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Steven Williams

Publications and source records attributed to Steven Williams.

6 recordsLinked to original sources

MorphiNet: A Graph Subdivision Network for Adaptive Bi-ventricle Surface Reconstruction

Cardiac Magnetic Resonance (CMR) imaging is widely used for heart model reconstruction and digital twin computational analysis because of its ability to visualize soft tissues and capture dynamic functions. However, CMR images have an anisotropic nature, characterized by large inter-slice distances and misalignments from cardiac motion. These limitations result in data loss and measurement inaccuracies, hindering the capture of detailed anatomical structures. In this work, we introduce MorphiNet, a novel network that reproduces heart anatomy learned from high-resolution Computed Tomography (CT) images, unpaired with CMR images. MorphiNet encodes the anatomical structure as gradient fields, deforming template meshes into patient-specific geometries. A multilayer graph subdivision network refines these geometries while maintaining a dense point correspondence, suitable for computational analysis. MorphiNet achieved state-of-the-art bi-ventricular myocardium reconstruction on CMR patients with tetralogy of Fallot with 0.3 higher Dice score and 2.6 lower Hausdorff distance compared to the best existing template-based methods. While matching the anatomical fidelity of comparable neural implicit function methods, MorphiNet delivered 50$\times$ faster inference. Cross-dataset validation on the Automated Cardiac Diagnosis Challenge confirmed robust generalization, achieving a 0.7 Dice score with 30\% improvement over previous template-based approaches. We validate our anatomical learning approach through the successful restoration of missing cardiac structures and demonstrate significant improvement over standard Loop subdivision. Motion tracking experiments further confirm MorphiNet's capability for cardiac function analysis, including accurate ejection fraction calculation that correctly identifies myocardial dysfunction in tetralogy of Fallot patients.

eess.IV

Strong Fiber from Uniaxial Fullerene Supramolecules Aligned with Carbon Nanotubes

Carbon nanotube (CNT) wires approach copper's specific conductivity and surpass carbon fiber's strength, with further improvement anticipated with greater aspect ratios and incorporation of dopants with long-range structural order. Fullerenes assemble into multitudes of process-dependent supramolecular crystals and, while initially insulating, they become marginally conductive (up to 0.05 MSm$^{-1}$) and superconductive ($T_c=18^\circ$K with K and 28$^\circ$K with Rb) after doping. These were small (100's $\mu$m long), soft (hardness comparable to indium), and typically unaligned, which hindered development of fullerene based wires. Individual fullerenes were previously incorporated into CNT fibers, although randomly without self-assembly into supramolecules. Here, a simple variation in established CNT acid extrusion creates a fiber composed of uniaxial chains of aligned fullerene supramolecules, self-assembled between aligned few-walled CNT bundles. This will provide a testbed for novel fullerene wire transport and prospects in CNT wire advancement.

cond-mat.mtrl-sci

Status of the PSF Reconstruction Work Package for MICADO ELT

MICADO is a workhorse instrument for the ESO ELT, allowing first light capability for diffraction limited imaging and long-slit spectroscopy at near-infrared wavelengths. The PSF Reconstruction (PSF-R) Team of MICADO is currently implementing, for the first time within all ESO telescopes, a software service devoted to the blind reconstruction of the PSF. This tool will work independently of the science data, using adaptive optics telemetry data, both for Single Conjugate (SCAO) and Multi-Conjugate Adaptive Optics (MCAO) allowed by the MORFEO module. The PSF-R service will support the state-of-the-art post-processing scientific analysis of the MICADO imaging and spectroscopic data. We provide here an update of the status of the PSF-R service tool of MICADO, after successfully fulfilling the Final Design Review phase, and discuss recent results obtained on simulated and real data gathered on instruments similar to MICADO.

astro-ph.IM

Fine-tuning neural excitation/inhibition for tailored ketamine use in treatment-resistant depression

The glutamatergic modulator ketamine has been shown to rapidly reduce depressive symptoms in patients with treatment-resistant major depressive disorder (TRD). Although its mechanisms of action are not fully understood, changes in cortical excitation/inhibition (E/I) following ketamine administration are well documented in animal models and could represent a potential biomarker of treatment response. Here, we analyse neuromagnetic virtual electrode timeseries collected from the primary somatosensory cortex in 18 unmedicated patients with TRD and in an equal number of age-matched healthy controls during a somatosensory 'airpuff' stimulation task. These two groups were scanned as part of a clinical trial of ketamine efficacy under three conditions: a) baseline; b) 6-9 hours following subanesthetic ketamine infusion; and c) 6-9 hours following placebo-saline infusion. We obtained estimates of E/I interaction strengths by using Dynamic Causal Modelling (DCM) on the timeseries, thereby allowing us to pinpoint, under each scanning condition, where each subject's dynamics lie within the Poincar\'e diagram - as defined in dynamical systems theory. We demonstrate that the Poincar\'e diagram offers classification capability for TRD patients, in that the further the patients' coordinates were shifted (by virtue of ketamine) toward the stable (top-left) quadrant of the Poincar\'e diagram, the more their depressive symptoms improved. The same relationship was not observed by virtue of a placebo effect - thereby verifying the drug-specific nature of the results. We show that the shift in neural dynamics required for symptom improvement necessitates an increase in both excitatory and inhibitory coupling. We present accompanying MATLAB code made available in a public repository, thereby allowing for future studies to assess individually-tailored treatments of TRD.

q-bio.QM

Fighting seizures with seizures: diffusion and stability in neural systems

Seizure activity is a ubiquitous and pernicious pathophysiology that, in principle, should yield to mathematical treatments of (neuronal) ensemble dynamics - and therefore interventions on stochastic chaos. A seizure can be characterised as a deviation of neural activity from a stable dynamical regime, i.e. one in which signals fluctuate only within a limited range. In silico treatments of neural activity are an important tool for understanding how the brain can achieve stability, as well as how pathology can lead to seizures and potential strategies for mitigating instabilities, e.g. via external stimulation. Here, we demonstrate that the (neuronal) state equation used in Dynamic Causal Modelling generalises to a Fokker-Planck formalism when propagation of neuronal activity along structural connections is considered. Using the Jacobian of this generalised state equation, we show that an initially unstable system can be rendered stable via a reduction in diffusivity (i.e., connectivity that disperses neuronal fluctuations). We show, for neural systems prone to epileptic seizures, that such a reduction can be achieved via external stimulation. Specifically, we show that this stimulation should be applied in such a way as to temporarily mirror epileptic activity in the areas adjoining an affected brain region - thus 'fighting seizures with seizures'. We offer proof of principle using simulations based on functional neuroimaging data collected from patients with idiopathic generalised epilepsy, in which we successfully suppress pathological activity in a distinct sub-network. Our hope is that this technique can form the basis for real-time monitoring and intervention devices that are capable of suppressing or even preventing seizures in a non-invasive manner.

q-bio.NC

Estimating required 'lockdown' cycles before immunity to SARS-CoV-2: Model-based analyses of susceptible population sizes, 'S0', in seven European countries including the UK and Ireland

We used Bayesian model inversion to estimate epidemic parameters from the reported case and death rates from seven countries using data from late January 2020 to April 5th 2020. Two distinct generative model types were employed: first a continuous time dynamical-systems implementation of a Susceptible-Exposed-Infectious-Recovered (SEIR) model and second: a partially observable Markov Decision Process (MDP) or hidden Markov model (HMM) implementation of an SEIR model. Both models parameterise the size of the initial susceptible population (S0), as well as epidemic parameters. Parameter estimation (data fitting) was performed using a standard Bayesian scheme (variational Laplace) designed to allow for latent unobservable states and uncertainty in model parameters. Both models recapitulated the dynamics of transmissions and disease as given by case and death rates. The peaks of the current waves were predicted to be in the past for four countries (Italy, Spain, Germany and Switzerland) and to emerge in 0.5-2 weeks in Ireland and 1-3 weeks in the UK. For France one model estimated the peak within the past week and the other in the future in two weeks. Crucially, Maximum a posteriori (MAP) estimates of S0 for each country indicated effective population sizes of below 20% (of total population size), under both the continuous time and HMM models. With a Bayesian weighted average across all seven countries and both models, we estimated that 6.4% of the total population would be immune. From the two models the maximum percentage of the effective population was estimated at 19.6% of the total population for the UK, 16.7% for Ireland, 11.4% for Italy, 12.8% for Spain, 18.8% for France, 4.7% for Germany and 12.9% for Switzerland. Our results indicate that after the current wave, a large proportion of the total population will remain without immunity.

q-bio.PE