In this paper we propose an innovative solution for a small size hybrid mobile robot called Epi.q-1. Overall dimensions are about 160 mm 1 360 mm 1 280 mm (height 1 length 1 width). The Epi.q-1 robot moves on flat, steep or uneven ground. It can climb over obstacles or steps, even if they are non-uniform in size. Its operating mode adapts to ground conditions and changes accordingly: from rolling (on wheels) to stepping (on legs)1 thanks to its great mobility it can follow complex routes. It is easy to control with just a few actuators. Robot locomotion drive-generating units employ an original driving mechanism, where degrees of freedom (DOFs) can be limited to some extent according to the operating conditions or thanks to a switching device. Locomotion units consist of a motor linked to a gear (double epicyclical chain) and an axial device (mini-motor and lead screw system) able to lock or unlock some DOFs of the kinematic chain. Moreover, the robot locomotion unit can change its size, from small to large and vice versa, in order to be able to reach restricted spaces and to overcome even quite tall obstacles. It was experimentally tested on flat ground and slopes. It can overcome 90 mm obstacles, that are 72% of the height of the locomotion unit, and climb stairs.

Intermittent pneumatic compression is a well-known technique, which can be used for several therapeutic treatments like sports recovery, lymphoedema drainage, deep vein thrombosis prevention or others, which may require very different operating characteristics as regards the desired pressure values and the operating velocity. The performance and the effectiveness of the device are often difficult to predict and must be usually optimized through empirical adjustments. This article presents a general method based on the mathematical modelling of a generic IPC system, aimed at studying and developing such a device with physical and dynamical characteristics suitable for the intended application.

The rapid hyperemia evoked by muscle compression is short lived and was recently shown to undergo a rapid decrease even in spite of continuing mechanical stimulation. The present study aims at investigating the mechanisms underlying this attenuation, which include local metabolic mechanisms, desensitization of mechanosensitive pathways, and reduced efficacy of the muscle pump. In 10 healthy subjects, short sequences of mechanical compressions ( = 3-6; 150 mmHg) of the lower leg were delivered at different interstimulus intervals (ranging from 20 to 160 s) through a customized pneumatic device. Hemodynamic monitoring included near-infrared spectroscopy, detecting tissue oxygenation and blood volume in calf muscles, and simultaneous echo-Doppler measurement of arterial (superficial femoral artery) and venous (femoral vein) blood flow. The results indicate that ) a long-lasting (>100 s) increase in local tissue oxygenation follows compression-induced hyperemia, ) compression-induced hyperemia exhibits different patterns of attenuation depending on the interstimulus interval,) the amplitude of the hyperemia is not correlated with the amount of blood volume displaced by the compression, and ) the extent of attenuation negatively correlates with tissue oxygenation ( = -0,78, < 0.05). Increased tissue oxygenation appears to be the key factor for the attenuation of hyperemia upon repetitive compressive stimulation. Tissue oxygenation monitoring is suggested as a useful integration in medical treatments aimed at improving local circulation by repetitive tissue compression. This study shows that ) the hyperemia induced by muscle compression produces a long-lasting increase in tissue oxygenation,) the hyperemia produced by subsequent muscle compressions exhibits different patterns of attenuation at different interstimulus intervals, and ) the extent of attenuation of the compression-induced hyperemia is proportional to the level of oxygenation achieved in the tissue. The results support the concept that tissue oxygenation is a key variable in blood flow regulation.

Intermittent Pneumatic Compression (IPC) devices can be used to analyze the mechanisms underlying several vascular phenomena, such as hyperaemia. Commercial devices have limited dynamics and do not allow the delivery of customizable compressive pressure patterns, making difficult the analysis of such phenomena, which may require the application of long stimulations with low amplitude as well as fast compressions with higher pressure level. To overcome these issues, a novel pneumo-tronic device aimed to the investigation of the physiological effects induced by limb compressions has been conceived and is presented in this work. The design requirements of the system, capable of delivering customizable compressive patterns in the range 0-200 mmHg, are outlined. The final prototype architecture is described, and a mathematical model of the entire system, also including the interaction between the device and the limb tissues, is proposed. The performance of the device has been evaluated in several conditions by means of simulations, whose results have been compared to the data collected from experimental trials in order to validate the model. The outcomes of both experimentation and simulation trials proved the effectiveness of the solution proposed. A possible employment of this device for the investigation of the rapid compression-induced hyperaemia is presented. Other potential applications concern the wide range of intermittent-pneumatic compression treatments.

A single muscle compression (MC) with accompanying hyperemia and hyper-oxygenation results in attenuation of a subsequent MC hyperemia, as long as the subsequent MC takes place when muscle oxygenation is still elevated. Whether this is due to the hyper-oxygenation, or compression-induced de-activation of mechano-sensitive structures is unclear. We hypothesized that increased oxygenation and not de-activation of mechano-sensitive structures was responsible for this attenuation and that both compression and contraction-induced hyperemia attenuate the hyperemic response to a subsequent muscle contraction, and vice-versa. Protocol-1) In eight subjects two MCs separated by a 25 s interval were delivered to the forearm without or with partial occlusion of the axillary artery, aimed at preventing hyperemia and increased oxygenation in response to the first MC. Tissue oxygenation [oxygenated (hemoglobin + myoglobin)/total (hemoglobin + myoglobin)] from forearm muscles and brachial artery blood flow were continuously monitored by means of spatially-resolved near-infrared spectroscopy (NIRS) and Doppler ultrasound, respectively. With unrestrained blood flow, the hyperemic response to the second MC was attenuated, compared to the first (5.7 ± 3.3 vs. 14.8 ± 3.9 ml, P < 0.05). This attenuation was abolished with partial occlusion of the auxillary artery (14.4 ± 3.9 ml). Protocol-2) In 10 healthy subjects, hemodynamic changes were assessed in response to MC and electrically stimulated contraction (ESC, 0.5 s duration, 20 Hz) of calf muscles, as single stimuli or delivered in sequences of two separated by a 25 s interval. When MC or ESC were delivered 25 s following MC or ESC the response to the second stimulus was always attenuated (range: 60–90%). These findings support a role for excess tissue oxygenation in the attenuation of mechanically-stimulated rapid dilation and rule out inactivation of mechano-sensitive structures. Furthermore, both MC and ESC rapid vasodilatation are attenuated by prior transient hyperemia, regardless of whether the hyperemia is due to MC or ESC. Previously, mechanisms responsible for this dilation have not been considered to be oxygen sensitive. This study identifies muscle oxygenation state as relevant blunting factor, and reveals the need to investigate how these feedforward mechanisms might actually be affected by oxygenation.