Marconi University

Superconducting Fault Current Limiters (SFCLs) have reached a mature Technology Readiness Level, making their deployment in power grids increasingly relevant. While applications in AC networks are well studied, HVDC grids pose distinct chal-lenges due to different fault dynamics and the reliance on Modular Multilevel Converters (MMCs). This work develops a mathematical model of a simplified DC grid including an SFCL based on High-Temperature Superconducting (HTS) tapes and an MMC repre-sented by an Averaged Value Model (AVM). The model couples net-work and converter dynamics with the nonlinear temperature- and current-dependent properties of the SFCL, enabling efficient para-metric studies under fault conditions. The analysis investigates key design parameters, such as the HTS tape length, highlighting their influence on SFCL and grid performance and providing guidelines for optimal device design.

The SAIFIN project (Satellite data and Artificial Intelligence for FINtech) develops a novel algorithmic trading system that integrates satellite imagery, financial data, and advanced artificial intelligence to enhance decision-making, particularly in commodity and agricultural markets. This paper presents the motivation, design, implementation, and validation of the SAIFIN framework. Leveraging alternative data and modular multi-agent architectures, SAIFIN aims to deliver robust, context-aware trading signals in diverse market conditions.

Abstract We report a case of young-onset PARK2 Parkinson’s disease complicated by severe, persistent insomnia, restless legs syndrome (RLS), and REM sleep behavior disorder (RBD), refractory to multiple conventional strategies. The clinical course included features consistent with levodopa-related rebound and augmentation, culminating in a systemic crisis with near-total sleep deprivation and night eating syndrome (NES). An N-of-1 precision approach was implemented by combining pharmacogenetics, molecule- and time-specific repositioning of medications (chronopharmacology), and continuous monitoring using consumer wearable sleep metrics and continuous glucose monitoring (CGM). Crucially, the optimization was conducted within an iterative human–AI loop in which a large language model (LLM) acted as a cognitive co-pilot to integrate multiplexed data streams, surface interaction risks, and generate prioritized hypotheses that were then clinically validated and implemented under continuous neurologist supervision. Key steps included discontinuation of evening levodopa, a strict pre-dinner ‘gastric-sparing’ window on an empty stomach to optimize absorption, and an evening synergy between low-dose pramipexole, pregabalin, and clonazepam. From September 2025 to February 2026, monthly wearable estimates showed deep sleep increasing from 5–8 min to 42–43 min and REM sleep increasing from 7–10 min to 45–50 min. In parallel, metabolic markers improved (HbA1c 7.2% to 6.8%, ALT/GPT 61 to 34 U/L within 12 months), with a 3 kg weight loss. This case illustrates a pragmatic framework for AI-augmented clinical reasoning in a complex multimorbid patient, demonstrating a path from pharmacoresistance to sustained clinical improvement.

A wealth of research in neuroscience and developmental psychology has documented the lasting detrimental effects of adverse early-life experiences on health and psychological well-being. To investigate these effects, researchers have developed self- and informant-report questionnaires, interview-based instruments, and experimental paradigms designed to assess exposure to early adversity, model its consequences under controlled laboratory conditions, and investigate the neurobiological mechanisms involved. In contrast, the role of positive early-life experiences in biobehavioral trajectories and adaptive functioning has received comparatively less empirical and theoretical attention. The existing work has largely conceptualized positive experiences in terms of their protective or buffering effects in the context of adversity, and/or their promotive role and independent contribution to physical and psychological well-being. Against this background, this narrative review comprehensively synthesizes (i) current definitions of positive early-life experiences, (ii) tools for their retrospective assessment, and (iii) experimental approaches aimed at manipulating and promoting such experiences in humans. Furthermore, this review advances time-sensitive and individual-centered attention for the study of positive early-life experiences, in which health- and well-being-promoting interventions are informed by an expanding understanding of normative human neuroplasticity as a heterosynchronous process and by dynamic, interdependent interactions operating across individual, family, and societal levels.

PurposeSelective inhibition of atrial proarrhythmicity can be therapeutic for reducing the atrial fibrillation (AF) burden. Atrial-selective K+-channel blockade (mainly Kv1.5 and Kv4.3 channels conducting the sustained IKur and transient Ito outward currents) promises to suppress AF with a favorable benefit-to-harm ratio. The mechanisms underlying the efficacy of K+ channel blockade under arrhythmic conditions and its association with electrophysiological and contractile remodeling in AF remain to be investigated.MethodsUsing our electromechanically coupled model MBS2023, we have simulated the effects of 4-aminopyridine (4-AP) and AVE0118 at different basic cycle lengths (2–0.25s). We have dissociated the primary and secondary responses to determine the drug’s underlying mechanisms of action. We have analyzed the effects of K+-channel blockers under arrhythmogenic conditions induced by either forward excitation-contraction coupling (ECC) or mechano-calcium feedback.ResultsAt the basal rate, the voltage-mediated increase in IKr induced by 4-AP shortens the action potential duration (APD) under sinus rhythm (SR), whereas a surge in ICaL prolongs APD under AF. 4-AP can exacerbate the vulnerability to phase 2 early afterdepolarizations (EADs) by slowing repolarization and prolonging myofilament activation. K+-channel blockade can decimate the susceptibility of delayed afterdepolarizations (DADs) by eliminating the cytosolic Ca2+ overload. The slowing of repolarization induced by 4-AP can suppress the reopening of Na+ channels during phase 3 EADs.ConclusionIn both types of EAD, a shorter, Ca2+-desensitized sarcomere can reduce the propensity for AF in the model. In general, K+ channel blockade has anti-arrhythmic potential to suppress phase 3 EADs by slowing repolarization.