Changes in non-invasive wave intensity parameters with variations of Savitzky-Golay filter settings

Ultrasound-measured waveforms, such as vessel diameter and blood flow velocity, are used to perform analysis of waves in the cardiovascular system. Wave intensity analysis is one of the tools used for this purpose. The waveforms are commonly filtered to eliminate high-frequency noise, however the filter settings affect the features of these signals and especially of their time derivatives, upon which wave intensity analysis is based. This study aims to investigate the alterations of wave intensity parameters with varying Savitzky-Golay filter settings, one of the most common smoothing algorithms used in this context. A broad spectrum of variations was observed in all the wave intensity variables. It is therefore important to always specify the filter settings applied to the signals in a wave intensity study, so that appropriate comparisons can be mad

Common carotid artery diameter, blood flow velocity and wave intensity responses at rest and during exercise in young healthy humans: a reproducibility study

The aim of this study was to assess the reproducibility of non-invasive, ultrasound-derived wave intensity (WI) in humans at the common carotid artery. Common carotid artery diameter and blood velocity of 12 healthy young participants were recorded at rest and during mild cycling, to assess peak diameter, change in diameter, peak velocity, change in velocity, time derivatives, non-invasive wave speed and WI. Diameter, velocity and WI parameters were fairly reproducible. Diameter variables exhibited higher reproducibility than corresponding velocity variables (intra-class correlation coefficient [ICC] = 0.79 vs. 0.73) and lower dispersion (coefficient of variation [CV] = 5% vs. 9%). Wave speed had fair reproducibility (ICC = 0.6, CV = 16%). WI energy variables exhibited higher reproducibility than corresponding peaks (ICC = 0.78 vs. 0.74) and lower dispersion (CV = 16% vs. 18%). The majority of variables had higher ICCs and lower CVs during exercise. We conclude that non-invasive WI analysis is reliable both at rest and during exercise

Non-invasive assessment of the common carotid artery hemodynamics with Increasing exercise workrate using wave intensity analysis

Non-invasively determined local wave speed (c) and wave intensity (WI) parameters provide insight into arterial stiffness and cardiac-vascular interactions in response to physiological perturbations. However, the effects of incremental exercise and subsequent recovery on c and WI are not fully established. We examined the changes in c and WI parameters in the common carotid artery (CCA) during exercise and recovery in 8 young healthy male athletes. Ultrasound measurements of CCA diameter (D) and blood flow velocity (U) were acquired at rest, during 5 stages of incremental exercise (up to 70% maximum workrate) and throughout 1 h of recovery and non-invasive WI analysis (DU approach) was performed. During exercise, c increased (+136%), showing increased stiffness with workrate. All peak and area of forward compression (FCW), backward compression (BCW) and forward expansion waves (FEW) increased during exercise (+452%, +700%, +900%, respectively). However, WI reflection indices and CCA resistance did not significantly change from rest to exercise. Further, wave speed and magnitude of all waves returned to baseline within 5 min of recovery, suggesting the effects of exercise in the investigated parameters of young healthy individuals were transient. In conclusion, incremental exercise was associated with an increase in local CCA stiffness and increases in all wave parameters, indicative of enhanced ventricular contractility and improved late-systolic blood flow deceleration

Implications of T loss in first wall armor and structural materials on T-self-sufficiency in future burning fusion devices

Future fusion reactors will have to breed enough tritium (T) to sustain continuous operation and to produce excess T to power up other fusion reactors. Therefore, T is a scarce resource that must not be lost inside the fusion power plants systems. The factor that describes the T production is the ‘tritium breeding ratio’ (TBR) which is the ratio of the breading rate in atoms per second to the burn rate in atoms per second. Its value is calculated from neutronics analyses of the breeding process in the blanket and coupled dynamics of the T processing plant. However, these calculations generally ignore the T transport and loss in the first wall by assuming essentially instantaneous recycling of the impinging T in-flux. In this paper the transport and retention of T in the main chamber first wall of a future EU-DEMO reactor is investigated based on the available material data and expected particle loads onto the wall. Two breeding blanket concepts are compared WCLL (water cooled lithium lead) and HCPB (helium cooled pebble bed) and the resulting wall-loss probabilities are compared with a simple balance model that describes the maximum allowable wall loss given a TBR to achieve T-self-sufficiency

Deletion of LBR N-terminal domains recapitulates Pelger-Huet anomaly phenotypes in mouse without disrupting X chromosome inactivation

Mutations in the gene encoding Lamin B receptor (LBR), a nuclear-membrane protein with sterol reductase activity, have been linked to rare human disorders. Phenotypes range from a benign blood disorder, such as Pelger-Huet anomaly (PHA), affecting the morphology and chromatin organization of white blood cells, to embryonic lethality as for Greenberg dysplasia (GRBGD). Existing PHA mouse models do not fully recapitulate the human phenotypes, hindering efforts to understand the molecular etiology of this disorder. Here we show, using CRISPR/Cas-9 gene editing technology, that a 236bp N-terminal deletion in the mouse Lbr gene, generating a protein missing the N-terminal domains of LBR, presents a superior model of human PHA. Further, we address recent reports of a link between Lbr and defects in X chromosome inactivation (XCI) and show that our mouse mutant displays minor X chromosome inactivation defects that do not lead to any overt phenotypes in vivo. We suggest that our N-terminal deletion model provides a valuable pre-clinical tool to the research community and will aid in further understanding the etiology of PHA and the diverse functions of LBR