ABSTRACT
OBJECTIVES: The criterion validity of the sphygmomanometer was evaluated, relative to the Force Frame strength testing system. Test-retest reliability was assessed for both hip adduction and abduction strength. DESIGN: Test-retest reliability study and criterion validity study. PARTICIPANTS: 50 asymptomatic, field-sport athletes. MAIN OUTCOME MEASURES: Maximal isometric hip adduction and abduction strength were measured. Interclass correlation coefficient(ICC2,1) with confidence intervals were calculated to evaluate reliability of peak strength values. A Pearson product-moment correlation coefficient(r) was calculated to examine criterion validity of the sphygmomanometer as a measure of force when compared to the ForceFrame. RESULTS: Intra-rater reliability for bilateral adduction testing using both ForceFrame and sphygmomanometer values revealed good-excellent reliability for both the 0° (ICC2.1 = 0.87-0.90) and 45° (ICC2.1 = 0.81-0.91) positions. ForceFrame values revealed good-excellent reliability for 0° abduction position and 45° abduction position. A good-moderate relationship (Pearson's r = 0.63) for 0° adduction position, and poor relationship (Pearson's r = 0.40) for 45° adduction position, were found between adduction squeeze values on ForceFrame and sphygmomanometer. CONCLUSION: Excellent reliability in hip adduction squeeze strength testing for both modes. However, there exists a 'good to moderate'-'fair' relationship between the Force Frame and sphygmomanometer.
Subject(s)
Muscle Strength , Sports , Humans , Reproducibility of Results , Sphygmomanometers , Athletes , Muscle Strength DynamometerABSTRACT
Patients with biallelic loss-of-function variants of AIRE suffer from autoimmune polyendocrine syndrome type-1 (APS-1) and produce a broad range of autoantibodies (auto-Abs), including circulating auto-Abs neutralizing most type I interferons (IFNs). These auto-Abs were recently reported to account for at least 10% of cases of life-threatening COVID-19 pneumonia in the general population. We report 22 APS-1 patients from 21 kindreds in seven countries, aged between 8 and 48 yr and infected with SARS-CoV-2 since February 2020. The 21 patients tested had auto-Abs neutralizing IFN-α subtypes and/or IFN-ω; one had anti-IFN-ß and another anti-IFN-ε, but none had anti-IFN-κ. Strikingly, 19 patients (86%) were hospitalized for COVID-19 pneumonia, including 15 (68%) admitted to an intensive care unit, 11 (50%) who required mechanical ventilation, and four (18%) who died. Ambulatory disease in three patients (14%) was possibly accounted for by prior or early specific interventions. Preexisting auto-Abs neutralizing type I IFNs in APS-1 patients confer a very high risk of life-threatening COVID-19 pneumonia at any age.
Subject(s)
Autoantibodies/immunology , COVID-19/immunology , Interferon Type I/immunology , Pneumonia/immunology , Polyendocrinopathies, Autoimmune/immunology , Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , SARS-CoV-2/immunology , Young AdultABSTRACT
Mitochondrial dysfunction is associated with insulin resistance and type 2 diabetes. It has thus been suggested that primary and/or genetic abnormalities in mitochondrial function may lead to accumulation of toxic lipid species in muscle and elsewhere, impairing insulin action on glucose metabolism. Alternatively, however, defects in insulin signaling may be primary events that result in mitochondrial dysfunction, or there may be a bidirectional relationship between these phenomena. To investigate this, we examined mitochondrial function in patients with genetic defects in insulin receptor (INSR) signaling. We found that phosphocreatine recovery after exercise, a measure of skeletal muscle mitochondrial function in vivo, was significantly slowed in patients with INSR mutations compared with that in healthy age-, fitness-, and BMI-matched controls. These findings suggest that defective insulin signaling may promote mitochondrial dysfunction. Furthermore, consistent with previous studies of mouse models of mitochondrial dysfunction, basal and sleeping metabolic rates were both significantly increased in genetically insulin-resistant patients, perhaps because mitochondrial dysfunction necessitates increased nutrient oxidation in order to maintain cellular energy levels.
