Parental socioeconomic position and midlife allostatic load:a study of potential mediators

Abstract Background The mechanisms underlying the association of parental socioeconomic position with later life allostatic load remain unclear. The present study aims to examine potential pathways underlying this association: personality, social relations, intelligence and education. Methods The study comprised 361 members of the Copenhagen Perinatal Cohort who participated in two subsequent follow-ups: the Prenatal Development Project (mean age 27 years) and the Copenhagen Aging and Midlife Biobank study (mean age 50 years). Allostatic load was based on 14 biomarkers representing the inflammatory, metabolic and cardiovascular system measured at midlife. Information on potential mediators was collected in young adulthood, and their role in the association of parental socioeconomic position with midlife allostatic load were examined in linear regression path analyses. Results Parental socioeconomic position at one year was inversely associated with midlife allostatic load (β = − 0.238, p < .001). No mediation effects were found for personality or social relations. In a model including intelligence and education, a significant indirect effect was found for education (β = − 0.151, p < .001). A significant direct effect remained (β = − 0.111, p = .040). Conclusions Parental socioeconomic position was inversely associated with allostatic load in midlife. Results suggest that part of this association was mediated by education. A better understanding of the non-cognitive pathways related to education is an important prerequisite for the development of effective intervention strategies

FastPathology: An open-source platform for deep learning-based research and decision support in digital pathology

Deep convolutional neural networks (CNNs) are the current state-of-the-art for digital analysis of histopathological images. The large size of whole-slide microscopy images (WSIs) requires advanced memory handling to read, display and process these images. There are several open-source platforms for working with WSIs, but few support deployment of CNN models. These applications use third-party solutions for inference, making them less user-friendly and unsuitable for high-performance image analysis. To make deployment of CNNs user-friendly and feasible on low-end machines, we have developed a new platform, FastPathology, using the FAST framework and C++. It minimizes memory usage for reading and processing WSIs, deployment of CNN models, and real-time interactive visualization of results. Runtime experiments were conducted on four different use cases, using different architectures, inference engines, hardware configurations and operating systems. Memory usage for reading, visualizing, zooming and panning a WSI were measured, using FastPathology and three existing platforms. FastPathology performed similarly in terms of memory to the other C++ based application, while using considerably less than the two Java-based platforms. The choice of neural network model, inference engine, hardware and processors influenced runtime considerably. Thus, FastPathology includes all steps needed for efficient visualization and processing of WSIs in a single application, including inference of CNNs with real-time display of the results. Source code, binary releases and test data can be found online on GitHub at https://github.com/SINTEFMedtek/FAST-Pathology/.Comment: 12 pages, 4 figures, submitted to IEEE Acces

Accelerated dynamic Fourier velocity encoding by exploiting velocity-spatio-temporal correlations

Objective: To describe how the information content in a Fourier velocity encoding (FVE) scan can be transformed into a very sparse representation and to develop a method that exploits the compactness of the data to significantly accelerate the acquisition. Materials and Methods: For validation, fully sampled FVE datasets were acquired in phantom and in vivo experiments. Fivefold and eightfold acceleration was simulated by using only one fifth or one eighth of the data for reconstruction in the proposed method based on the k-t BLAST framework. Reconstructed images were compared quantitatively to those from the fully sampled data. Results: Velocity spectra in the accelerated datasets were comparable to the spectra from fully sampled datasets. The detected peak velocities remained accurate even at eightfold acceleration, and the overall shape of the spectra was well preserved. Slight temporal smoothing was seen in the accelerated datasets. Conclusion: A novel technique for accelerating time-resolved FVE scan is presented. It is possible to accelerate FVE to acquisition speeds comparable to a standard time-resolved phase-contrast sca

Prosthetic heart valve evaluation by magnetic resonance imaging

Objective: To evaluate the potential of magnetic resonance imaging (MRI) for evaluation of velocity fields downstream of prosthetic aortic valves. Furthermore, to provide comparative data from bileaflet aortic valve prostheses in vitro and in patients. Methods: A pulsatile flow loop was set up in a 7.0 Tesla MRI scanner to study fluid velocity data downstream of a 25 mm aortic bileaflet heart valve prosthesis. Three dimensional surface plots of velocity fields were displayed. In six NYHA class I patients blood velocity profiles were studied downstream of their St. Jude Medical aortic valves using a 1.5 Tesla MRI whole-body scanner. Blood velocity data were displayed as mentioned above. Results: Fluid velocity profiles obtained from in vitro studies 0.25 valve diameter downstream of the valve exhibited significant details about the cross sectional distribution of fluid velocities. This distribution completely reflected the valve design. Blood velocity profiles in humans were considerably smoother and in some cases skewed with the highest velocities toward the anterior-right ascending aortic wall. Conclusion: Display and interpretation of fluid and blood velocity data obtained downstream of prosthetic valves is feasible both in vitro and in vivo using the MRI technique. An in vitro model with a straight tube and the test valve oriented orthogonally to the long axis of the test tube does not entail fluid velocity profiles which are compatible to those obtained from humans, probably due to the much more complex human geometry, and variable alignment of the valve with the ascending aorta. With the steadily improving quality of MRI scanners this technique has significant potential for comparative in vitro and in vivo hemodynamic evaluation of heart valve

Ischaemia-reperfusion injury impairs tissue plasminogen activator release in man

AIMS: Ischaemia-reperfusion (IR) injury causes endothelium-dependent vasomotor dysfunction that can be prevented by ischaemic preconditioning. The effects of IR injury and preconditioning on endothelium-dependent tissue plasminogen activator (t-PA) release, an important mediator of endogenous fibrinolysis, remain unknown. METHODS AND RESULTS: Ischaemia-reperfusion injury (limb occlusion at 200 mmHg for 20 min) was induced in 22 healthy subjects. In 12 subjects, IR injury was preceded by local or remote ischaemic preconditioning (three 5 min episodes of ipsilateral or contralateral limb occlusion, respectively) or sham in a randomized, cross-over trial. Forearm blood flow (FBF) and endothelial t-PA release were assessed using venous occlusion plethysmography and venous blood sampling during intra-arterial infusion of acetylcholine (5-20 µg/min) or substance P (2-8 pmol/min). Acetylcholine and substance P caused dose-dependent increases in FBF (P&lt;0.05 for all). Substance P caused a dose-dependent increase in t-PA release (P&lt;0.05 for all). Acetylcholine and substanceP-mediated vasodilatation and substanceP-mediated t-PA release were impaired following IR injury (P&lt;0.05 for all). Neither local nor remote ischaemic preconditioning protected against the impairment of substance P-mediated vasodilatation or t-PA release. CONCLUSION: Ischaemia-reperfusion injury induced substanceP-mediated, endothelium-dependent vasomotor and fibrinolytic dysfunction in man that could not be prevented by ischaemic preconditioning. CLINICAL TRIAL REGISTRATION INFORMATION: Reference number: NCT00789243, URL: http://clinicaltrials.gov/ct2/show/NCT00789243?term=NCT00789243andrank=1