Portable Ultrasound Research System for Use in Automated Bladder Monitoring with Machine-Learning-Based Segmentation.

We developed a new mobile ultrasound device for long-term and automated bladder monitoring without user interaction consisting of 32 transmit and receive electronics as well as a 32-element phased array 3 MHz transducer. The device architecture is based on data digitization and rapid transfer to a consumer electronics device (e.g., a tablet) for signal reconstruction (e.g., by means of plane wave compounding algorithms) and further image processing. All reconstruction algorithms are implemented in the GPU, allowing real-time reconstruction and imaging. The system and the beamforming algorithms were evaluated with respect to the imaging performance on standard sonographical phantoms (CIRS multipurpose ultrasound phantom) by analyzing the resolution, the SNR and the CNR. Furthermore, ML-based segmentation algorithms were developed and assessed with respect to their ability to reliably segment human bladders with different filling levels. A corresponding CNN was trained with 253 B-mode data sets and 20 B-mode images were evaluated. The quantitative and qualitative results of the bladder segmentation are presented and compared to the ground truth obtained by manual segmentation.

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome.

INTRODUCTION: In addition to its effects on platelet function, recent studies suggest that inhaled nitric oxide (NO) also influences the function of circulating leukocytes. Therefore, the aim of this work was to investigate the formation of platelet-leukocyte aggregates (PLAs) and platelet and leukocyte cell surface receptor expression during NO therapy in patients with acute respiratory distress syndrome. METHODS: In 16 patients responding to NO therapy with an improvement in oxygenation (NO group) and in four nonresponders (control), platelet P-selectin expression, platelet fibrinogen binding, the expression CD11a on leukocytes, and the formation of PLAs were investigated at 0, 60, 120, and 180 mins of therapy or at corresponding time points by means of flow cytometry. In addition, PLA was investigated in 30 healthy volunteers during NO inhalation, in five mechanically ventilated patients without acute respiratory distress syndrome and without NO inhalation, and during NO incubation in platelet-rich plasma of ten healthy volunteers in vitro. RESULTS: NO therapy inhibited PLA formation at 60 (13% +/- 4% in the NO group vs. 19% +/- 7% in the control group, p <.01) and 120 mins (14% +/- 4% vs. 18% +/- 7%, p <.05) and slightly decreased CD11a expression at 60 mins (152 +/- 22 arbitrary units vs. 187 +/- 36 arbitrary units, p <.05). Furthermore, besides inhibiting platelet fibrinogen binding, NO also led to a significant inhibition of P-selectin expression at 120 (38% +/- 4% vs. 43% +/- 5%, p <.05) and 180 mins (34% +/- 5% vs. 43% +/- 6%, p <.01), demonstrating a significant correlation between changes in P-selectin expression and PLA formation. In contrast, PLA formation was not influenced by mechanical ventilation in patients without acute respiratory distress syndrome. These results were further supported by additional studies showing inhibition of PLA formation in healthy volunteers as well. CONCLUSIONS: NO-dependent inhibition of PLA formation in patients with acute respiratory distress syndrome can be explained by the inhibition in platelet P-selectin expression. Thus, this study provides rational evidence of systemic antileukocytic and antiplatelet properties of NO therapy in the clinical setting.