This paper presents a low-power wireless strain sensor that can be remotely powered by a light source and can be dynamically interrogated with a low-cost wireless interrogator. Based on a conventional thin film strain gauge, the wireless sensor is capable of measuring both static and vibration deformations. The low power wireless operation was achieved via amplitude modulation of the antenna backscattering using a high frequency oscillatory signal whose frequency is controlled by the low-frequency strain signal. The wireless strain sensor can be powered continuously by harvesting the energy supplied from a remote light source using a small solar panel. A micro-processor based wireless interrogator was developed to recover the strain information from the wirelessly received signals dynamically. The implementation and characterization of the wireless strain sensor and wireless interrogator are presented.

This paper presents a wireless strain sensor that consumes about 9 mW. To achieve such an ultra-low power operation, a voltage-controlled oscillator (VCO) is utilized to convert the direct-current (DC) strain signal to a high frequency oscillatory signal. This oscillatory signal is then transmitted using an unpowered wireless transponder (Huang et al 2011 Smart Mater. Struct. 20 015017). A photocell-based energy harvester was developed to power the wireless strain sensor. The energy harvested from a flash light placed at 65 cm away is sufficient to power the wireless strain sensor continuously. The implementation of the wireless strain sensor and its characterization are presented.

Although acute hypoxia is of utmost pathophysiologic relevance in health and disease, studies on its effects on both the macro- and microcirculation are scarce. Herein, we provide a comprehensive analysis of the effects of acute normobaric hypoxia on human macro- and microcirculation. 20 healthy participants were enrolled in this study. Hypoxia was induced in a normobaric hypoxia chamber by decreasing the partial pressure of oxygen in inhaled air stepwisely (pO2; 21.25 kPa (0 k), 16.42 kPa (2 k), 12.63 kPa (4 k) and 9.64 kPa (6 k)). Macrocirculatory effects were assessed by cardiac output measurements, microcirculatory changes were investigated by sidestream dark-field imaging in the sublingual capillary bed and videocapillaroscopy at the nailfold. Exposure to hypoxia resulted in a decrease of systemic vascular resistance (p < 0.0001) and diastolic blood pressure (p = 0.014). Concomitantly, we observed an increase in heart rate (p < 0.0001) and an increase of cardiac output (p < 0.0001). In the sublingual microcirculation, exposure to hypoxia resulted in an increase of total vessel density, proportion of perfused vessels and perfused vessel density. Furthermore, we observed an increase in peripheral capillary density. Exposure to acute hypoxia results in vasodilatation of resistance arteries, as well as recruitment of microvessels of the central and peripheral microcirculation. The observed macro- and microcirculatory effects are most likely a result from compensatory mechanisms to ensure adequate tissue oxygenation.

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