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[Display omitted] • N400 and P600 ERPs evoked in adolescents ignoring sentences with semantic errors. • Semantic processing is fundamentally different in passive versus active contexts. • We provide 22 control adolescent high-density electrophysiological BIDs datasets. Language comprehension requires semantic processing of individual words and their context within a sentence. Well-characterized event-related potential (ERP) components (the N400 and late positivity component (LPC/P600)) provide neuromarkers of semantic processing, and are robustly evoked when semantic errors are introduced into sentences. These measures are useful for evaluating semantic processing in clinical populations, but it is not known whether they can be evoked in more severe neurodevelopmental disorders where explicit attention to the sentence inputs cannot be objectively assessed (i.e., when sentences are passively listened to). We evaluated whether N400 and LPC/P600 could be detected in adolescents who were explicitly ignoring sentence inputs. Specifically, it was asked whether explicit attention to spoken inputs was required for semantic processing, or if a degree of automatic processing occurs when the focus of attention is directed elsewhere? High-density ERPs were acquired from twenty-two adolescents (12–17 years), under two experimental conditions: 1. individuals actively determined whether the final word in a sentence was congruent or incongruent with sentence context, or 2. passively listened to background sentences while watching a video. When sentences were ignored, N400 and LPC/P600 were robustly evoked to semantic errors, albeit with reduced amplitudes and protracted/delayed latencies. Statistically distinct topographic distributions during passive versus active paradigms pointed to distinct generator configurations for semantic processing as a function of attention. Covert semantic processing continues in neurotypical adolescents when explicit attention is withdrawn from sentence inputs. As such, this approach could be used to objectively investigate semantic processing in populations with communication deficits. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is highly prevalent in the Australian community, ranking amongst the highest globally. The consequences of AF are significant. Stroke, dementia and heart failure risk are increased substantially, hospitalisations are amongst the highest for all cardiovascular causes, and Australians living with AF suffer from substantial symptoms that impact quality of life. Australian research has made a significant impact at the global level in advancing the care of patients living with AF. However, new strategies are required to reduce the growing incidence of AF and its associated healthcare demand. The Australian Cardiovascular Alliance (ACvA) has led the development of an arrhythmia clinical theme with the objective of tackling major research priorities to achieve a reduction in AF burden across Australia. In this summary, we highlight these research priorities with particular focus on the strengths of Australian research and the strategies needed to move forward in reducing incident AF and improving outcomes for those who live with this chronic condition. [ABSTRACT FROM AUTHOR]

Recognizing objects by smell is a crucial ability for many species. To accomplish this, the brain must associate activity patterns of olfactory sensory neurons with the objects that elicited them. Recognition is hard because objects are dynamic entities whose molecular composition varies due to extrinsic and intrinsic factors and because background odors are often present. These factors lead to variability in receptor activation patterns evoked by any given object. Currently, the behavioral ability to overcome these sources of variance and the underlying neuronal mechanisms are poorly understood. We propose that extraction of invariant object representations is a major function of the elaborate olfactory cortical network. Revealing the limits of olfactory capabilities, and the neuronal mechanisms that enable them, calls for integration of natural sources of stimulus variability in experimental paradigms. Many animal species use olfaction to extract information about objects in their environment. Yet, the specific molecular signature that any given object emits varies due to various factors. Here, we detail why such variability makes chemosensory-mediated object recognition such a hard problem, and we propose that a major function of the elaborate chemosensory network is to overcome it. We describe previous work addressing different elements of the problem and outline future research directions that we consider essential for a full understanding of object-oriented olfaction. In particular, we call for extensive representation of olfactory object variability in chemical, behavioral, and electrophysiological analyses. While written with an emphasis on macrosmatic mammalian species, our arguments apply to all organisms that employ chemosensation to navigate complex environments. [ABSTRACT FROM AUTHOR]

• Tonic painful stimulation entailed a decrease in EEG alpha power, together with cardiac, electrodermal and pupil activation. • Taking in isolation, none of these activities was specific to pain. • Powerful discrimination between painful and non-painful conditions was achieved only when EEG and autonomic changes were combined. To assess the value of combining brain and autonomic measures to discriminate the subjective perception of pain from other sensory-cognitive activations. 20 healthy individuals received 2 types of tonic painful stimulation delivered to the hand: electrical stimuli and immersion in 10 Celsius degree (°C) water, which were contrasted with non-painful immersion in 15 °C water, and stressful cognitive testing. High-density electroencephalography (EEG) and autonomic measures (pupillary, electrodermal and cardiovascular) were continuously recorded, and the accuracy of pain detection based on combinations of electrophysiological features was assessed using machine learning procedures. Painful stimuli induced a significant decrease in contralateral EEG alpha power. Cardiac, electrodermal and pupillary reactivities occurred in both painful and stressful conditions. Classification models, trained on leave-one-out cross-validation folds, showed low accuracy (61–73%) of cortical and autonomic features taken independently, while their combination significantly improved accuracy to 93% in individual reports. Changes in cortical oscillations reflecting somatosensory salience and autonomic changes reflecting arousal can be triggered by many activating signals other than pain; conversely, the simultaneous occurrence of somatosensory activation plus strong autonomic arousal has great probability of reflecting pain uniquely. Combining changes in cortical and autonomic reactivities appears critical to derive accurate indexes of acute pain perception. [ABSTRACT FROM AUTHOR]

Single-lead electrocardiogram (ECG) devices may allow detection and diagnosis of cardiac rhythms. However, data on their accuracy for detecting cardiac arrhythmias beyond atrial fibrillation are limited. We aimed to determine the accuracy of the AliveCor KardiaMobile (AC) (AliveCor Inc, Mountain View, CA, USA) for the diagnosis of arrhythmias against gold standard cardiac electrophysiology study (EPS). Patients undergoing clinically indicated EPS underwent simultaneous rhythm recording with an AC, standard 12-lead ECG, and EP catheters for intracardiac electrograms. Rhythms recorded during EPS were classified based on electrogram, 12-lead ECG, and clinical findings. Blinded reviewers provided differential diagnoses for the single-lead AC tracings; a separate reviewer compared diagnoses made between the AC tracings and EPS findings. In 49 patients, 843 cardiac rhythms were captured during 502 AC recordings. Analysis of tracings containing sinus rhythm (n=273) returned an overall accuracy of 92%, with sensitivity and specificity values of 93% and 92%, respectively. Accuracy for tracings per rhythm was atrial fibrillation 91% (n=51); supraventricular tachycardia accuracy was 89% (n=191), ventricular tachycardia 91% (n=198), ventricular fibrillation 98% (n=11), and asystole 100% (n=5). Accuracy for supraventricular ectopy was 93% (n=28) and for premature ventricular complexes was 91% (n=86). Overall accuracy was 94% for solitary rhythms and 93% in tracings from patients with baseline bundle branch block. When compared against the gold standard EPS diagnosis, the interpretation of arrhythmias recorded by an AliveCor single-lead ECG device had reasonable diagnostic accuracy. [ABSTRACT FROM AUTHOR]

The ability to value rewards is crucial for adaptive behavior and is influenced by the time and effort required to obtain them. Impairments in these computations have been observed in patients with schizophrenia and may be present in individuals with subclinical psychotic symptoms (PS). In this study, we employed delay and effort-discounting tasks with food rewards in thirty-nine participants divided into high and low levels of PS. We investigated the underlying mechanisms of effort-discounting through computational modelling of dopamine prefrontal and subcortical circuits and the electrophysiological biomarker of both delay and effort-discounting alterations through resting-state frontal alpha asymmetry (FAA). Results revealed greater delay discounting in the High PS group compared to the Low PS group but no differences in the effort discounting task. However, in this task, the same levels of estimated dopamine release were associated with a lower willingness to exert effort for high-calorie food rewards in High PS participants compared to Low PS participants. Although there were no significant differences in FAA between the High PS and Low PS groups, FAA was significantly associated with the severity of participants' negative symptoms. Our study suggests that the dysfunction in temporal and effort cost computations, seen in patients with schizophrenia, may be present in individuals with subclinical PS. These findings provide valuable insight into the early vulnerability markers (behavioral, computational, and electrophysiological) for psychosis, which may aid in the development of preventive interventions. These findings are preliminary and warrant further investigation. [ABSTRACT FROM AUTHOR]

Congenital myasthenic syndromes (CMS) are a group of genetic disorders characterized by impaired neuromuscular transmission. CMS typically present at a young age with fatigable muscle weakness, often with an abnormal response after repetitive nerve stimulation (RNS). Pharmacologic treatment can improve symptoms, depending on the underlying defect. Prevalence is likely underestimated. This study reports on patients with CMS followed in Belgium in 2022. Data were gathered retrospectively from the medical charts. Only likely pathogenic and pathogenic variants were included in the analysis. We identified 37 patients, resulting in an estimated prevalence of 3.19 per 1,000,000. The patients harbored pathogenic variants in CHRNE , RAPSN , DOK7 , PREPL , CHRNB1 , CHRNG , COLQ , MUSK , CHRND , GFPT1, and GMPPB. CHRNE was the most commonly affected gene. Most patients showed disease onset at birth, during infancy, or during childhood. Symptom onset was at adult age in seven patients, caused by variants in CHRNE , DOK7 , MUSK , CHRND, and GMPPB. Severity and distribution of weakness varied, as did the presence of respiratory involvement, feeding problems, and extraneuromuscular manifestations. RNS was performed in 23 patients of whom 18 demonstrated a pathologic decrement. Most treatment responses were predictable based on the genotype. This is the first pooled characterization of patients with CMS in Belgium. We broaden the phenotypical spectrum of pathogenic variants in CHRNE with adult-onset CMS. Systematically documenting larger cohorts of patients with CMS can aid in better clinical characterization and earlier recognition of this rare disease. We emphasize the importance of establishing a molecular genetic diagnosis to tailor treatment choices. [ABSTRACT FROM AUTHOR]

Both alcohol use disorder (AUD) and cognitive decline include disruption in the balance of excitation and inhibition in the cortex, but the potential role of alcohol use on excitation and inhibition on the aging brain is unclear. We examined the effect of moderate voluntary binge alcohol consumption on the aged, pre-disease neuronal environment by measuring intrinsic excitability and spontaneous neurotransmission on prefrontal cortical pyramidal (excitatory, glutamatergic) and non-pyramidal (inhibitory, GABAergic) neurons following a prolonged period of abstinence from alcohol in mice. Results highlight that binge alcohol consumption has lasting impacts on the electrophysiological properties of prefrontal cortical neurons. A profound increase in excitatory events onto layer 2/3 non-pyramidal neurons following alcohol consumption was seen, along with altered intrinsic excitability of pyramidal neurons, which could have a range of effects on cognitive disorder progression, such as Alzheimer's Disease, in humans. These results indicate that moderate voluntary alcohol influences the pre-disease environment in aging and highlight the need for further mechanistic investigation into this risk factor. [Display omitted] • Moderate voluntary alcohol disrupts prefrontal cortical signaling at protracted ages in mice. • Glutamatergic events onto GABA neurons are increased 6 months following alcohol exposure. • Pyramidal and GABA neurons show altered intrinsic excitability 6 months after alcohol exposure. [ABSTRACT FROM AUTHOR]

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Coordinated detection of changes in metabolic state by the nervous system is fundamental for survival. Hypothalamic pro-opiomelanocortin (POMC) neurons play a critical role in integrating metabolic signals, including leptin levels. They also coordinate adaptative responses and thus represent an important relay in the regulation of energy balance. Despite a plethora of work documenting the effects of individual hormones, nutrients, and neuropeptides on POMC neurons, the importance for crosstalk and additive effects between such signaling molecules is still underexplored. The ability of the metabolic state and the concentrations of nutrients, such as glucose, to influence leptin's effects on POMC neurons appears critical for understanding the function and complexity of this regulatory network. Here, we summarize the current knowledge on the effects of leptin on POMC neuron electrical excitability and discuss factors potentially contributing to variability in these effects, with a particular focus on the mouse models that have been developed and the importance of extracellular glucose levels. This review highlights the importance of the metabolic "environment" for determining hypothalamic neuronal responsiveness to metabolic cues and for determining the fundamental effects of leptin on the activity of hypothalamic POMC neurons. [ABSTRACT FROM AUTHOR]

This special article is a continuation of an annual series for the Journal of Cardiothoracic and Vascular Anesthesia , highlighting the latest developments in the field of electrophysiology, particularly concerning cardiac anesthesiologists. The selected topics in the specialty for 2023 include consensus statements on left atrial appendage closure, outcomes in patients with atrial fibrillation and heart failure after ablation, further developments in the field of pulse field ablation, alternate defibrillation strategies for refractory ventricular fibrillation, updates on conduction system pacing, new devices such as the Aurora EV system and AVEIR leadless pacemaker system, artificial intelligence and its use in electrocardiogram-based diagnosis and latest evidence regarding the impact of anesthetic techniques on patient outcomes undergoing electrophysiology procedures. [ABSTRACT FROM AUTHOR]

A rotational activation pattern (RAP) around the localized line of a conduction block often correlates with sites specific to the critical zones of ventricular tachycardia (VT). The wavefront direction during substrate mapping affects manifestation of the RAP and line of block. The purpose of this study was to investigate the most optimal cardiac rhythm for identifying RAP and line of block in substrate mapping. We retrospectively evaluated 71 maps (median 3205 points/map) in 46 patients (65 ± 15 years; 33% with ischemic cardiomyopathy) who underwent high-density substrate mapping and ablation of scar-related VT. Appearance of a RAP during sinus, right ventricular (RV)-paced, left ventricular (LV)-paced, and biventricular-paced rhythms was investigated. RAP was identified in 24 of 71 maps (34%) in the region where wavefronts from a single direction reached but not in the region where wavefronts from multiple directions centripetally collided. The probability of identifying the RAP depended on scar location; that is, anteroseptal and inferoseptal, inferior and apical, and basal lateral RAPs were likely to be identified during sinus/atrial, RV-paced, and LV-paced rhythms, respectively. In 13 patients, the RAP was not evident in the baseline map but became apparent during remapping in the other rhythm, in which the wavefront reached the site earlier within the entire activation time. The optimal rhythm for substrate mapping depends on the spatial distribution of the area of interest. A paced rhythm with pacing sites near the scar may facilitate the identification of critical VT zones. [ABSTRACT FROM AUTHOR]

Bradyarrhythmias including sinus bradycardia and atrioventricular (AV) block are frequently encountered in endurance athletes especially at night. While these are well tolerated by the young athlete, there is evidence that generally from the fifth decade of life onward, such arrhythmias can degenerate into pathological symptomatic bradycardia requiring pacemaker therapy. For many years, athletic bradycardia and AV block have been attributed to high vagal tone, but work from our group has questioned this widely held assumption and demonstrated a role for intrinsic electrophysiological remodeling of the sinus node and the AV node. In this article, we argue that bradyarrhythmias in the veteran athlete arise from the cumulative effects of exercise training, the circadian rhythm and aging on the electrical activity of the nodes. We consider contemporary strategies for the treatment of symptomatic bradyarrhythmias in athletes and highlight potential therapies resulting from our evolving mechanistic understanding of this phenomenon. [Display omitted] [ABSTRACT FROM AUTHOR]

• DMV contains cardiac and pulmonary parasympathetic motoneurons controlling ventricular function and airways secretion. • DMV pulmonary motoneurons are more depolarized and excitable than cardiac. • DMV pulmonary motoneurons have both lower magnitude of A-type K+ currents and level of Kv4.2 expression than cardiac. • DMV pulmonary motoneurons receive greater excitatory synaptic inputs and have highly dendritic complexity than cardiac. The dorsal motor nucleus of the vagus (DMV) contains parasympathetic motoneurons that project to the heart and lungs. These motoneurons control ventricular excitability/contractility and airways secretions/blood flow, respectively. However, their electrophysiological properties, morphology and synaptic input activity remain unknown. One important ionic current described in DMV motoneurons controlling their electrophysiological behaviour is the A-type mediated by voltage-dependent K+ (Kv) channels. Thus, we compared the electrophysiological properties, synaptic activity, morphology, A-type current density, and single cell expression of Kv subunits, that contribute to macroscopic A-type currents, between DMV motoneurons projecting to either the heart or lungs of adult male rats. Using retrograde labelling, we visualized distinct DMV motoneurons projecting to the heart or lungs in acutely prepared medullary slices. Subsequently, whole cell recordings, morphological reconstruction and single motoneuron qRT-PCR studies were performed. DMV pulmonary motoneurons were more depolarized, electrically excitable, presented higher membrane resistance, broader action potentials and received greater excitatory synaptic inputs compared to cardiac DMV motoneurons. These differences were in part due to highly branched dendritic complexity and lower magnitude of A-type K+ currents. By evaluating expression of channels that mediate A-type currents from single motoneurons, we demonstrated a lower level of Kv4.2 in pulmonary versus cardiac motoneurons, whereas Kv4.3 and Kv1.4 levels were similar. Thus, with the distinct electrical, morphological, and molecular properties of DMV cardiac and pulmonary motoneurons, we surmise that these cells offer a new vista of opportunities for genetic manipulation providing improvement of parasympathetic function in cardiorespiratory diseases such heart failure and asthma. [ABSTRACT FROM AUTHOR]

During the COVID-19 pandemic, professional societies recommended deferral of elective procedures for optimal resource utilization. We sought to assess changes in procedural trends and outcomes of electrophysiology (EP) procedures during the pandemic. National Inpatient Sample databases were used to identify all EP procedures performed in the United States (2016–2020) by International Classification of Diseases, Tenth Revision codes. We evaluated trends in utilization, cost/revenue, and outcomes from EP procedures performed. An estimated 1.35 million EP procedures (82% devices and 18% catheter ablations) were performed (2016–2020) with significant yearly uptrend. During the pandemic, there was a substantial decline in EP procedure utilization from a 5-year peak of 298 cases/million population in the second quarter of 2019 to a nadir of 220 cases in the second quarter of 2020. In 2020, the pandemic was associated with the loss of 50,233 projected EP procedures (39,337 devices and 10,896 ablations) with subsequent revenue loss of $7.06 billion. This deficit was driven by revenue deficit from dual-chamber permanent pacemaker (PPM) utilization ($2.88 billion, 49.3% of lost cases), ablation procedures ($1.84 billion, 21.7% of lost cases), and implantable cardioverter-defibrillator implantation ($1.36 billion, 12.0% of lost cases). To the contrary, there was a 9.4% increase in the utilization of leadless PPM. EP device implantation during the pandemic was associated with higher adverse in-hospital events (9.4% vs 8.0%; P <.001). In the United States, the significant decline in EP procedures during the pandemic was primarily driven by the reduction in dual-chamber PPM utilization, followed by arrhythmia ablation and implantable cardioverter-defibrillator implantation. There was a substantial increase in leadless PPM utilization during the pandemic. [ABSTRACT FROM AUTHOR]

[Display omitted] • Chronic Unpredictable mild stress (CUMS) increased serum Corticosterone level. • UCMS increased oxidative stress status and neuro-inflammation and decreasing BDNF and Ki67 in the brain. • Oxidative stress and neuro-inflammation followed by learning and memory impairment in adolescent male rats. • Ascorbic acid (AA) improved learning and memory impairment. • Vit C decreased serum corticosterone level, brain oxidative stress damage and increased BDNF and neurogenesis. The present research study aimed to investigate the role of Ascorbic acid (AA) on synaptic plasticity, learning, and memory impairment induced by unpredicted chronic mild stress (CUMS) in adolescent male rats. Adolescent male rats were divided into: 1) vehicle, 2) CUMS, 3–5) CUMS plus various doses of AA by oral gavage (CUMS-10/100/400 mg/kg), and 6) AA400 mg/kg by oral gavage. In Morris Water Maze, the time latency decreased, while the time spent in the target quadrant increased in CUMS group treated with AA at the dose of 400 mg/kg. In passive avoidance, the latency of entering into the dark chamber decreased in CUMS group treated with AA (400 mg/kg). In biochemical test results, nitrite and MDA significantly decreased, while thiol content, SOD, and catalase activity in CUMS group that received AA400mg/kg was increased. IL-10, BDNF and Ki67 increased, while TNF-a and AChE activity were decreased in CUMS group treated with AA simultaneously. The results of our study showed that chronic stress during adolescence could cause learning and memory disorders as well as synaptic plasticity. In addition, we showed that AA can prevent this problem by reducing oxidative stress, inflammation, increasing the amount of BDNF, and neurogenesis. [ABSTRACT FROM AUTHOR]

Aging is associated with the slowdown of neuronal processing and cognitive performance in the brain; however, the exact cellular mechanisms behind this deterioration in humans are poorly elucidated. Recordings in human acute brain slices prepared from tissue resected during brain surgery enable the investigation of neuronal changes with age. Although neocortical fast-spiking cells are widely implicated in neuronal network activities underlying cognitive processes, they are vulnerable to neurodegeneration. Herein, we analyzed the electrical properties of 147 fast-spiking interneurons in neocortex samples resected in brain surgery from 106 patients aged 11–84 years. By studying the electrophysiological features of action potentials and passive membrane properties, we report that action potential overshoot significantly decreases and spike half-width increases with age. Moreover, the action potential maximum-rise speed (but not the repolarization speed or the afterhyperpolarization amplitude) significantly changed with age, suggesting a particular weakening of the sodium channel current generated in the soma. Cell passive membrane properties measured as the input resistance, membrane time constant, and cell capacitance remained unaffected by senescence. Thus, we conclude that the action potential in fast-spiking interneurons shows a significant weakening in the human neocortex with age. This may contribute to the deterioration of cortical functions by aging. • Recordings in human acute brain slices prepared from tissue resected during brain surgery enable investigating neuronal changes with age. • Action potential in fast-spiking interneurons shows a significant weakening in the human neocortex with age. • Neuron intrinsic excitability, measured as the input resistance, membrane time constant, and cell capacitance remained unaffected by senescence. • These changes in neurons' electrical activity may contribute to the deterioration of cortical functions with age. [ABSTRACT FROM AUTHOR]

Esophageal thermal injury is one of the most devastating complications of atrial radiofrequency ablation, and its diagnosis can be challenging. In this report, we highlight the novel use of free water as a contrast material to better visualize the esophageal lumen in a patient with anaphylaxis to Iodinated contrast media and Gadolinium who recently underwent atrial fibrillation ablation. This becomes particularly handy in patients with contrast allergy, and further emphasizes the role of multimodality imaging. [Display omitted] • MR hydrography is a novel technique that can be used for evaluation of esophageal perforation after RF ablation procedures. • This technique is useful in a subset of patients with contrast allergy in whom multimodality imaging evaluation is necessary. • This report forms the basis of a new imaging technique that could potentially be used in clinical practice in the future. [ABSTRACT FROM AUTHOR]

This study aimed to assess the efficacy of a screening questionnaire, based on historical criteria, in distinguishing between seizures and syncope in patients experiencing their first episode of transient loss of consciousness (TLOC) in a neurology emergency department. A prospective cohort of 159 patients with initial TLOC episodes underwent clinical observation and answered a nine-question screening questionnaire. The questionnaire's predictive ability was compared to final diagnoses determined through detailed neurology, electrophysiology, and cardiology assessments during a minimum 12-month follow-up. Logistic regression (LR) analysis was performed with final diagnosis as the outcome variable. The calibration and discrimination of the models were assessed. revealed that the screening score accurately classified 72.33% of patients. Among those with positive screening scores, 65 (67.71%) had seizures compared to 31 (32.29%) with syncope. Introducing a novel risk-scoring model incorporating age and gender, in addition to the screening score, significantly improved performance achieving an accurate classification rate of 81.48%. Among patients with a positive prediction, 63 (80.77%) had seizure, whereas 15 (19.23%) had syncope. Employing a structured questionnaire based on common historical criteria is a valuable tool for distinguishing between seizure and syncope in the dynamic setting of the emergency department. [ABSTRACT FROM AUTHOR]

Differentiating between atypical atrioventricular nodal reentrant tachycardia (AVNRT) and orthodromic reciprocating tachycardia utilizing a septal accessory pathway is a complex challenge. The purpose of this study was to describe the "local VA index," a straightforward method based on signals from the coronary sinus catheter, to distinguish between these arrhythmias during tachycardia and entrainment. The ventriculoatrial (VA) interval on the coronary sinus catheter is measured during tachycardia and entrainment, at the site of earliest atrial activity. The difference between these 2 situations defines the "local VA index." We also propose a mechanism to clarify the limitations of historical pacing maneuvers, such as postpacing interval minus tachycardia cycle length (PPI-TCL) and stimulus–atrial interval minus ventriculoatrial interval (SA-VA), by examining nodal decrement and intraventricular conduction delay. In a retrospective study of 75 patients referred for supraventricular tachycardia evaluation, 37 were diagnosed with atrioventricular reentrant tachycardia (AVRT) with orthodromic reciprocating tachycardia, and 38 with AVNRT (27 typical, 11 atypical). In comparison to AVRT patients, AVNRT patients exhibited longer PPI-TCL (176 ± 47 ms vs 113 ± 42 ms; P <.01) and SA-VA (138 ± 47 ms vs 64 ± 28 ms; P <.01). The AVRT group had mean local VA index of –1 ± 13 ms, whereas the AVNRT group had a significantly longer index of 91 ± 46 ms (P <.01). An optimal threshold for differentiation was a local VA index of 40 ms. Importantly, there was no significant correlation between pacing cycle length and nodal decrement as well as intraventricular delay related to pathway location. This interindividual variability might explain misleading interpretations of PPI-TCL and SA-VA. This novel approach is advantageous because of its simplicity and effectiveness, requiring only 2 diagnostic catheters. A local VA interval difference <40 ms provides a clear distinction for AVRT. [ABSTRACT FROM AUTHOR]

• This study investigated the cortical silent period (CSP) characteristics in stronger biceps (power = 3–5) and weaker triceps (power = 1–3) after SCI. • The CSP from the biceps had a longer duration, whereas it was delayed and shallow for the triceps in individuals with SCI. • The CSP characteristics were associated with upper arm functional ability supporting their relevance for motor recovery after SCI. Corticospinal inhibitory mechanisms are relevant to functional recovery but remain poorly understood after spinal cord injury (SCI). Post-injury characteristics of contralateral silent period (CSP), a measure of corticospinal inhibition evaluated using transcranial magnetic stimulation (TMS), is inconsistent in literature. We envisioned that investigating CSP across muscles with varying degrees of weakness may be a reasonable approach to resolve inconsistencies and elucidate the relevance of corticospinal inhibition for upper extremity function following SCI. We studied 27 adults with chronic C1-C8 SCI (age 48.8 ± 16.1 years, 3 females) and 16 able-bodied participants (age 33.2 ± 11.8 years, 9 females). CSP characteristics were assessed across biceps (muscle power = 3–5) and triceps (muscle power = 1–3) representing stronger and weaker muscles, respectively. We assessed functional abilities using the Capabilities of the Upper Extremity Test (CUE-T). Participants with chronic SCI had prolonged CSPs for biceps but delayed and diminished CSPs for triceps compared to able-bodied participants. Early-onset CSPs for biceps and longer, deeper CSPs for triceps correlated with better CUE-T scores. Corticospinal inhibition is pronounced for stronger biceps but diminished for weaker triceps muscle in SCI indicating innervation relative to the level of injury matters in the study of CSP. Nevertheless, corticospinal inhibition or CSP holds relevance for upper extremity function following SCI. [ABSTRACT FROM AUTHOR]

The highly selective α2-adrenoceptor agonist dexmedetomidine is a commonly used sedative drug for patients undergoing anesthesia and intensive care treatment. Several studies have indicated that dexmedetomidine may have a potential role in preventing and treating perioperative tachyarrhythmias. However, the specific effect and mechanism of action of dexmedetomidine in this context remain unclear. Dexmedetomidine is known to regulate the electrophysiologic function of the myocardium by inhibiting the function of the sinus node and atrioventricular node, as well as affecting myocardial repolarization. This paper aims to provide a theoretical basis for the prevention and treatment of perioperative arrhythmias by summarizing the effects of dexmedetomidine on myocardial electrophysiologic function and its impact on different types of arrhythmias. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a neurodegeneration disease with α -synuclein accumulated in the substantia nigra pars compacta (SNpc) and most of the dopaminergic neurons are lost in SNpc while patients are diagnosed with PD. Exploring the pathology at an early stage contributes to the development of the disease-modifying strategy. Although the "gut–brain" hypothesis is proposed to explain the underlying mechanism, where the earlier lesioned site in the brain of gastric α -synuclein and how α -synuclein further spreads are not fully understood. Here we report that caudal raphe nuclei (CRN) are the early lesion site of gastric α -synuclein propagating through the spinal cord, while locus coeruleus (LC) and substantia nigra pars compacta (SNpc) were further affected over a time frame of 7 months. Pathological α -synuclein propagation via CRN leads to neuron loss and disordered neuron activity, accompanied by abnormal motor and non-motor behavior. Potential neuron circuits are observed among CRN, LC, and SNpc, which contribute to the venerability of dopaminergic neurons in SNpc. These results show that CRN is the key region for the gastric α -synuclein spread to the midbrain. Our study provides valuable details for the "gut–brain" hypothesis and proposes a valuable PD model for future research on early PD intervention. This study shows gastric α -synuclein propagates through the spinal cord to the caudal raphe nuclei, and further induces lesions in the locus coeruleus and substantia nigra via potential neuronal circuits. [Display omitted] [ABSTRACT FROM AUTHOR]

Precordial Bipolar Leads (PBLs) provide new electrocardiographic information derived from standard 12‑lead ECG recordings. To explore the usefulness of PBLs in patients with acute circumflex coronary artery (CxCA) occlusion. Twelve patients undergoing elective percutaneous transluminal coronary angioplasty (PTCA) were studied before and after acute CxCA occlusion and their data were processed with new methods based on PBLs. The findings were: 1. In right PBL V2-V1, a strong systolic current of injury moving in the left-to-right direction coexists with a strong right-to-left current of injury displayed in left standard unipolar precordial leads (V4, V5 and V6). 2. Ischemic changes lead to a significant increase (approximately 10 ms) in the QRS duration in different leads, although changes in the QRS loop rotation and folding were absent. 3. In the transverse, sagittal, and frontal planes, superimposing two PBLs and the corresponding Regional VCG facilitates the location of the J-point. 4. In the Regional VCGs of this group of patients, J-point and ST segment shifts produced an image that reminds the Greek letter omega (Ω). 5. The currents of injury flowing in opposite directions could result in electrical cancellation that minimizes ECG changes in the standard 12‑lead recordings. Computerized processing of digital, standard 12‑lead ECG recordings, provides new valuable diagnostic data in patients with acute CxCA occlusion. The loops revealed important information related to systolic currents of injury. Because these methods use routine 12‑lead ECG data, the procedure is based only in software applications. Twelve patients undergoing PTCA were studied before and after acute CxCA occlusion and their data were processed with the new methods based on Precordial Bipolar Leads (PBLs) to explore their usefulness. The results showed strong systolic currents of injury in different and sometimes opposite directions in the right-to-left axis and ischemic alterations in the time and amplitude of the QRS waves. The superimposition of two-dimensional coordinates planes (x-y, x-z or z-y) helped to locate the J-point and to display the Regional VCG omega sign (Ω) of myocardial injury. In conclusion, computerized processing of digital ECG data provides new diagnostic information in patients with acute CxCA occlusion. [ABSTRACT FROM AUTHOR]

Accurate estimation of accessory pathway (AP) localization in patients with ventricular pre-excitation or Wolff-Parkinson-White (WPW) syndrome remains a diagnostic challenge. Existing algorithms have contributed significantly to this area, but alternative algorithms can offer additional perspectives and approaches to AP localization. This study introduces and evaluates the diagnostic accuracy of the EPM algorithm in AP localization, comparing it with established algorithms Arruda and EASY. A retrospective analysis was conducted on 138 patients from Hospital São Paulo who underwent catheter ablation. Three blinded examiners assessed the EPM algorithm's diagnostic accuracy against the Arruda and EASY algorithms. The gold standard for comparison was the radioscopic position of the AP where radiofrequency ablation led to pre-excitation disappearance on the ECG. EPM showed a diagnostic accuracy of 51.45%, closely aligning with Arruda (53.29%) and EASY (44.69%). Adjacency accuracy for EPM was 70.67%, with Arruda at 66.18% and EASY at 72.22%. Sensitivity for EPM in distinguishing left vs. right APs was 95.73%, with a specificity of 74.33%. For identifying septal vs. lateral right APs, EPM sensitivity was 82.79% with a specificity of 46.15%. These measures were comparable to those of Arruda and EASY. Inter-observer variability was excellent for EPM, with Kappa statistics over 0.9. The EPM algorithm emerges as a reliable tool for AP localization, offering a systematic approach beneficial for therapeutic decision-making in electrophysiology. Its comparable diagnostic accuracy and excellent inter-observer variability underscore its potential clinical applicability. Future research may further validate its efficacy in a broader clinical setting. [Display omitted] • EPM stands as a reliable electrocardiographic tool for AP localization, enhancing electrophysiology outcomes. • EPM aligns with established algorithms, showing 51.45% diagnostic and 70.67% adjacency accuracy. • EPM's real-world diagnostic rates parallel retrospective studies, validating its clinical use. [ABSTRACT FROM AUTHOR]

The transition from wakefulness to sleep is neither an 'all-or-none' nor a linear phenomenon. It is a specific period characterized by fluctuations between various transient and local neural patterns with high inter- and intraindividual variability. During the SOP, there is an intricate interplay between the internal and external information sources that feed neurocognitive processing. Individuals can still respond to some external stimuli while having dream-like experiences. Drowsiness is often linked to negative cognitive effects (e.g., attention lapses). However, growing evidence indicates that the SOP may serve key cognitive functions (e.g., memory and creativity). About one-third of the population suffers from sleep-onset difficulties. A better understanding of the SOP could help to identify key markers for diagnosing and treating these disorders. Sleep is crucial for many vital functions and has been extensively studied. By contrast, the sleep-onset period (SOP), often portrayed as a mere prelude to sleep, has been largely overlooked and remains poorly characterized. Recent findings, however, have reignited interest in this transitional period and have shed light on its neural mechanisms, cognitive dynamics, and clinical implications. This review synthesizes the existing knowledge about the SOP in humans. We first examine the current definition of the SOP and its limits, and consider the dynamic and complex electrophysiological changes that accompany the descent to sleep. We then describe the interplay between internal and external processing during the wake-to-sleep transition. Finally, we discuss the putative cognitive benefits of the SOP and identify novel directions to better diagnose sleep-onset disorders. [ABSTRACT FROM AUTHOR]

Assessments of action semantics consistently reveal markers of Parkinson's disease (PD). However, neurophysiological signatures of the domain remain under-examined in this population, especially under conditions that allow patients to process stimuli without stringent time constraints. Here we assessed event-related potentials and time-frequency modulations in healthy individuals (HPs) and PD patients during a delayed-response semantic judgment task involving related and unrelated action-picture pairs. Both groups had shorter response times for related than for unrelated trials, but they exhibited discrepant electrophysiological patterns. HPs presented significantly greater N400 amplitudes as well as theta enhancement and mu desynchronization for unrelated relative to related trials. Conversely, N400 and theta modulations were abolished in the patients, who further exhibited a contralateralized cluster in the mu range. None of these patterns were associated with the participants' cognitive status. Our results suggest that PD involves multidimensional neurophysiological disruptions during action-concept processing, even under task conditions that elicit canonical behavioral effects. New constraints thus emerge for translational neurocognitive models of the disease. • We examined EEG markers of action concept relatedness in Parkinson's disease (PD). • Patients and controls were faster to process related than unrelated action trials. • Underlying N400 and theta effects were robust in controls and absent in patients. • Accompanying mu rhythms were contralateralized in patients. • Key neural signatures of action relatedness and grounding are altered in PD. [ABSTRACT FROM AUTHOR]

[Display omitted] • ACM is characterized by histopathological and electrophysiological remodelling. • This remodelling leads to adverse clinical outcomes. • Several factors play a critical role in ACM pathogenesis. • These factors include aging, metabolic disorders, pressure overload and genetics. • Noninvasive clinical tools can characterize ACM. • These tools include electrocardiography, cardiac imaging and serum biomarkers. • The tools are helpful in the prediction of adverse clinical outcomes. • The outcomes include atrial fibrillation, stroke, heart failure and dementia. Atrial cardiomyopathy is defined as any complex of structural, architectural, contractile or electrophysiological changes affecting atria, with the potential to produce clinically relevant manifestations. Most of our knowledge about the mechanistic aspects of atrial cardiomyopathy is derived from studies investigating animal models of atrial fibrillation and atrial tissue samples obtained from individuals who have a history of atrial fibrillation. Several noninvasive tools have been reported to characterize atrial cardiomyopathy in patients, which may be relevant for predicting the risk of incident atrial fibrillation and its related outcomes, such as stroke. Here, we provide an overview of the pathophysiological mechanisms involved in atrial cardiomyopathy, and discuss the complex interplay of these mechanisms, including aging, left atrial pressure overload, metabolic disorders and genetic factors. We discuss clinical tools currently available to characterize atrial cardiomyopathy, including electrocardiograms, cardiac imaging and serum biomarkers. Finally, we discuss the clinical impact of atrial cardiomyopathy, and its potential role for predicting atrial fibrillation, stroke, heart failure and dementia. Overall, this review aims to highlight the critical need for a clinically relevant definition of atrial cardiomyopathy to improve treatment strategies. [ABSTRACT FROM AUTHOR]

Ventricular arrhythmia in hypertrophic cardiomyopathy (HCM) relates to adverse structural change and genetic status. Cardiovascular magnetic resonance (CMR)–guided electrocardiographic imaging (ECGI) noninvasively maps cardiac structural and electrophysiological (EP) properties. The purpose of this study was to establish whether in subclinical HCM (genotype [G]+ left ventricular hypertrophy [LVH]−), ECGI detects early EP abnormality, and in overt HCM, whether the EP substrate relates to genetic status (G+/G−LVH+) and structural phenotype. This was a prospective 211-participant CMR-ECGI multicenter study of 70 G+LVH−, 104 LVH+ (51 G+/53 G−), and 37 healthy volunteers (HVs). Local activation time (AT), corrected repolarization time, corrected activation-recovery interval, spatial gradients (G AT /G RTc), and signal fractionation were derived from 1,000 epicardial sites per participant. Maximal wall thickness and scar burden were derived from CMR. A support vector machine was built to discriminate G+LVH− from HV and low-risk HCM from those with intermediate/high-risk score or nonsustained ventricular tachycardia. Compared with HV, subclinical HCM showed mean AT prolongation (P = 0.008) even with normal 12-lead electrocardiograms (ECGs) (P = 0.009), and repolarization was more spatially heterogenous (G RTc : P = 0.005) (23% had normal ECGs). Corrected activation-recovery interval was prolonged in overt vs subclinical HCM (P < 0.001). Mean AT was associated with maximal wall thickness; spatial conduction heterogeneity (G AT) and fractionation were associated with scar (all P < 0.05), and G+LVH+ had more fractionation than G−LVH+ (P = 0.002). The support vector machine discriminated subclinical HCM from HV (10-fold cross-validation accuracy 80% [95% CI: 73%-85%]) and identified patients at higher risk of sudden cardiac death (accuracy 82% [95% CI: 78%-86%]). In the absence of LVH or 12-lead ECG abnormalities, HCM sarcomere gene mutation carriers express an aberrant EP phenotype detected by ECGI. In overt HCM, abnormalities occur more severely with adverse structural change and positive genetic status. [Display omitted] [ABSTRACT FROM AUTHOR]

In the same way that beauty lies in the eye of the beholder, what a stimulus does to the brain is determined not simply by the nature of the stimulus but by the nature of the brain that is receiving the stimulus at that instant in time. Over the past decades, therapeutic brain stimulation has typically applied open-loop fixed protocols and has largely ignored this principle. Only recent neurotechnological advancements have enabled us to predict the nature of the brain (i.e., the electrophysiological brain state in the next instance in time) with sufficient temporal precision in the range of milliseconds using feedforward algorithms applied to electroencephalography time-series data. This allows stimulation exclusively whenever the targeted brain area is in a prespecified excitability or connectivity state. Preclinical studies have shown that repetitive stimulation during a particular brain state (e.g., high-excitability state), but not during other states, results in lasting modification (e.g., long-term potentiation) of the stimulated circuits. Here, we survey the evidence that this is also possible at the systems level of the human cortex using electroencephalography-informed transcranial magnetic stimulation. We critically discuss opportunities and difficulties in developing brain state–dependent stimulation for more effective long-term modification of pathological brain networks (e.g., in major depressive disorder) than is achievable with conventional fixed protocols. The same real-time electroencephalography-informed transcranial magnetic stimulation technology will allow closing of the loop by recording the effects of stimulation. This information may enable stimulation protocol adaptation that maximizes treatment response. This way, brain states control brain stimulation, thereby introducing a paradigm shift from open-loop to closed-loop stimulation. [ABSTRACT FROM AUTHOR]

Peripheral nerve injuries are common and serious conditions. The effect of Neurotropin® (NTP), a nonprotein extract derived from the inflamed skin of rabbits inoculated with vaccinia virus, on peripheral nerve regeneration has not been fully elucidated. However, it has analgesic properties via the activation of descending pain inhibitory systems. Therefore, the current study aimed to determine the effects of NTP on peripheral nerve regeneration. We examined axonal outgrowth of dorsal root ganglion (DRG) neurons using immunocytochemistry in vitro. In addition, nerve regeneration was evaluated functionally, electrophysiologically, and histologically in a rat sciatic nerve crush injury model in vivo. Furthermore, gene expression of neurotrophic factors in the injured sciatic nerves and DRGs was evaluated. In the dorsal root ganglion neurons in vitro , NTP promoted axonal outgrowth at a concentration of 10 mNU/mL. Moreover, the systemic administration of NTP contributed to the recovery of motor and sensory function at 2 weeks, and of sensory function, nerve conduction velocity, terminal latency, and axon-remyelination 4 weeks after sciatic nerve injury. In the gene expression assessment, insulin-like growth factor 1 and vascular endothelial growth factor expressions were increased in the injured sciatic nerve 2 days postoperatively. Therefore, NTP might be effective in not only treating chronic pain but also promoting peripheral nerve regeneration after injury. [ABSTRACT FROM AUTHOR]

• SCAF4 is associated with focal epilepsy accompanied by multisystem disorders, including skeletal, genitourinary abnormalities, etc. • Used whole-exome sequencing, genetic analysis and computational modelling to verify the pathogenicity of SCAF4 variants. • Abnormal epileptiform signals and skeletal development have been found in scaf4a/b knockout zebrafish compared to the wild-type. The SCAF4 gene encodes serine/arginine-related carboxyl-terminal domain-associated factor 4, which is highly expressed in the brain and potentially affects neurodevelopment. However, the functional significance of SCAF4 variants in human diseases remains unknown. Trio-based whole-exome sequencing was performed in three individuals with focal epilepsy. Bioinformatics tools were used to assess the pathogenicity of SCAF4 variants. Knockout scaf4a/b zebrafish were created using CRISPR-Cas9 used to validate the phenotype. SCAF4 variants were identified in three individuals from three unrelated families with focal epilepsy. All patients had focal seizures and focal discharges on EEG recordings, with intellectual disability or motor retardation, skeletal abnormalities, and one had cryptorchidism. However, no recurrence was observed after short-term ASMs treatment. The identified SCAF4 variants included two nonsense variants and one compound heterozygous variant, consisting of a missense and an in-frame variant. A low frequency of SCAF4 variants was observed in gnomAD in this study. Computational modelling has suggested that missense variants lead to functional impairments. In zebrafish, abnormal epileptiform signals, skeletal development, and neurodevelopment have been found in scaf4a/b knockout compared to wild-type zebrafish. These results indicate that SCAF4 is associated with focal epilepsy accompanied by multisystem disorders. Otherwise, the management of patients with SCAF4 variants requires more attention to multisystem involvement. [ABSTRACT FROM AUTHOR]

Humans and other primates skillfully navigate the complex cognitive interplay of cooperative behaviors. However, the neural resources we rely on to do so are poorly understood. Franch et al. found that neuronal activity in a visual-frontal domain general cortical network is shaped during the training of a cooperative behavior to highlight relevant sensory inputs. [ABSTRACT FROM AUTHOR]

Microbial fuel cells (MFCs) are an important tool that generates electricity from waste biomass. Polymer electron membrane supported dual-chamber MFCs are one of the most tested microbial fuel cells. The most important factor affecting performance in this system is the proton transfer capability of the membrane. In this study, zirconia based metal organic frameworks (Zr-MOF) doped porous membranes were produced, characterized and used in dual chamber (H-type) MFC to generate electricity from animal manure (Cow manure). The effects of MOF ratio on membrane's physical, chemical properties, and on the cell performance were investigated. The incorporation of MOF into the PVDF matrix improved the water retention property of the membrane. The Zr-MOF addition increased the mechanical strength from 0.55 MPa to 1.52 MPa. The cation exchange capacity increased from 1.04 mmol/g to 2.41 mmol/g. It significantly increased the cell electricity production from 0.186V to 0.49V. The power density values are obtained as 5.02 and 13.8 mW/m2 with the pristine and Zr-MOF(4)-PVDF membranes, respectively. • H type MFC with porous PVDF membrane was investigated. • Zr-MOF was synthesized and used for filler in PVDF membrane. • Zr-MOF addition increased the mechanical strength from 0.55 to 1.52 MPa. • The cation exchange capacity increased from 1.04 to 2.41 mmol/g. • The cell electricity production increased from 0.186V to 0.49V. [ABSTRACT FROM AUTHOR]

An increasing number of patients undergoing elective or emergency surgery in the United States have a cardiovascular implantable electronic device. Practice advisories and consensus statements have been issued by the American Society of Anesthesiologists and the Heart Rhythm Society, advocating a multidisciplinary approach. Unfortunately, anesthesia providers often find themselves in a situation in which they are left to manage these devices independently. At the University of Washington Medical Center, an anesthesiology-based service to manage these devices has existed for more than a decade. Many problems with devices have been observed, including confusing rhythms, failure of magnets to provide the desired change in device function, and actual device malfunction. With these clinical case examples taken from the authors' collective experience, this article provides an in-depth understanding of some key electrophysiology principles relevant to cardiovascular implantable electronic device function and appropriate perioperative management. [ABSTRACT FROM AUTHOR]

• TBS failed to induce LTP in pyramidal neurons or NGF interneurons in the CA1 hippocampus of male or female RTT mice. • STP did not differ in pyramidal neurons or NGF interneurons of the CA1 hippocampus of male or female RTT mice. • E/I balance is altered in CA1 NGF interneurons in male RTT mice, but not in pyramidal neurons or in female RTT mice. • Pyramidal neurons and NGF interneurons have increased intrinsic excitability in male RTT mice. Rett syndrome (RTT) is a debilitating neurodevelopmental disorder caused by mutations in the X-linked methyl-CpG-binding protein 2 (MeCP2) gene, resulting in severe deficits in learning and memory. Alterations in synaptic plasticity have been reported in RTT, however most electrophysiological studies have been performed in male mice only, despite the fact that RTT is primarily found in females. In addition, most studies have focused on excitation, despite the emerging evidence for the important role of inhibition in learning and memory. Here, we performed an electrophysiological characterization in the CA1 region of the hippocampus in both males and females of RTT mouse models with a focus on neurogliaform (NGF) interneurons, given that they are the most abundant dendrite-targeting interneuron subtype in the hippocampus. We found that theta-burst stimulation (TBS) failed to induce long-term potentiation (LTP) in either pyramidal neurons or NGF interneurons in male or female RTT mice, with no apparent changes in short-term plasticity (STP). This failure to induce LTP was accompanied by excitation/inhibition (E/I) imbalances and altered excitability, in a sex- and cell-type specific manner. Specifically, NGF interneurons of male RTT mice displayed increased intrinsic excitability, a depolarized resting membrane potential, and decreased E/I balance, while in female RTT mice, the resting membrane potential was depolarized. Understanding the role of NGF interneurons in RTT animal models is crucial for developing targeted treatments to improve cognition in individuals with this disorder. [ABSTRACT FROM AUTHOR]

Electrophysiological and interventional procedures have been increasingly used to reduce morbidity and mortality in patients experiencing cardiovascular diseases. Although antithrombotic therapies are critical to reduce the risk of stroke or other thromboembolic events, they can nonetheless increase the bleeding hazard. This is even more true in an aging population undergoing cardiac procedures in which the combination of oral anticoagulants and antiplatelet therapies would further increase the hemorrhagic risk. Hence, the timing, dose, and combination of antithrombotic therapies should be carefully chosen in each case. However, the maze of society guidelines and consensus documents published so far have progressively led to a hazier scenario in this setting. Aim of this review is to provide—in a single document—a quick, evidenced-based practical summary of the antithrombotic approaches used in different cardiac electrophysiology and interventional procedures to guide the busy clinician and the cardiac proceduralist in their everyday practice. [Display omitted] • Cardiac electrophysiological and other interventional procedures can usually be performed safely without interrupting (or only briefly interrupting) oral anticoagulants. • OAC can be combined with a single antiplatelet agent and is feasible in patients with AF undergoing PCI. • The long-term antithrombotic strategy should be individualized based on the balance of thromboembolic and hemorrhagic risks. [ABSTRACT FROM AUTHOR]

The renal collecting duct is continuously exposed to a wide spectrum of fluid flow rates and osmotic gradients. Expression of a mechanoactivated Piezo1 channel is the most prominent in the collecting duct. However, the status and regulation of Piezo1 in functionally distinct principal and intercalated cells (PCs and ICs) of the collecting duct remain to be determined. We used pharmacological Piezo1 activation to quantify Piezo1-mediated [Ca2+]i influx and single-channel activity separately in PCs and ICs of freshly isolated collecting ducts with fluorescence imaging and electrophysiological tools. We also employed a variety of systemic treatments to examine their consequences on Piezo1 function in PCs and ICs. Piezo1 selective agonists, Yoda-1 or Jedi-2, induced a significantly greater Ca2+ influx in PCs than in ICs. Using patch clamp analysis, we recorded a Yoda-1-activated nonselective channel with 18.6 ± 0.7 pS conductance on both apical and basolateral membranes. Piezo1 activity in PCs but not ICs was stimulated by short-term diuresis (injections of furosemide) and reduced by antidiuresis (water restriction for 24 h). However, prolonged stimulation of flow by high K+ diet decreased Yoda-1-dependent Ca2+ influx without changes in Piezo1 levels. Water supplementation with NH4Cl to induce metabolic acidosis stimulated Piezo1 activity in ICs but not in PCs. Overall, our results demonstrate functional Piezo1 expression in collecting duct PCs (more) and ICs (less) on both apical and basolateral sides. We also show that acute changes in fluid flow regulate Piezo1-mediated [Ca2+]i influx in PCs, whereas channel activity in ICs responds to systemic acid-base stimuli. [ABSTRACT FROM AUTHOR]

This study evaluated whether a novel standardized heparin dosing protocol used during atrial fibrillation catheter ablation resulted in a higher percentage of therapeutic activated clotting time (ACT) values compared to historic nonstandardized procedures. A retrospective cohort study This study was conducted at Ochsner Medical Center, the largest tertiary-care teaching hospital in New Orleans, LA Patients undergoing catheter-based atrial fibrillation ablation The authors implemented a standardized heparin protocol, and enrolled 202 patients between November 2020 and March 2021. The historic controls consisted of 173 patients who underwent atrial fibrillation ablation between April 2020 and September 2020. Heparin administration in the control group was based on physician preference and was nonstandardized. The primary endpoint was the percentage of intraprocedural ACTs in therapeutic range (≥300 to <450 s). Secondary endpoints included first measured ACT at ≥300 s and percent of measured ACTs in the supratherapeutic range (>450 s). Comparisons were performed using chi-squared tests or Fisher exact tests. Patients in the intervention group had a higher mean percentage of ACTs in the therapeutic range compared to the control group (84.9% vs. 75.8%, p<0.001). More patients in the intervention group reached therapeutic ACT on the first measurement compared to the control group (70.3% vs. 31.2%, p<0.001). During catheter-based cardiac ablation procedures, a novel standardized unfractionated heparin dosing protocol resulted in a higher percentage of ACTs in the target range, and a higher proportion of initial ACTs in the therapeutic range compared with baseline nonstandardized heparin dosing. [ABSTRACT FROM AUTHOR]

DBS has been shown to be an effective intervention for neurological disorders. However, the intervention is complex and many aspects have not been understood. Various clinical situations have no solution and follow trial and error approaches. Dystonia is a movement disorder characterized by involuntary muscle contractions, which gives rise to abnormal movements and postures. Status dystonicus (SD) represents a life-threatening condition that requires urgent assessment and management. Electrophysiological markers for risk of symptom worsening and SD related patterns of evolution in patients treated with long-term deep brain stimulation (DBS), and specially under the effect of withdrawal and renewals of simulation are needed. To this end, we study the variability of neural synchronization as a mechanism for symptom generation under successive perturbations to a system, i.e. withdrawals and renewals of neuromodulation, through computational simulation of clinical profiles under different plasticity conditions. The simulation shows that the neuroplasticity makeup influences the variability of oscillation synchronization patterns in virtual "patients". The difference between the effect of different electrophysiological signatures is remarkable and under a certain condition (equal medium long term potentiation and long term depression) the situation resembles that of a stable equilibrium, putatively making the sudden worsening or change less likely. Stability of variability can only be observed in this condition and is clearly distinct from other scenarios. Our results demonstrate that the neuroplasticity makeup affects the variability of the oscillatory synchrony. This i) informs the shaping of the electrophysiological makeup and ii) might serve as a marker for clinical behavior. • Variability of electrophysiological data is useful information for DBS patient management. • Modelling variability data sheds light on physiological signatures usually not accessible with in vivo data. • Risks associated with changes to neuromodulation can be elucidated via variability analysis. [ABSTRACT FROM AUTHOR]

To investigate the frequency, characteristics, and associated factors of systemic lupus erythematosus-related peripheral neuropathy (SLE-PN) using nerve conduction study (NCS). A retrospective chart review was conducted at the Rheumatology clinics of King Abdulaziz University Hospital, Jeddah, Saudi Arabia from 2016 to 2020. Eligibility included systemic lupus erythematosus (SLE) diagnosed patients with at least one NCS result in their clinical records. Demographic, clinical, and biological characteristics were collected. Among 101 female SLE patients, abnormal NCS findings were observed in 11 (10.9%) patients. Of those with abnormal NCS, 27.3% showed mixed axonal and demyelinated motor neuropathy, 18.2% had sensory-motor axonal neuropathy, another 18.2% presented with axonal left common peroneal neuropathy, and the same percentage was observed for axonal sensory neuropathy. Comparisons between abnormal and normal NCS groups in a study population revealed that the abnormal NCS group had significantly higher proportions of non-Saudi nationality, lupus nephritis, seizures, and high SLICC DI. Furthermore, this group was associated with higher ANA titers and exhibited a non-significant trend towards increased positive anti-DNA frequency. Multivariate analysis identified non-Saudi nationality and the presence of end-organ damage as two significant predictors of SLE-related PN. Peripheral neuropathy in SLE patients in Saudi Arabia is not uncommon, specifically those with heightened disease activity, organ damage, or disadvantaged socioeconomic backgrounds. Predominantly, the condition presents as axonopathy impacting sensory nerves, with possible motor involvement. The critical role of electrophysiological studies in early detection and improved patient management is high lightened. [ABSTRACT FROM AUTHOR]

Intensive care unit-acquired weakness (ICUAW) is an acute clinical weakness that occurs in approximately 50% of ICU patients and is directly attributable to their critical care stay where other causes of weakness have been excluded. The condition is characterized by diffuse limb and respiratory muscle weakness with a relative sparing of the cranial/facial muscles and the autonomic nervous system. Patients with ICUAW are classified into three conditions: critical illness polyneuropathy (CIP), critical illness myopathy (CIM) or critical illness neuromyopathy (CINM) based on clinical criteria and further defined by electrophysiological studies and muscle biopsies. ICUAW is often a manifestation of immobility or a systemic inflammatory response syndrome, especially in long-term ventilated patients who have had systemic sepsis/multi-organ failure or exposure to high-dose corticosteroids, neuromuscular blockers or hyperglycaemia. It is associated with prolonged weaning from mechanical ventilation, increased mortality/length of ICU stay and long-term disability. [ABSTRACT FROM AUTHOR]

Background: While the microstructure of the left ventricle (LV) has been largely described, only a few studies investigated the right ventricular insertion point (RVIP). It was accepted that the aggregate cardiomyocytes organization was much more complex due to the intersection of the ventricular cavities but a precise structural characterization in the human heart was lacking even if clinical phenotypes related to right ventricular wall stress or arrhythmia were observed in this region. Methods: MRI-derived anatomical imaging (150 µm3) and diffusion tensor imaging (600 µm3) were performed in large mammalian whole hearts (human: N = 5, sheep: N = 5). Fractional anisotropy, aggregate cardiomyocytes orientations and tractography were compared within both species. Aggregate cardiomyocytes orientation on one ex-vivo sheep whole heart was then computed using structure tensor imaging (STI) from 21 µm isotropic acquisition acquired with micro computed tomography (MicroCT) imaging. Macroscopic and histological examination were performed. Lastly, experimental cardiomyocytes orientation distribution was then compared to the usual rule-based model using electrophysiological (EP) modeling. Electrical activity was modeled with the monodomain formulation. Results: The RVIP at the level of the inferior ventricular septum presented a unique arrangement of aggregate cardiomyocytes. An abrupt, mid-myocardial change in cardiomyocytes orientation was observed, delimiting a triangle-shaped region, present in both sheep and human hearts. FA's histogram distribution (mean ± std: 0.29 ± 0.06) of the identified region as well as the main dimension (22.2 mm ± 5.6 mm) was found homogeneous across samples and species. Averaged volume is 0.34 cm3 ± 0.15 cm3. Both local activation time (LAT) and morphology of pseudo-ECGs were strongly impacted with delayed LAT and change in peak-to-peak amplitude in the simulated wedge model. Conclusion: The study was the first to describe the 3D cardiomyocytes architecture of the basal inferoseptal left ventricle region in human hearts and identify the presence of a well-organized aggregate cardiomyocytes arrangement and cardiac structural discontinuities. The results might offer a better appreciation of clinical phenotypes like RVIP-late gadolinium enhancement or uncommon idiopathic ventricular arrhythmias (VA) originating from this region. [ABSTRACT FROM AUTHOR]

Background: Electrocardiographic imaging (ECGI) generates electrophysiological (EP) biomarkers while cardiovascular magnetic resonance (CMR) imaging provides data about myocardial structure, function and tissue substrate. Combining this information in one examination is desirable but requires an affordable, reusable, and high-throughput solution. We therefore developed the CMR-ECGI vest and carried out this technical development study to assess its feasibility and repeatability in vivo. Methods: CMR was prospectively performed at 3T on participants after collecting surface potentials using the locally designed and fabricated 256-lead ECGI vest. Epicardial maps were reconstructed to generate local EP parameters such as activation time (AT), repolarization time (RT) and activation recovery intervals (ARI). 20 intra- and inter-observer and 8 scan re-scan repeatability tests. Results: 77 participants were recruited: 27 young healthy volunteers (HV, 38.9 ± 8.5 years, 35% male) and 50 older persons (77.0 ± 0.1 years, 52% male). CMR-ECGI was achieved in all participants using the same reusable, washable vest without complications. Intra- and inter-observer variability was low (correlation coefficients [rs] across unipolar electrograms = 0.99 and 0.98 respectively) and scan re-scan repeatability was high (rs between 0.81 and 0.93). Compared to young HV, older persons had significantly longer RT (296.8 vs 289.3 ms, p = 0.002), ARI (249.8 vs 235.1 ms, p = 0.002) and local gradients of AT, RT and ARI (0.40 vs 0.34 ms/mm, p = 0,01; 0.92 vs 0.77 ms/mm, p = 0.03; and 1.12 vs 0.92 ms/mm, p = 0.01 respectively). Conclusion: Our high-throughput CMR-ECGI solution is feasible and shows good reproducibility in younger and older participants. This new technology is now scalable for high throughput research to provide novel insights into arrhythmogenesis and potentially pave the way for more personalised risk stratification. Clinical trial registration: Title: Multimorbidity Life-Course Approach to Myocardial Health—A Cardiac Sub-Study of the MRC National Survey of Health and Development (NSHD) (MyoFit46). National Clinical Trials (NCT) number: NCT05455125. URL: https://clinicaltrials.gov/ct2/show/NCT05455125?term=MyoFit&draw=2&rank=1 [ABSTRACT FROM AUTHOR]

• Functional connectivity changes in Alzheimer's disease are already detectable at the prodromal phase, Mild Cognitive Impairment. • An early non-invasive detection of electrophysiological biomarkers is a priority. • Alpha temporo-parietal desynchronization could be a potential early neurophysiological biomarker. Early synchrony alterations have been observed through electrophysiological techniques in Mild Cognitive Impairment (MCI), which is considered the intermediate phase between healthy aging (HC) and Alzheimer's disease (AD). However, the documented direction (hyper/hypo-synchronization), regions and frequency bands affected are inconsistent. This meta-analysis intended to elucidate existing evidence linked to potential neurophysiological biomarkers of AD. We conducted a random-effects meta-analysis that entailed the unbiased inclusion of Non-statistically Significant Unreported Effect Sizes ("MetaNSUE") of electroencephalogram (EEG) and magnetoencephalogram (MEG) studies investigating functional connectivity changes at rest along the healthy-pathological aging continuum, searched through PubMed, Scopus, Web of Science and PsycINFO databases until June 2023. Of the 3852 articles extracted, we analyzed 12 papers, and we found an alpha synchrony decrease in MCI compared to HC, specifically between temporal-parietal (d = -0.26) and frontal-parietal areas (d = -0.25). Alterations of alpha synchrony are present even at MCI stage. Synchrony measures may be promising for the detection of the first hallmarks of connectivity alterations, even at the prodromal stages of the AD, before clinical symptoms occur. [ABSTRACT FROM AUTHOR]

This article reviews various opportunities to translate established and novel tools and techniques used in adult electrophysiology to pediatrics and the adult congenital heart disease population. There is a specific focus on preoperative management of special population, implantation techniques, and postoperative programming of devices. [ABSTRACT FROM AUTHOR]

[Display omitted] [ABSTRACT FROM AUTHOR]

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