Accuracy and Precision of Wearable Devices for Real-Time Monitoring of Swimming Athletes

none4noNowadays, the use of wearable devices is spreading in different fields of application, such as healthcare, digital health, and sports monitoring. In sport applications, the present trend is to continuously monitor the athletes’ physiological parameters during training or competitions to maximize performance and support coaches. This paper aims to evaluate the performances in heart rate assessment, in terms of accuracy and precision, of both wrist-worn and chest-strap commercial devices used during swimming activity, considering a test population of 10 expert swimmers. Three devices were employed: Polar H10 cardiac belt, Polar Vantage V2, and Garmin Venu Sq smartwatches. The former was used as a reference device to validate the data measured by the two smartwatches. Tests were performed both in dry and wet conditions, considering walking/running on a treadmill and different swimming styles in water, respectively. The measurement accuracy and precision were evaluated through standard methods, i.e., Bland–Altman plot, analysis of deviations, and Pearson’s correlation coefficient. Results show that both precision and accuracy worsen during swimming activity (with an absolute increase of the measurement deviation in the range of 13–56 bpm for mean value and 49–52 bpm for standard deviation), proving how water and arms movement act as relevant interference inputs. Moreover, it was found that wearable performance decreases when activity intensity increases, highlighting the need for specific research for wearable applications in water, with a particular focus on swimming-related sports activitiesCosoli, Gloria; Antognoli, Luca; Veroli, Valentina; Scalise, LorenzoCosoli, Gloria; Antognoli, Luca; Veroli, Valentina; Scalise, Lorenz

PARTICULATE MATTER-INDUCED PROCOAGULANT MICROPARTICLE GENERATION BY HUMAN MONONUCLEAR CELLS: A POSSIBLE NOVEL LINK BETWEEN AIRBORNE POLLUTANTS AND CARDIOVASCULAR DISEASES

n/

The Role of Dietary Fibre in Enteral Nutrition in Sepsis Prevention and Therapy: A Narrative Review.

OBJECTIVE This narrative review summarises the current evidence on the role of dietary fibre in enteral nutrition in the prevention and therapy of sepsis, with a focus on critically ill patients. The aim is to discuss the implications for clinical practice and identify future directions for policy and research. RESOURCES We searched MEDLINE and Google Scholar for records on sepsis, critically ill, enteral nutrition, and dietary fibre. We included all types of articles such as meta-analyses, reviews, clinical trials, preclinical studies, and in vitro studies. Data were evaluated for significance and clinical relevance. Synopsis of Review: Despite the ongoing debate, enteral nutrition containing dietary fibres showed great potential in attenuating sepsis-related outcomes and preventing the incidence of sepsis in critically ill patients on enteral nutrition. Dietary fibres target different underlying mechanisms such as microbiota, mucosal barrier integrity, local cellular immune response, and systemic inflammation. We discuss the clinical potential and concerns that currently exist with the standard implementation of dietary fibre in enterally fed intensive care patients. Additionally, we identified research gaps that should be addressed to determine effectiveness and the role of dietary fibres in sepsis itself and its associated outcomes

miR-19a and miR-20a and tissue factor expression in activated human peripheral blood mononuclear cells

Background and Aims. To investigate the behaviour of miR-19a and miR-20a, two microRNAs involved in posttranscriptional modulation of TF expression in peripheral blood mononuclear cells (PBMCs) exposed to high glucose (HG) and lipopolysaccharide (LPS), and to evaluate the involvement of angiotensin II in that process. Methods. TF Procoagulant Activity (PCA, one-stage clotting assay), antigen (Ag, ELISA), and miR-19a and miR-20a levels (specific TaqMan® MicroRNA Assays) were evaluated in PBMCs exposed to high glucose (HG, 50 mM), LPS (100 ng/mL), and Olmesartan (OLM, 10−6 M), an angiotensin II type 1 receptor antagonist. Results. HG increased TF expression and decreased both miRs as compared to control glucose conditions (11.1 mM). In HG-activated PBMCs, LPS stimulated TF expression and downregulated miR-20a, an effect reverted by OLM (10−6 M); miR-19a expression was unchanged by LPS in both CG and HG conditions. Conclusions. miR-19a and miR-20a are inhibited by inflammatory stimuli active on TF expression and their response differs by the stimulus under investigation; angiotensin II may participate in that mechanism

Particulate matter induces prothrombotic microparticle shedding by human mononuclear and endothelial cells

Particulate airborne pollution is associated with increased cardiopulmonary morbidity. Microparticles are extracellular vesicles shed by cells upon activation or apoptosis involved in physiological processes such as coagulation and inflammation, including airway inflammation. We investigated the hypothesis that particulate matter causes the shedding of microparticles by human mononuclear and endothelial cells.Cells, isolated from the blood and the umbilical cords of normal donors, were cultured in the presence of particulate from a standard reference. Microparticles were assessed in the supernatant as phosphatidylserine concentration. Microparticle-associated tissue factor was assessed by an one-stage clotting assay. Nanosight technology was used to evaluate microparticle size distribution.Particulate matter induces a dose- and time- dependent, rapid (1 h) increase in microparticle generation in both cells. These microparticles express functional tissue factor. Particulate matter increases intracellular calcium concentration and phospholipase C inhibition reduces microparticle generation. Nanosight analysis confirmed that upon exposure to particulate matter both cells express particles with a size range consistent with the definition of microparticles (50-1000 nm).Exposure of mononuclear and endothelial cells to particulate matter upregulates the generation of microparticles at least partially mediated by calcium mobilization. This observation might provide a further link between airborne pollution and cardiopulmonary morbidity

The effect of high glucose on the inhibitory action of C21, a selective AT2R agonist, of LPS-stimulated tissue factor expression in human mononuclear cells

Background: Intimate links connect tissue factor (TF), the principal initiator of the clotting cascade, to inflammation, a cross-talk amplified by locally generated Angiotensin (AT) II, the effector arm of the Renin Angiotensin System (RAS). C21, a selective AT2R agonist, downregulates the transcriptional expression of TF in LPS-activated peripheral blood mononuclear cell(PBMC)s implying the existence of ATII type 2 receptor (AT2R)s whose stimulation attenuates inflammation-mediated procoagulant responses. High glucose, by activating key signalling pathways and increasing the cellular content of RAS components, augments TF expression and potentiates the inhibitory effect of AT1R antagonists. It is unknown, however, the impact of that stimulus on AT2R-mediated TF inhibition, an information useful to understand more precisely the role of that signal transduction pathway in the inflammation-mediated coagulation process. TF antigen (ELISA), procoagulant activity (PCA, 1-stage clotting assay) and TF-mRNA (real-time polymerase chain reaction) were assessed in PBMCs activated by LPS, a pro-inflammatory and procoagulant stimulus, exposed to either normal (N) or HG concentrations (5.5 and 50 mM respectively). Results: HG upregulated TF expression, an effect abolished by BAY 11-7082, a NFκB inhibitor. C21 inhibited LPS-stimulated PCA, TFAg and mRNA to an extent independent of glucose concentration but the response to Olmesartan, an AT1R antagonist, was quite evidently potentiated by HG. Conclusions: HG stimulates LPS-induced TF expression through mechanisms completely dependent upon NFkB activation. Both AT2R-stimulation and AT1R-blockade downregulate inflammation-mediated procoagulant response in PBMCs but HG impacts differently on the two different signal transduction pathway

Non enzymatic upregulation of tissue factor expression by gamma-glutamyl transferase in human peripheral blood mononuclear cells

Background Besides maintaining intracellular glutathione stores, gamma-glutamyltransferase(GGT) generates reactive oxygen species and activates NFkB, a redox-sensitive transcription factor key in the induction of Tissue Factor (TF) gene expression, the principal initiator of the clotting cascade. Thus, GGT might be involved in TF-mediated coagulation processes, an assumption untested insofar. Methods Experiments were run with either equine, enzymatically active GGT or human recombinant (hr) GGT, a wheat germ-derived protein enzymatically inert because of missing post-translational glycosylation. TF Procoagulant Activity (PCA, one-stage clotting assay), TF antigen(ELISA) and TFmRNA(real-time PCR) were assessed in unpooled human peripheral blood mononuclear cell(PBMC) suspensions obtained from healthy donors through discontinuous Ficoll/Hystopaque density gradient. Results Equine GGT increased PCA, an effect insensitive to GGT inhibition by acivicin suggesting mechanisms independent of its enzymatic activity, a possibility confirmed by the maintained stimulation in response to hrGGT, an enzymatically inactive molecule. Endotoxin(LPS) contamination of GGT preparations was excluded by heat inactivation studies and direct determination(LAL method) of LPS concentrations <0.1 ng/mL practically devoid of procoagulant effect. Inhibition by anti-GGT antibodies corroborated that conclusion. Upregulation by hrGGT of TF antigen and mRNA and its downregulation by BAY-11-7082, a NFkB inhibitor, and N-acetyl-L-cysteine, an antioxidant, was consistent with a NFkB-driven, redox-sensitive transcriptional site of action. Conclusions GGT upregulates TF expression independent of its enzymatic activity, a cytokine-like behaviour mediated by NFκB activation, a mechanism contributing to promote acute thrombotic events, a possibility in need, however, of further evaluation