Validity of activity trackers, smartphones, and phone applications to measure steps in various walking conditions.

To examine the validity of popular smartphone accelerometer applications and a consumer activity wristband compared to a widely used research accelerometer while assessing the impact of the phone's position on the accuracy of step detection. Twenty volunteers from 2 different age groups (Group A: 18-25 years, n = 10; Group B 45-70 years, n = 10) were equipped with 3 iPhone SE smartphones (placed in pants pocket, shoulder bag, and backpack), 1 Samsung Galaxy S6 Edge (pants pocket), 1 Garmin Vivofit 2 wristband, and 2 ActiGraph wGTX+ devices (worn at wrist and hip) while walking on a treadmill (1.6, 3.2, 4.8, and 6.0 km/h) and completing a walking course. All smartphones included 6 accelerometer applications. Video observation was used as gold standard. Validity was evaluated by comparing each device with the gold standard using mean absolute percentage errors (MAPE). The MAPE of the iPhone SE (all positions) and the Garmin Vivofit was small (<3) for treadmill walking ≥3.2 km/h and for free walking. The Samsung Galaxy and hip-worn ActiGraph showed small MAPE only for treadmill walking at 4.8 and 6.0 km/h and for free walking. The wrist-worn ActiGraph showed high MAPE (17-47) for all walking conditions. The iPhone SE and the Garmin Vivofit 2 are accurate tools for step counting in different age groups and during various walking conditions, even during slow walking. The phone's position does not impact the accuracy of step detection, which substantially improves the versatility for physical activity assessment in clinical and research settings.

Mechanisms of cytokine cascade activation in patients with sepsis: normal cytokine transcription despite reduced CD14 receptor expression.

BACKGROUND: Lipopolysaccharide causes activation of monocytes/macrophages with excessive secretion of cytokines resulting in hypotension and shock in patients with sepsis. Lipopolysaccharide may induce these responses by interacting with lipopolysaccharide-binding protein and then binding to the cell surface protein CD14 or by acting directly with CD11-CD18 on monocytes/macrophages. The role of CD14 and CD11-CD18 in the activation of macrophages with enhanced cytokine transcription in patients with septic shock remains to be determined. METHODS: To study this, heparinized blood was obtained from 16 patients with septic shock on days 0, 1, 3, 5, 7, and 10 and compared with 20 control patients. The expression of CD14 and CD11b on monocytes in whole blood was measured by direct immunofluorescence and flow cytometry. Moreover, whole blood was stimulated with lipopolysaccharide (1 microgram/ml) for 0, 1, 2, 4, 8, and 24 hours, and messenger RNA expression for tumor necrosis factor-alpha, interleukin-beta (IL-1 beta), and IL-6 was determined on isolated peripheral blood mononuclear cells with Northern blot analysis. RESULTS: Both CD14 expression and receptor density on monocytes from whole blood were markedly suppressed (-63% on day 3; p < 0.05) in the septic group compared with controls. Although CD11b expression was also decreased (-24% on day 1; p < 0.05), receptor density on monocytes was slightly increased in the septic group in comparison with the control group. Kinetics and intensity of messenger RNA expression for tumor necrosis factor-alpha, IL-1 beta, and IL-6 were similar in both groups. CONCLUSIONS: These data indicate that in patients with septic shock, lipopolysaccharide-mediated signaling and cytokine transcription are unchanged despite a significant reduction of CD14 expression and density on monocytes. Thus, lipopolysaccharide-induced activation of monocytes from patients with sepsis may occur through direct binding of lipopolysaccharide to the CD11-CD18 complex or other lipopolysaccharide receptors, whereas binding of the lipopolysaccharide-lipopolysaccharide-binding protein complex to the CD14 receptor may not play a pivotal role in sepsis.