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Detecting fluid imbalance in patients with chronic heart failure can be challenging. Use of a pocket-sized ultrasound device (PSUD) in addition to physical examination can be helpful to assess this important information.To evaluate the feasibility for nurses without prior experience of ultrasonography to examine fluid imbalance by the use of a PSUD on heart failure patients.Four heart failure nurses and an expert cardiologist participated. The nurses underwent a four-hour PSUD training programme. One hundred and four heart failure outpatients were included. The examinations obtained information of pulmonary congestion, pleural effusion and the diameter of the vena cava inferior.Examinations took nine minutes on average. In 28% and 14% of the patients, pulmonary congestion and pleural effusion respectively were found by the nurses. The sensitivities and specificities for nurses' findings were 79% and 91%, and, 88% and 93% respectively. The inter-operator agreement between the nurses and the cardiologist reached a substantial level (kappa values: 0.71 and 0.66). The inter-operator agreement for vena cava inferior reached a fair level (kappa value=0.39). Bland-Altman plots of the level of agreement revealed a mean difference of vena cava inferior diameter of 0.11 cm, while the 95% lower and upper limits ranged from -0.78 cm to 1.00 cm.After brief training, heart failure nurses can reliably identify pulmonary congestion and pleural effusion with a PSUD. Assessment of vena cava inferior was less valid. PSUD readings, when added to the history and a physical examination, can improve nurse assessment of fluid status in patients with heart failure.

The ability of neutrophils to sense and move to sites of infection is essential for our defense against pathogens. For motility, lamellipodium extension and stabilization are prerequisites, but how cells form such membrane protrusions is still obscure. Using contrast-enhanced video microscopy and Transwell® assays, we show that water-selective aquaporin channels regulate lamellipodium formation and neutrophil motility. Addition of anti-aquaporin-9 antibodies, HgCl2, or tetraethyl ammonium inhibited the function(s) of the channels and blocked motility-related shape changes. On human neutrophils, aquaporin-9 preferentially localized to the cell edges, where N-formyl peptide receptors also accumulated, as assessed with fluorescence microscopy. To directly visualize water fluxes at cell edges, cells were loaded with high dilution-sensitive, self-quenching concentrations of fluorophore. In these cells, motile regions always displayed increased fluorescence compared with perinuclear regions. Our observations provide the first experimental support for motility models where water fluxes play a pivotal role in cell-volume increases accompanying membrane extensions.