Functional Electrical Stimulation for Foot Drop in Post-Stroke People: Quantitative Effects on Step-to-Step Symmetry of Gait Using a Wearable Inertial Sensor.

The main purpose of the present study was to assess the effects of foot drop stimulators (FDS) in individuals with stroke by means of spatio-temporal and step-to-step symmetry, harmonic ratio (HR), parameters obtained from trunk accelerations acquired using a wearable inertial sensor. Thirty-two patients (age: 56.84 ± 9.10 years; 68.8% male) underwent an instrumental gait analysis, performed using a wearable inertial sensor before and a day after the 10-session treatment (PRE and POST sessions). The treatment consisted of 10 sessions of 20 min of walking on a treadmill while using the FDS device. The spatio-temporal parameters and the HR in the anteroposterior (AP), vertical (V), and mediolateral (ML) directions were computed from trunk acceleration data. The results showed that time had a significant effect on the spatio-temporal parameters; in particular, a significant increase in gait speed was detected. Regarding the HRs, the HR in the ML direction was found to have significantly increased (+20%), while those in the AP and V directions decreased (approximately 13%). Even if further studies are necessary, from these results, the HR seems to provide additional information on gait patterns with respect to the traditional spatio-temporal parameters, advancing the assessment of the effects of FDS devices in stroke patients.

Na+/H+ exchanger isoform 1 activity in AQP2-expressing cells can be either proliferative or anti-proliferative depending on extracellular pH.

We have previously shown in renal cells that expression of the water channel Aquaporin-2 increases cell proliferation by a regulatory volume mechanism involving Na+/H+ exchanger isoform 2. Here, we investigated if Aquaporin-2 (AQP2) also modulates Na+/H+ exchanger isoform 1-dependent cell proliferation. We use two AQP2-expressing cortical collecting duct models: one constitutive (WT or AQP2-transfected RCCD1 cell line) and one inducible (control or vasopressin-induced mpkCCDc14 cell line). We found that Aquaporin-2 modifies Na+/H+ exchanger isoform 1 (NHE1) contribution to cell proliferation. In Aquaporin-2-expressing cells, Na+/H+ exchanger isoform 1 is anti-proliferative at physiological pH. In acid media, Na+/H+ exchanger isoform 1 contribution turned from anti-proliferative to proliferative only in AQP2-expressing cells. We also found that, in AQP2-expressing cells, NHE1-dependent proliferation changes parallel changes in stress fiber levels: at pH 7.4, Na+/H+ exchanger isoform 1 would favor stress fiber disassembly and, under acidosis, NHE1 would favor stress fiber assembly. Moreover, we found that Na+/H+ exchanger-dependent effects on proliferation linked to Aquaporin-2 relied on Transient Receptor Potential Subfamily V calcium channel activity. In conclusion, our data show that, in collecting duct cells, the water channel Aquaporin-2 modulates NHE1-dependent cell proliferation. In AQP2-expressing cells, at physiological pH, the Na+/H+ exchanger isoform 1 function is anti-proliferative and, at acidic pH, Na+/H+ exchanger isoform 1 function is proliferative. We propose that Na+/H+ exchanger isoform 1 modulates proliferation through an interplay with stress fiber formation.