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Cardiography is an indispensable element of health care. However, the accessibility of at-home cardiac monitoring is limited by device complexity, accuracy, and cost. We have developed a real-time algorithm for heart rate monitoring and beat detection implemented in a custom-built, affordable system. These measurements were processed from seismocardiography (SCG) and gyrocardiography (GCG) signals recorded at the sternum, with concurrent electrocardiography (ECG) used as a reference. Our system demonstrated the feasibility of non-invasive electro-mechanical cardiac monitoring on supine, stationary subjects at a cost of $100, and with the SCG-GCG and ECG algorithms decoupled as standalone measurements. Testing was performed on 25 subjects in the supine position when relaxed, and when recovering from physical exercise, to record 23,984 cardiac cycles at heart rates in the range of 36-140 bpm. The correlation between the two measurements had r 2 coefficients of 0.9783 and 0.9982 for normal (averaged) and instantaneous (beat identification) heart rates, respectively. At a sampling frequency of 250 Hz, the average computational time required was 0.088 s per measurement cycle, indicating the maximum refresh rate. A combined SCG and GCG measurement was found to improve accuracy due to fundamentally different noise rejection criteria in the mutually orthogonal signals. The speed, accuracy, and simplicity of our system validated its potential as a real-time, non-invasive, and affordable solution for outpatient cardiac monitoring in situations with negligible motion artifact., Competing Interests: The authors declare no conflict of interest. The funders had no direct role in the design of the study; in the collection, analysis, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Cardio-respiratory activity originating in the chest creates vibrations that diffuse through the organs to the thoracic wall. The vibrational waves were detected in all six degrees of freedom by an inertial motion sensor at the xiphoid process of the sternum. Vibrational cardiography (VCG) combines the detection of vibrations via acceleration, termed as seismocardiography, and gyration, termed as gyrocardiography. The objective of this study was to determine the effect of static respiration volume on the morphology of cardiac-induced waveforms in the VCG signal. In this study, 24 subjects were tested while holding breath at peak inhalation, and at peak exhalation. Ensemble averages of the waveforms showed larger variations in the signal when the lungs were inhaled for both the primary and secondary heart sounds. Inter-subject variability was accounted for by averaging all waveforms and calculating the root mean squared value over a sliding window of 60 milliseconds. The peak amplitudes of both heart sounds were consistently larger for high lung volumes. However, the ratio of primary to the secondary heart sound was found to be inversely proportional to lung volume. These opposing effects offer a strong analysis tool for the determination of relative inhalation volume using VCG morphology alone.

Human mesenchymal stem/stromal cells (MSCs) have been reported to produce an M2-like, alternatively activated phenotype in macrophages. In addition, MSCs mediate effective bacterial clearance in pre-clinical sepsis models. Thus, MSCs have a paradoxical antimicrobial and anti-inflammatory response that is not understood.Here, we studied the phenotypic and functional response of monocyte-derived human macrophages to MSC exposure in vitro MSCs induced two distinct, coexistent phenotypes: M2-like macrophages (generally elongated morphology, CD163 + , acute phagosomal acidification, low NOX2 expression and limited phagosomal superoxide production) and M1-like macrophages characterised by high levels of phagosomal superoxide production. Enhanced phagosomal reactive oxygen species production was also observed in alveolar macrophages from a rodent model of pneumonia-induced sepsis. The production of M1-like macrophages was dependent on prostaglandin E 2 and phosphatidylinositol 3-kinase. MSCs enhanced human macrophage phagocytosis of unopsonised bacteria and enhanced bacterial killing compared with untreated macrophages. Bacterial killing was significantly reduced by blockade of NOX2 using diphenyleneiodonium, suggesting that M1-like cells are primarily responsible for this effect. MSCs also enhanced phagocytosis and polarisation of M1-like macrophages derived from patients with severe sepsis.The enhanced antimicrobial capacity (M1-like) and inflammation resolving phenotype (M2-like) may account for the paradoxical effect of these cells in sepsis in vivo ., Competing Interests: Conflict of interest: G.F. Curley reports grants paid to his institution from the Government of Ontario, Ministry of Research and Innovation (Early Researcher Award), Canadian Institute of Health Research (Operating Grant CIHR-312714) and St Michael's Hospital Translational Innovation Fund (TIF Award Winner 2015), during the conduct of the study. J.G. Laffey reports grants from the Canadian Institutes for Health Research and salary support from the Dept of Anesthesia, University of Toronto, during the conduct of the study., (Copyright ©ERS 2018.)

The cystic fibrosis (CF)-causing mutant, deltaF508-CFTR, is misfolded and fails to traffic out of the endoplasmic reticulum (ER) to the cell surface. Introduction of second site mutations that disrupt a diarginine (RXR)-based ER retention motif in the first nucleotide binding domain rescues the trafficking defect of deltaF508-CFTR, supporting a role for these motifs in mediating ER retention of the major mutant. To determine if these RXR motifs mediate retention of the native deltaF508-CFTR protein in situ, we generated peptides that mimic these motifs and should antagonize mistrafficking mediated via their aberrant exposure. Here we show robust rescue of deltaF508-CFTR in cell lines and in respiratory epithelial tissues by transduction of RXR motif-mimetics, showing that abnormal accessibility of this motif is a key determinant of mistrafficking of the major CF-causing mutant.