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Digital devices are the essential building blocks of any modern electronic system. Fibres containing digital devices could enable fabrics with digital system capabilities for applications in physiological monitoring, human-computer interfaces, and on-body machine-learning. Here, a scalable preform-to-fibre approach is used to produce tens of metres of flexible fibre containing hundreds of interspersed, digital temperature sensors and memory devices with a memory density of ~7.6 × 10 5 bits per metre. The entire ensemble of devices are individually addressable and independently operated through a single connection at the fibre edge, overcoming the perennial single-fibre single-device limitation and increasing system reliability. The digital fibre, when incorporated within a shirt, collects and stores body temperature data over multiple days, and enables real-time inference of wearer activity with an accuracy of 96% through a trained neural network with 1650 neuronal connections stored within the fibre. The ability to realise digital devices within a fibre strand which can not only measure and store physiological parameters, but also harbour the neural networks required to infer sensory data, presents intriguing opportunities for worn fabrics that sense, memorise, learn, and infer situational context. Implementation of digital electronics into fibres can enable real time monitoring of human physiological functions. Loke et al. show how digital functionalities can be incorporated into thin flexible polymeric fibre strands and applied for on-body machine-learning and intelligent textiles.

Thirst is a motivational state that drives behaviors to obtain water for fluid homeostasis. We identified two types of central brain interneurons that regulate thirsty water seeking in Drosophila , that we term the Janu neurons. Janu-GABA, a local interneuron in the subesophageal zone, is activated by water deprivation and is specific to thirsty seeking. Janu-AstA projects from the subesophageal zone to the superior medial protocerebrum, a higher order processing area. Janu-AstA signals with the neuropeptide Allatostatin A to promote water seeking and to inhibit feeding behavior. NPF ( Drosophila NPY) neurons are postsynaptic to Janu-AstA for water seeking and feeding through the AstA-R2 galanin-like receptor. NPF neurons use NPF to regulate thirst and hunger behaviors. Flies choose Janu neuron activation, suggesting that thirsty seeking up a humidity gradient is rewarding. These findings identify novel central brain circuit elements that coordinate internal state drives to selectively control motivated seeking behavior.

In early December 2019, the coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) first emerged in Wuhan, China. As of May 10th, 2020, a total of over 4 million COVID-19 cases and 280,000 deaths have been reported globally, reflecting the raised infectivity and severity of this virus. Amongst hospitalised COVID-19 patients, there is a high prevalence of established cardiovascular disease (CVD). There is evidence showing that COVID-19 may exacerbate cardiovascular risk factors and preexisting CVD or may lead to cardiovascular complications. With intensive care units operating at maximum capacity and such staggering mortality rates reported, it is imperative during this time-sensitive COVID-19 outbreak to identify patients with an increased risk of adverse outcomes and/or myocardial injury. Preliminary findings from COVID-19 studies have shown the association of biomarkers of acute cardiac injury and coagulation with worse prognosis. While these biomarkers are recognised for CVD, there is emerging prospect that they may aid prognosis in COVID-19, especially in patients with cardiovascular comorbidities or risk factors that predispose to worse outcomes. Consequently, the aim of this review is to identify cardiovascular prognostic factors associated with morbidity and mortality in COVID-19 and to highlight considerations for incorporating laboratory testing of biomarkers of cardiovascular performance in COVID-19 to optimise outcomes.

The coronavirus disease 2019 (COVID-19) pandemic has resulted in over 6 million deaths and significant morbidity across the globe. Alongside common respiratory symptoms, COVID-19 is associated with a variety of cardiovascular complications in the acute and post-acute phases of infection. The suggested pathophysiological mechanisms that underlie these complications include direct viral infection of the myocardium via the angiotensin-converting enzyme 2 (ACE2) protein and a cytokine release syndrome that results in indirect inflammatory damage to the heart. Patients with pre-existing cardiovascular disease and co-morbidities are generally more susceptible to the cardiac manifestations of COVID-19. However, studies have identified a variety of complications in low-risk individuals, including young adults and children. Myocarditis and paediatric inflammatory multisystem syndrome temporally associated with COVID-19 (PIMS) are among the adverse events reported in the acute phase of infection. Furthermore, patients have reported cardiac symptoms persisting beyond the acute phase in post-COVID syndrome. This review summarises the acute and chronic cardiac consequences of COVID-19 in low-risk patients, explores the pathophysiology behind them, and discusses new predictive factors for poor outcomes.

Hypertensive heart disease (HHD) continues to be a leading cause of cardiovascular morbidity and mortality worldwide, necessitating the evolution of evidence-based management strategies. This literature review examines the most recent updates from the 2023 and 2024 hypertension guidelines issued by the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC). These guidelines are compared with previous key recommendations, such as the 2017 American College of Cardiology/American Heart Association guidelines and the 2018 ESC/ESH guidelines. The updated recommendations reflect a paradigm shift in the approach to hypertension diagnosis and management, including a stricter systolic blood pressure (BP) target of 120–129 mmHg, which underscores the importance of early and precise BP control. The difference between the classification of “elevated BP” and hypertension in the ESC versus ESH guidelines, particularly, regarding their implications for early detection and prevention of HHD, are critically examined, highlighting areas of clinical and academic debate. The introduction of a new “elevated BP” category (120–139/70–89 mmHg) highlights a proactive strategy aimed at identifying at-risk individuals earlier in the disease course to prevent progression to HHD. Additionally, the divergent roles of hypertension-mediated organ damage (HMOD), including HHD, in risk stratification as recommended by the ESC and ESH are discussed, emphasising their significance in tailoring management approaches. For patients with resistant hypertension, the 2023 and 2024 updates also endorse innovative therapies, such as renal denervation, an interventional procedure that has demonstrated significant promise in managing treatment-resistant cases. This review synthesises these updates, focusing on their implications for clinical practice in diagnosing and managing HHD. By emphasising aggressive intervention and the integration of novel treatment modalities, the review aims to bridge existing gaps in earlier approaches to hypertension management. The critical evaluation of guideline discrepancies and evolving evidence seeks to provide clinicians with a nuanced understanding to optimise outcomes for patients with HHD, particularly considering emerging therapeutic possibilities and more stringent BP control targets.

The link between neuroinflammation and neurogenesis is an area of intensive research in contemporary neuroscience. The burgeoning amount of evidence accumulated over the past decade has been incredible, and now there remains the figuring out of minutia to give us a more complete picture of what individual, synergistic, and antagonistic events are occurring between neurogenesis and neuroinflammation. An intricate study of the inflammatory microenvironment influenced by the presence of the various inflammatory components like cytokines, chemokines, and immune cells is essential for: 1) understanding how neurogenesis can be affected in such a specialized niche and 2) applying the knowledge gained for the treatment of cognitive and/or motor deficits arising from inflammation-associated diseases like stroke, traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease. This review is written to provide the reader with up-to-date information explaining how these inflammatory components are effecting changes on neurogenesis.

Aging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.

Inherited heart diseases (IHDs) are caused by genetic mutations that disrupt the physiological structure and function of the heart. Understanding the mechanisms behind these diseases is crucial for developing personalised interventions in cardiovascular medicine. Development of induced pluripotent stem cells, which can then be differentiated to any nucleated adult cell type, has enabled the creation of personalised single-cell and multicellular models, providing unprecedented insights into the pathophysiology of IHDs. This review provides a comprehensive overview of recent advancements in human iPSC models used to dissect the molecular and genetic underpinnings of common IHDs. We examine multicellular models and tissue engineering approaches, such as cardiac organoids, engineered heart tissue, and multicellular co-culture systems, which simulate complex intercellular interactions within heart tissue. Recent advancements in stem cell models offer a more physiologically relevant platform to study disease mechanisms, enabling researchers to observe cellular interactions, study disease progression, and identify therapeutic strategies. By leveraging these innovative models, we can gain deeper insights into the molecular and cellular mechanisms underlying IHDs, ultimately paving the way for more effective diagnostic and therapeutic strategies.