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Abstract-Therapeutic strategies against free radicals have mostly focused on the augmentation of antioxidant defenses (eg, vitamins C and E). A novel approach is to prevent free radical generation by the enzyme system xanthine oxidase. We examined whether the inhibition of xanthine oxidase with allopurinol can improve endothelial function in subjects with type 2 diabetes and coexisting mild hypertension compared with control subjects of a similar age. We examined 23 subjects (11 patients with type 2 diabetes and 12 healthy age-matched control subjects) in 2 parallel groups. The subjects were administered 300 mg allopurinol in a randomized, placebo-controlled study in which both therapies were administered for 1 month. Endothelial function was assessed with bilateral venous occlusion plethysmography, in which the forearm blood flow responses to intra-arterial infusions of endothelium-dependent and -independent vasodilators were measured. Allopurinol significantly increased the mean forearm blood flow response to acetylcholine by 30% (3.16Ϯ1.21 versus 2.54Ϯ0.76 mL ⅐ 100 mL Ϫ1 ⅐ min Ϫ1 allopurinol versus placebo; Pϭ0.012, 95% CI 0.14, 1.30) but did not affect the nitroprusside response in patients with type 2 diabetes. There was no significant impact on either endothelium-dependent or -independent vascular responses in age-matched control subjects. Allopurinol improved endothelial function to near-normal levels. Regarding markers of free radical activity, the level of malondialdehyde was significantly reduced (0.30Ϯ0.04 versus 0.34Ϯ0.05 mol/L for allopurinol versus placebo, Pϭ0.03) in patients with type 2 diabetes but not in control subjects. The xanthine oxidase inhibitor allopurinol improves endothelial dysfunction in patients with type 2 diabetes with mild hypertension but not in matched control subjects. In the former group, allopurinol restored endothelial function to near-normal levels.

Background:Field expedient screening tools that can identify individuals at an elevated risk for injury are needed to minimize time loss in American football players. Previous research has suggested that poor dynamic balance may be associated with an elevated risk for injury in athletes; however, this has yet to be examined in college football players.Hypothesis:To determine if dynamic balance deficits are associated with an elevated risk of injury in collegiate football players. It was hypothesized that football players with lower performance and increased asymmetry in dynamic balance would be at an elevated risk for sustaining a noncontact lower extremity injury.Study Design:Prospective cohort study.Methods:Fifty-nine collegiate American football players volunteered for this study. Demographic information, injury history, and dynamic balance testing performance were collected, and noncontact lower extremity injuries were recorded over the course of the season. Receiver operator characteristic curves were calculated based on performance on the Star Excursion Balance Test (SEBT), including composite score and asymmetry, to determine the population-specific risk cut-off point. Relative risk was then calculated based on these variables, as well as previous injury.Results:A cut-off point of 89.6% composite score on the SEBT optimized the sensitivity (100%) and specificity (71.7%). A college football player who scored below 89.6% was 3.5 times more likely to get injured.Conclusion:Poor performance on the SEBT may be related to an increased risk for sustaining a noncontact lower extremity injury over the course of a competitive American football season.Clinical Relevance:College football players should be screened preseason using the SEBT to identify those at an elevated risk for injury based upon dynamic balance performance to implement injury mitigation strategies to this specific subgroup of athletes.

Background-Increased oxidative stress in chronic heart failure is thought to contribute to endothelial dysfunction.Xanthine oxidase produces oxidative stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic heart failure. Methods and Results-We performed a randomized, placebo-controlled, double-blind crossover study on 11 patients with New York Heart Association class II-III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo. Endothelial function was assessed by standard forearm venous occlusion plethysmography with acetylcholine, nitroprusside, and verapamil. Plasma malondialdehyde levels were also compared to assess significant changes in oxidative stress. Allopurinol significantly increased the forearm blood flow response to acetylcholine (percentage change in forearm blood flow [meanϮSEM]: 181Ϯ19% versus 120Ϯ22% allopurinol versus placebo; Pϭ0.003). There were no significant differences in the forearm blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitroprusside or verapamil. Plasma malondialdehyde was significantly reduced with allopurinol treatment (346Ϯ128 nmol/L versus 461Ϯ101 nmol/L, allopurinol versus placebo; Pϭ0.03), consistent with reduced oxidative stress with allopurinol therapy. Conclusions-We have shown that allopurinol improves endothelial dysfunction in chronic heart failure. This raises the distinct possibility that allopurinol might reduce cardiovascular events and even improve exercise capacity in chronic heart failure.

The purpose of this study was to determine if an off-season intervention program was effective in improving Functional Movement Screen(™) (FMS) scores in professional American football players. Pre- and post-intervention FMS scores were obtained on 62 subjects who completed a 7-week off-season intervention program. A repeated measures ANOVA was conducted to determine the effectiveness of the training program on FMS scores. A chi-square was performed to determine if there were a greater number of players who met the injury threshold and if asymmetries were reduced following intervention. Logistic regression was used to predict what factors were associated with failure (post-test score of <14). There was a positive main effect for time (P<0.01) and a greater number of individuals with a score >14 following the intervention. At post-test, 41 players were free of asymmetry as compared with 31 at the pre-test. The strongest predictor of program failure was a low squat score at pre-test. This study demonstrated that fundamental movement characteristics do change with a standardized intervention. Further research is required to determine if injury risk is reduced when a player's score improves beyond the established cut-off of 14 and/or asymmetry is resolved.

The Functional Movement Screen (FMS) is a series of 7 tests that categorize fundamental movement. Each test is scored on an ordinal scale with 4 categories. The purpose of this study was to determine the interrater reliability of the FMS. Forty healthy subjects were videotaped while performing the FMS. The videos were independently scored by 4 raters, including 2 experts who instruct FMS training courses and 2 novices who completed a standardized training course on the FMS. Interrater reliability was analyzed using the weighted kappa statistic. The novice raters demonstrated excellent or substantial agreement on 14 of the 17 tests, whereas the expert raters did the same on 13 of the 17 tests. When the novice raters were paired with the expert raters, all 17 components demonstrated excellent or substantial agreement. These data indicate that the FMS can confidently be applied by trained individuals. This would suggest that the FMS can be confidently used to assess the movement patterns of athletes and to make decisions related to interventions for performance enhancement, and the FMS may assist in identifying athletes at risk for injury.

SummaryBackgroundRemote ischaemic conditioning with transient ischaemia and reperfusion applied to the arm has been shown to reduce myocardial infarct size in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). We investigated whether remote ischaemic conditioning could reduce the incidence of cardiac death and hospitalisation for heart failure at 12 months.MethodsWe did an international investigator-initiated, prospective, single-blind, randomised controlled trial (CONDI-2/ERIC-PPCI) at 33 centres across the UK, Denmark, Spain, and Serbia. Patients (age >18 years) with suspected STEMI and who were eligible for PPCI were randomly allocated (1:1, stratified by centre with a permuted block method) to receive standard treatment (including a sham simulated remote ischaemic conditioning intervention at UK sites only) or remote ischaemic conditioning treatment (intermittent ischaemia and reperfusion applied to the arm through four cycles of 5-min inflation and 5-min deflation of an automated cuff device) before PPCI. Investigators responsible for data collection and outcome assessment were masked to treatment allocation. The primary combined endpoint was cardiac death or hospitalisation for heart failure at 12 months in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT02342522) and is completed.FindingsBetween Nov 6, 2013, and March 31, 2018, 5401 patients were randomly allocated to either the control group (n=2701) or the remote ischaemic conditioning group (n=2700). After exclusion of patients upon hospital arrival or loss to follow-up, 2569 patients in the control group and 2546 in the intervention group were included in the intention-to-treat analysis. At 12 months post-PPCI, the Kaplan-Meier-estimated frequencies of cardiac death or hospitalisation for heart failure (the primary endpoint) were 220 (8·6%) patients in the control group and 239 (9·4%) in the remote ischaemic conditioning group (hazard ratio 1·10 [95% CI 0·91–1·32], p=0·32 for intervention versus control). No important unexpected adverse events or side effects of remote ischaemic conditioning were observed.InterpretationRemote ischaemic conditioning does not improve clinical outcomes (cardiac death or hospitalisation for heart failure) at 12 months in patients with STEMI undergoing PPCI.FundingBritish Heart Foundation, University College London Hospitals/University College London Biomedical Research Centre, Danish Innovation Foundation, Novo Nordisk Foundation, TrygFonden.