Secondary attributes included defender speed in the lateral direction during the early epoch, and angle of attack (i.e., angle between the respective velocity vectors of the attacker and defender) during the late epoch. The model was then used to predict outcomes of one-versus-one contests from the second session (accuracy = 0.643; area under the receiver operating characteristic (ROC) curve = 0.712). Moreover, decision trees provide an intuitive framework for relating spatial-temporal concepts to coaches, and the suitability of decision trees for analysing the features of one-versus-one exchanges are discussed.

11ß-HSD1 contributes to age-related metabolic decline in male mice.

The aged phenotype shares several metabolic similarities with that of circulatory glucocorticoid excess (Cushing's syndrome), including type 2 diabetes, obesity, hypertension, and myopathy. We hypothesise that local tissue generation of glucocorticoids by 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1), which converts 11-dehydrocorticosterone to active corticosterone in rodents (corticosterone to cortisol in man), plays a role in driving age-related chronic disease. In this study, we have examined the impact of ageing on glucocorticoid metabolism, insulin tolerance, adiposity, muscle strength, and blood pressure in both wildtype (WT) and transgenic male mice with a global deletion of 11ß-HSD1 (11ß-HSD1-/-) following 4 months high-fat feeding. We found that high fat-fed 11ß-HSD1-/- mice were protected from age-related glucose intolerance and hyperinsulinemia when compared to age/diet-matched WTs. By contrast, aged 11ß-HSD1-/- mice were not protected from the onset of sarcopenia observed in the aged WTs. Young 11ß-HSD1-/- mice were partially protected from diet-induced obesity; however, this partial protection was lost with age. Despite greater overall obesity, the aged 11ß-HSD1-/- animals stored fat in more metabolically safer adipose depots as compared to the aged WTs. Serum analysis revealed both WT and 11ß-HSD1-/- mice had an age-related increase in morning corticosterone. Surprisingly, 11ß-HSD1 oxo-reductase activity in the liver and skeletal muscle was unchanged with age in WT mice and decreased in gonadal adipose tissue. These data suggest that deletion of 11ß-HSD1 in high fat-fed, but not chow-fed, male mice protects from age-related insulin resistance and supports a metabolically favourable fat distribution.

Regulation of 11ß-HSD1 by GH/IGF-1 in key metabolic tissues may contribute to metabolic disease in GH deficient patients.

Patients with growth hormone deficiency (GHD) have many clinical features in common with Cushing's syndrome (glucocorticoid excess) - notably visceral obesity, insulin resistance, muscle myopathy and increased vascular mortality. Within key metabolic tissues, 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) converts cortisone to the active glucocorticoid, cortisol (11-dehydrocorticosterone and corticosterone in rodents respectively), and thus amplifies local glucocorticoid action. We hypothesize that 11ß-HSD1 expression is negatively regulated by growth hormone (GH), and that GHD patients have elevated 11ß-HSD1 within key metabolic tissues (leading to increased intracellular cortisol generation) which contributes to the clinical features of this disease. To identify the impact of GH excess/resistance on 11ß-HSD1 in vivo, we measured mRNA expression in key metabolic tissues of giant mice expressing the bovine GH (bGH) gene, dwarf mice with a disrupted GH receptor (GHRKO) gene and mice expressing a gene encoding a GH receptor antagonist (GHA). Additionally, we assessed urine steroid markers of 11ß-HSD1 activity in both GHRKO and bGH animals. 11ß-HSD1 expression was decreased in gastrocnemius muscle (0.43-fold, p < 0.05), subcutaneous adipose (0.53-fold, p < 0.05) and epididymal adipose tissue (0.40-fold, p < 0.05), but not liver, in bGH mice compared to WT controls. This was paralleled by an increased percentage of 11-DHC (inactive glucocorticoid) present in the urine of bGH mice compared to WT controls (2.5-fold, p < 0.01) - consistent with decreased systemic 11ß-HSD1 activity. By contrast, expression of 11ß-HSD1 was increased in the liver of GHRKO (2.7-fold, p < 0.05) and GHA mice (2.0-fold, p < 0.05) compared to WT controls, but not gastrocnemius muscle, subcutaneous adipose tissue or epididymal adipose tissue. In summary, we have demonstrated a negative relationship between GH action and 11ß-HSD1 expression which appears to be tissue specific. These data provide evidence that increased intracellular cortisol production within key tissues may contribute to metabolic disease in GHD patients.

Electrohydrodynamic atomisation driven design and engineering of opportunistic particulate systems for applications in drug delivery, therapeutics and pharmaceutics.

Electrohydrodynamic atomisation (EHDA) technologies have evolved significantly over the past decade; branching into several established and emerging healthcare remits through timely advances in the engineering sciences and tailored conceptual process designs. More specifically for pharmaceutical and drug delivery spheres, electrospraying (ES) has presented itself as a high value technique enabling a plethora of different particulate structures. However, when coupled with novel formulations (e.g. co-flows) and innovative device aspects (e.g., materials and dimensions), core characteristics of particulates are manipulated and engineered specifically to deliver an application driven need, which is currently lacking, ranging from imaging and targeted delivery to controlled release and sensing. This demonstrates the holistic nature of these emerging technologies; which is often overlooked. Parametric driven control during particle engineering via the ES method yields opportunistic properties when compared to conventional methods, albeit at ambient conditions (e.g., temperature and pressure), making this extremely valuable for sensitive biologics and molecules of interest. Furthermore, several processing (e.g., flow rate, applied voltage and working distance) and solution (e.g., polymer concentration, electrical conductivity and surface tension) parameters impact ES modes and greatly influence the production of resulting particles. The formation of a steady cone-jet and subsequent atomisation during ES fabricates particles demonstrating monodispersity (or near monodispersed), narrow particle size distributions and smooth or textured morphologies; all of which are successfully incorporated in a one-step process. By following a controlled ES regime, tailored particles with various intricate structures (hollow microspheres, nanocups, Janus and cell-mimicking nanoparticles) can also be engineered through process head modifications central to the ES technique (single-needle spraying, coaxial, multi-needle and needleless approaches). Thus, intricate formulation design, set-up and combinatorial engineering of the EHDA process delivers particulate structures with a multitude of applications in tissue engineering, theranostics, bioresponsive systems as well as drug dosage forms for specific delivery to diseased or target tissues. This advanced technology has great potential to be implemented commercially, particularly on the industrial scale for several unmet pharmaceutical and medical challenges and needs. This review focuses on key seminal developments, ending with future perspectives addressing obstacles that need to be addressed for future advancement.

Low energy defibrillation in human cardiac tissue: a simulation study.

We aim to assess the effectiveness of feedback-controlled resonant drift pacing as a method for low energy defibrillation. Antitachycardia pacing is the only low energy defibrillation approach to have gained clinical significance, but it is still suboptimal. Low energy defibrillation would avoid adverse side effects associated with high voltage shocks and allow the application of implantable cardioverter defibrillator (ICD) therapy, in cases where such therapy is not tolerated today. We present results of computer simulations of a bidomain model of cardiac tissue with human atrial ionic kinetics. Reentry was initiated and low energy shocks were applied with the same period as the reentry, using feedback to maintain resonance. We demonstrate that such stimulation can move the core of reentrant patterns, in the direction that depends on the location of the electrodes and the time delay in the feedback. Termination of reentry is achieved with shock strength one-order-of-magnitude weaker than in conventional single-shock defibrillation. We conclude that resonant drift pacing can terminate reentry at a fraction of the shock strength currently used for defibrillation and can potentially work where antitachycardia pacing fails, due to the feedback mechanisms. Success depends on a number of details that these numerical simulations have uncovered.

Microsensor technology to help monitor removable appliance wear.

Retention is routinely prescribed after orthodontic treatment to prevent relapse. Orthodontists often notice a discrepancy between what a patient reports about retainer wear and what a clinical examination shows. In these cases, is the patient misreporting wear, or is the retainer at fault? Scientific Compliance (Atlanta, Ga) has invented, patented, and produced the Smart Retainer environmental microsensor that can be easily incorporated into many types of removable orthodontic appliances to monitor compliance. The technology behind the Smart Retainer environmental microsensor is possible because of recent reductions in electronic component sizes and power requirements. A proprietary USB-powered Smart Reader uses wireless technology to download information about actual usage from the Smart Retainer. The information is decrypted and analyzed, and can be shown to the patient in easy-to-understand charts. The orthodontist can use this information to discuss actual retainer usage vs prescribed retainer usage with the patient or parent and make data-driven recommendations about future retention.

Stable increased formulation atomization using a multi-tip nozzle device.

Electrohydrodynamic atomization (EHDA) is an emerging technique for the production of micron and nano-scaled particles. The process often involves Taylor cone enablement, which results in a fine spray yielding formulated droplets, which then undergo drying during deposition. In this work, novel multi-tip emitter (MTE) devices were designed, engineered and utilized for potential up-scaled EHDA, by comparison with a conventional single-needle system. To demonstrate this, the active ketoprofen (KETO) was formulated using polyvinylpyrrolidone (PVP) polymer as the matrix material. Here, PVP polymer (5% w/v) solution was prepared using ethanol and distilled water (80:20) as the vehicle. KETO was incorporated as 5% w/w of PVP. Physical properties of resulting solutions (viscosity, electrical conductivity, density and surface tension) were obtained. Formulations were electrosprayed through both single and novel MTEs under EHDA conditions at various flow rates (5-300 µl/min) and applied voltages (0-30 kV). The atomization process using MTEs and single nozzle was monitored at using various process parameters via a digital optical camera. Resulting particles were collected 200 mm below processing heads and were analyzed using differential scanning calorimetry (DSC), thermal gravimetric analysis (TGA), X-ray diffraction (XRD) and scanning electron microscopy (SEM). Digital recordings confirmed stable MTE jetting at higher flow rates. Electron micrographs confirmed particle size variation arising due to nozzle head design and evidenced stable jetting derived greater near-uniform particles. DSC, XRD and TGA confirm KETO molecules were encapsulated and dispersed into PVP polymer particles. In conclusion, novel MTE devices enabled stable atomization even at higher flow rates when compared to conventional single-needle device. This indicates an exciting approach for scaling up (EHDA) in contrast to current efforts focusing on multiple-nozzle and pore-based processing outlets.

The acceleration and deceleration profiles of elite female soccer players during competitive matches.

OBJECTIVES: The aim of this study was to determine the acceleration (≥2ms-2) and deceleration (≤-2ms-2) profiles of elite female soccer players during competitive matches. DESIGN: Single cohort, observational study. METHODS: An Optical Player Tracking system was used to determine acceleration (≥2ms-2) and deceleration (≤-2ms-2) variables for twelve elite female players across seven competitive matches. RESULTS: In total, players performed 423 (±126) accelerations and 430 (±125) decelerations per match. It was shown that the number of accelerations (p=0.003-0.034, partial η2=0.229-321) and decelerations (p=0.012-0.031, partial η2=0.233-275) at different intensities (based on the start and final velocity) varied according to player position. Mean and maximum distance per effort was 1-4m and 2-8m, respectively, and differed between each intensity category (p<0.001, partial η2=0.753-0.908). The mean time between efforts was 14s for both accelerations (±5s) and decelerations (±4s) and fluctuated between 15min time periods (p<0.001, partial η2=0.148-0.206). CONCLUSIONS: The acceleration and deceleration profiles varied according to player position and time period of the match. The results of this study can be used to design match-specific acceleration and deceleration drills to enhance change of speed ability.

When Is a Sprint a Sprint? A Review of the Analysis of Team-Sport Athlete Activity Profile.

The external load of a team-sport athlete can be measured by tracking technologies, including global positioning systems (GPS), local positioning systems (LPS), and vision-based systems. These technologies allow for the calculation of displacement, velocity and acceleration during a match or training session. The accurate quantification of these variables is critical so that meaningful changes in team-sport athlete external load can be detected. High-velocity running, including sprinting, may be important for specific team-sport match activities, including evading an opponent or creating a shot on goal. Maximal accelerations are energetically demanding and frequently occur from a low velocity during team-sport matches. Despite extensive research, conjecture exists regarding the thresholds by which to classify the high velocity and acceleration activity of a team-sport athlete. There is currently no consensus on the definition of a sprint or acceleration effort, even within a single sport. The aim of this narrative review was to examine the varying velocity and acceleration thresholds reported in athlete activity profiling. The purposes of this review were therefore to (1) identify the various thresholds used to classify high-velocity or -intensity running plus accelerations; (2) examine the impact of individualized thresholds on reported team-sport activity profile; (3) evaluate the use of thresholds for court-based team-sports and; (4) discuss potential areas for future research. The presentation of velocity thresholds as a single value, with equivocal qualitative descriptors, is confusing when data lies between two thresholds. In Australian football, sprint efforts have been defined as activity >4.00 or >4.17 m·s-1. Acceleration thresholds differ across the literature, with >1.11, 2.78, 3.00, and 4.00 m·s-2 utilized across a number of sports. It is difficult to compare literature on field-based sports due to inconsistencies in velocity and acceleration thresholds, even within a single sport. Velocity and acceleration thresholds have been determined from physical capacity tests. Limited research exists on the classification of velocity and acceleration data by female team-sport athletes. Alternatively, data mining techniques may be used to report team-sport athlete external load, without the requirement of arbitrary or physiologically defined thresholds.

25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 exert distinct effects on human skeletal muscle function and gene expression.

Age-associated decline in muscle function represents a significant public health burden. Vitamin D-deficiency is also prevalent in aging subjects, and has been linked to loss of muscle mass and strength (sarcopenia), but the precise role of specific vitamin D metabolites in determining muscle phenotype and function is still unclear. To address this we quantified serum concentrations of multiple vitamin D metabolites, and assessed the impact of these metabolites on body composition/muscle function parameters, and muscle biopsy gene expression in a retrospective study of a cohort of healthy volunteers. Active serum 1,25-dihydroxyvitamin D3 (1α,25(OH)2D3), but not inactive 25-hydroxyvitamin D3 (25OHD3), correlated positively with measures of lower limb strength including power (rho = 0.42, p = 0.02), velocity (Vmax, rho = 0.40, p = 0.02) and jump height (rho = 0.36, p = 0.04). Lean mass correlated positively with 1α,25(OH)2D3 (rho = 0.47, p = 0.02), in women. Serum 25OHD3 and inactive 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) had an inverse relationship with body fat (rho = -0.30, p = 0.02 and rho = -0.33, p = 0.01, respectively). Serum 25OHD3 and 24,25(OH)2D3 were also correlated with urinary steroid metabolites, suggesting a link with glucocorticoid metabolism. PCR array analysis of 92 muscle genes identified vitamin D receptor (VDR) mRNA in all muscle biopsies, with this expression being negatively correlated with serum 25OHD3, and Vmax, and positively correlated with fat mass. Of the other 91 muscle genes analysed by PCR array, 24 were positively correlated with 25OHD3, but only 4 were correlated with active 1α,25(OH)2D3. These data show that although 25OHD3 has potent actions on muscle gene expression, the circulating concentrations of this metabolite are more closely linked to body fat mass, suggesting that 25OHD3 can influence muscle function via indirect effects on adipose tissue. By contrast, serum 1α,25(OH)2D3 has limited effects on muscle gene expression, but is associated with increased muscle strength and lean mass in women. These pleiotropic effects of the vitamin D 'metabolome' on muscle function indicate that future supplementation studies should not be restricted to conventional analysis of the major circulating form of vitamin D, 25OHD3.