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Chronic obstructive pulmonary disease (COPD) is a tobacco-related chronic inflammatory disease of the lungs with still increasing prevalence worldwide. Wearable smart devices endorsed with accelerometers capable of recording health-related information including physical activity is becoming popular, and some of them have been validated for using in some diseased states but not in COPD. In this study, we tested the potential usefulness of smart watch to evaluate physical activity in COPD. Validation of the smart watch was done by correlating with data obtained from two types of accelerometer. Ten male patients (mean age: 73.9 ± 2.3 years old) with stable COPD that consulted the outpatient department of Matsusaka Municipal Hospital were enrolled in the study. The uniaxial accelerometry sensor Lifecorder the triaxial accelerometry sensor Actigraph and Smart watch (Apple inc., Cupertino, CA) were carried by all patients and the number of steps, energy expenditure in calories, time of exercise and distance walked were measured. The duration and intensity of physical activity and the number of steps recorded by the Lifecorder were significantly, proportionally and strongly correlated with all physical activity parameters measured by the Smart watch. Similarly, the number of steps and the amount of calorie measured by Actigraph was significantly correlated with all smart watch activity parameters. These findings suggest that the ability of monitoring physical activity in COPD patients by wearable smart watches is comparable to devices generally used in clinical practice.

OBJECTIVE: The purpose of this study was to assess the relationship of composite physiologic index (CPI) with 6-minute walking test (6MWT) parameters in patients with idiopathic interstitial pneumonias (IIPs). METHODS: Thirty five patients (male: 31, female: 4, average age: 72.5 ± 6.8 years old) with IIPs that consulted the Outpatient Department and underwent 6MWT at the Respiratory Center of Matsuzaka Municipal Hospital were enrolled in the present investigation. Correlation of CPI with parameters including 6-min walking distance (6MWD), maximum arterial oxygen saturation of pulse oxymetry (SpO2max), SpO2 minimun (SpO2min), modified Borg scale at rest and at the end of 6MWT was retrospectively evaluated. Pearson-moment correlation was used to evaluate the relationship between parameters. Univariate and multivariate analyses between parameters were performed. A p RESULTS: CPI was significantly correlated with 6MWD (r=-0.574, p CONCLUSION: The results of this study showed a significant relationship of 6MWD with CPI, thereby suggesting the potential usefulness of 6MWD as a predictor of prognosis in patients with IIPs.

Hepcidin is a key regulator of systemic iron metabolism and its expression is modulated by hepatitis C virus (HCV) infection. Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 act as negative regulators of the Jak/signal transducers and activators of transcription signaling pathway. In this study, we investigated how HCV infection modulates SOCS-1 and SOCS-3 production and how these SOCS proteins affect hepcidin production. The effects of SOCS-1 and SOCS-3 on hepcidin production were investigated using a complete genome, HCV replicon system. Unexpectedly, basal expression levels of hepcidin (HAMP) mRNA and the bioactive form of hepcidin protein, hepcidin-25, were significantly higher in replicon cells. Regardless of HCV infection, STAT3 was activated in response to interleukin-6 (IL-6), but this activation was greater in replicon cells than in cured cells. Basal expression of the SOCS-3 protein was enhanced, but basal expression of SOCS-1 protein was reduced, in replicon cells. Expression of SOCS-3 increased dramatically in response to IL-6 stimulation but expression of SOCS-1 was not induced by IL-6. Interestingly, silencing of SOCS-1 and SOCS-3 gene expression enhanced STAT3 activation and HAMP gene expression. In addition, overexpression of SOCS-1 protein strongly suppressed STAT3 activation and HAMP gene expression. This in vitro study shows that SOCS-3 expression was enhanced but SOCS-1 expression was reduced by HCV infection. The upregulation of hepcidin induced by IL-6 was found to be negatively regulated by SOCS-1 and SOCS-3. The modulation of SOCS1 and SOCS3 in HCV-infected hepatocytes may explain, at least in part, the relative shortage of hepcidin production in CH-C.