6th vital sign app: Testing validity and reliability for measuring gait speed.

BACKGROUND: Gait speed tests are useful predictors of different health outcomes in people. These tests can be administered by the convenience of one's smartphone. RESEARCH QUESTION: Is the 6th Vital Sign app valid and reliable for measuring gait speed? METHODS: The study used a prospective test-retest design. Fifteen college subjects were asked to walk at their normal pace for 2 min. Each subject performed two trials. Speed was recorded by the 6th Vital Sign app, Brower timing gates, and by hand-measurement of distance walked divided by the 2 min. Criterion validity was assessed by paired t-tests, Cohen's D effect sizes, and Pearson correlation tests. Inter-trial reliability within each device was assessed with Pearson correlation tests. RESULTS: Speed measured by the app was significantly lower than speed measured by gates (p = 0.004) and by hand-measurement (p = 0.009). The difference between gates and hand-measurement was not significant (p = 0.684). The speed measured by gates and hand-measurement were very highly correlated (r = 0.974), but speed measured by app was only moderately correlated with gates (r = 0.370) and hand-measurement (r = 0.365). The inter-trial reliability was fairly high with correlations r = 0.916, 0.944, and 0.941 when speed was measured by the app, gates, and hand-measurement, respectively. SIGNIFICANCE: The app tended to underestimate speed when compared to gate and hand-measurements. Therefore, we conclude that the 6th Vital Sign app is not valid for use for clinical diagnosis or prognosis.

Loss of DJ-1 impairs antioxidant response by altered glutamine and serine metabolism.

The oncogene DJ-1 has been originally identified as a suppressor of PTEN. Further on, loss-of-function mutations have been described as a causative factor in Parkinson's disease (PD). DJ-1 has an important function in cellular antioxidant responses, but its role in central metabolism of neurons is still elusive. We applied stable isotope assisted metabolic profiling to investigate the effect of a functional loss of DJ-1 and show that DJ-1 deficient neuronal cells exhibit decreased glutamine influx and reduced serine biosynthesis. By providing precursors for GSH synthesis, these two metabolic pathways are important contributors to cellular antioxidant response. Down-regulation of these pathways, as a result of loss of DJ-1 leads to an impaired antioxidant response. Furthermore, DJ-1 deficient mouse microglia showed a weak but constitutive pro-inflammatory activation. The combined effects of altered central metabolism and constitutive activation of glia cells raise the susceptibility of dopaminergic neurons towards degeneration in patients harboring mutated DJ-1. Our work reveals metabolic alterations leading to increased cellular instability and identifies potential new intervention points that can further be studied in the light of novel translational medicine approaches.