Tea, one of the most widely consumed beverages globally, exhibits remarkable genomic diversity in its underlying flavour and health-related compounds. In this study, we present the construction and analysis of a tea pangenome comprising a total of 11 genomes, with a focus on three newly sequenced genomes comprising the purple-leaved assamica cultivar \"Zijuan\", the temperature-sensitive sinensis cultivar \"Anjibaicha\" and the wild accession \"L618\" whose assemblies exhibited excellent quality scores as they profited from latest sequencing technologies. Our analysis incorporates a detailed investigation of transposon complement across the tea pangenome, revealing shared patterns of transposon distribution among the studied genomes and improved transposon resolution with long read technologies, as shown by long terminal repeat (LTR) Assembly Index analysis. Furthermore, our study encompasses a gene-centric exploration of the pangenome, exploring the genomic landscape of the catechin pathway with our study, providing insights on copy number alterations and gene-centric variants, especially for Anthocyanidin synthases. We constructed a gene-centric pangenome by structurally and functionally annotating all available genomes using an identical pipeline, which both increased gene completeness and allowed for a high functional annotation rate. This improved and consistently annotated gene set will allow for a better comparison between tea genomes. We used this improved pangenome to capture the core and dispensable gene repertoire, elucidating the functional diversity present within the tea species. This pangenome resource might serve as a valuable resource for understanding the fundamental genetic basis of traits such as flavour, stress tolerance, and disease resistance, with implications for tea breeding programmes.

Non-invasive brain stimulation (NIBS) approaches have seen a rise in utilization in both clinical and basic neuroscience in recent years. Here, we concentrate on the two methods that have received the greatest research: transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS). Both approaches have yielded pertinent data regarding the cortical excitability in subjects in good health as well as pertinent advancements in the management of various clinical disorders. NIBS is a helpful method for comprehending the cortical control of the ANS. Previous research has shown that there are notable changes in muscular sympathetic nerve activity when the motor cortex is modulated. Furthermore, in NIBS investigations, the ANS has been employed more frequently as an outcome measure to comprehend the overall impacts of these methods, including their safety profile. Though there is ample proof that brain stimulation has autonomic effects on animals, new research on the connection between NIBS and the ANS has produced contradictory findings. In order to better understand NIBS processes and ANS function, it is crucial to take into account the reciprocal relationship that exists between central modulation and ANS function.

Cardiovascular disease stands as a leading global cause of mortality. Nucleotide-binding Oligomerization Domain-like Receptor Protein 3 (NLRP3) inflammasome is widely acknowledged as pivotal factor in specific cardiovascular disease progression, such as myocardial infarction, heart failure. Recent investigations underscore a close interconnection between autonomic nervous system (ANS) dysfunction and cardiac inflammation. It has been substantiated that sympathetic nervous system activation and vagus nerve stimulation (VNS) assumes critical roles withinNLRP3 inflammasome pathway regulation, thereby contributing to the amelioration of cardiac injury and enhancement of prognosis in heart diseases. This article reviews the nexus between NLRP3 inflammasome and cardiovascular disorders, elucidating the modulatory functions of the sympathetic and vagus nerves within the ANS with regard to NLRP3 inflammasome. Furthermore, it delves into the potential therapeutic utility of NLRP3 inflammasome to be targeted by VNS. This review serves as a valuable reference for further exploration into the potential mechanisms underlying VNS in the modulation of NLRP3 inflammasome.

Sport coaches increasingly rely on external load metrics for designing effective training programs. However, their accuracy in estimating internal load is inconsistent, and their ability to predict autonomic nervous system (ANS) deterioration is unknown. This study aimed to evaluate the relationships between internal and external training load metrics and ANS recovery and function in college football players. Football athletes were recruited from a D1 college in the southeastern US and prospectively followed for 27 weeks. Internal load was estimated via exercise cardiac load (ECL; average training heartrate (HR) × session duration) and measured with an armband monitor equipped with electrocardiographic capabilities (Warfighter MonitorTM (WFM), Tiger Tech Solutions, Miami, FL, USA). External load was estimated via the summation and rate of acceleration and decelerations as measured by a triaxial accelerometer using the WFM and an accelerometer-based (ACCEL) device (Catapult Player Load, Catapult Sports, Melbourne, Australia) worn on the mid-upper back. Baseline HR, HR variability (HRV) and HR recovery served as the indicators for ANS recovery and function, respectively. For HRV, two, time-domain metrics were measured: the standard deviation of the NN interval (SDNN) and root mean square of the standard deviation of the NN interval (rMSSD). Linear regression models evaluated the associations between ECL, ACCEL, and the indicators of ANS recovery and function acutely (24 h) and cumulatively (one- and two-week). Athletes (n = 71) were male and, on average, 21.3 ± 1.4 years of age. Acute ECL elicited stronger associations for 24 h baseline HR (R2 0.19 vs. 0.03), HR recovery (R2 0.38 vs. 0.07), SDNN (R2 0.19 vs. 0.02) and rMSSD (R2 0.19 vs. 0.02) compared to ACCEL. Similar results were found for one-week: 24 h baseline HR (R2 0.48 vs. 0.05), HR recovery (R2 0.55 vs. 0.05), SDNN (R2 0.47 vs. 0.05) and rMSSD (R2 0.47 vs. 0.05) and two-week cumulative exposures: 24 h baseline HR (R2 0.52 vs. 0.003), HR recovery (R2 0.57 vs. 0.05), SDNN (R2 0.52 vs. 0.003) and rMSSD (R2 0.52 vs. 0.002). Lastly, the ACCEL devices weakly correlated with ECL (rho = 0.47 and 0.43, p < 0.005). Our findings demonstrate that ACCEL poorly predicted ANS deterioration and underestimated internal training load. ACCEL devices may \"miss\" the finite window for preventing ANS deterioration by potentially misestimating training loads acutely and cumulatively.

Predictive coding framework posits that our brain continuously monitors changes in the environment and updates its predictive models, minimizing prediction errors to efficiently adapt to environmental demands. However, the underlying neurophysiological mechanisms of these predictive phenomena remain unclear. The present study aimed to explore the systemic neurophysiological correlates of predictive coding processes during passive and active auditory processing. Electroencephalography (EEG), functional near-infrared spectroscopy (fNIRS), and autonomic nervous system (ANS) measures were analyzed using an auditory pattern-based novelty oddball paradigm. A sample of 32 healthy subjects was recruited. The results showed shared slow evoked potentials between passive and active conditions that could be interpreted as automatic predictive processes of anticipation and updating, independent of conscious attentional effort. A dissociated topography of the cortical hemodynamic activity and distinctive evoked potentials upon auditory pattern violation were also found between both conditions, whereas only conscious perception leading to imperative responses was accompanied by phasic ANS responses. These results suggest a systemic-level hierarchical reallocation of predictive coding neural resources as a function of contextual demands in the face of sensory stimulation. Principal component analysis permitted to associate the variability of some of the recorded signals.

Heart rate variability (HRV) measurements have emerged as a valuable tool for understanding the functioning of the autonomic nervous system (ANS) and assessing the health outcomes of obstructive sleep apnea (OSA) in patients. Sleep and the ANS exert a mutual influence on each other. Sleep promotes relaxation and recovery of the ANS. Conversely, ANS activity plays a role in regulating the onset and maintenance of sleep. The impact of continuous positive airway pressure (CPAP) therapy on patient recovery levels was investigated by assessing the restoration of ANS activity using HRV indicators. The study included patients with OSA who had been on CPAP for at least eight weeks. The patients were divided into two groups, namely the experimental group (CPAP-compliant) and the control group (CPAP-non-compliant). The study included a total of 38 patients, with 20 in the CPAP-compliant group and 18 in the CPAP-non-compliant group. The HRV analysis included time- and frequency-domain measures. Data was collected in various resting conditions, including lying down, standing, regular breathing, and under physiological stress induced by deep breathing and the Valsalva maneuver. After CPAP treatment, there was an increase in the average values for SDNN for deep breathing and Valsalva maneuvers. The mean changes in SDNN for CPAP-non-compliant versus CPAP-compliant groups for normal breathing increased from 32.50±5.33 to 42.40±8.03, while the values for Valsalva increased from 20.16±2.47 to 25.45±3.03. Despite the observed variations in SDNN, there was no significant change in the average change in heart rate (∆ HR), except during the Valsalva maneuver. Post-CPAP values for the Valsalva ratio were significantly decreased in deep breathing. The E:I ratio for the CPAP-compliant group during normal breathing was 1.08±.16 compared to 1.55±.09; t (36) =-11.15, p <0.001 in the CPAP-non-compliant group. During deep breathing, the ratio was 1.36±.15 versus 1.59±.24; t (36) =-3.578, p <0.001. The high frequency (HF)nu mean values for deep breathing were 34.06±5.546 compared to 35.00±6.358; t (36) = -.485, p=.630. For the Valsalva maneuver, the values were 29.94±4.721 versus 26.95±6.621; t (36) =1.589, p=.060. The HF/low frequency (LF) ratio was found to be significant only in supine, standing, and normal breathing. The utilization of CPAP therapy was found to be effective in achieving and sustaining autonomic balance during tasks like standing and engaging in regular breathing patterns. During activities that involve intense physical effort, like the Valsalva maneuver, the HRV metrics did not indicate any significant balance between sympathetic and parasympathetic activity. However, using CPAP therapy for a prolonged period can be beneficial in consistently improving the sympathovagal balance in these patients.

We introduce McDAPS, an interactive software for assessing autonomic imbalance from non-invasive multi-channel physiological recordings. McDAPS provides a graphical user interface for data visualization, beat-to-beat processing and interactive analyses. The software extracts beat-to-beat RR interval systolic blood pressure, diastolic blood pressure, the pulse amplitude of photoplethysmogram and the pulse-to-pulse interval. The analysis modules include stationary and time-varying power spectral analyses, moving-correlation analysis and univariate analyses. Analyses can also be performed in batch mode if multiple datasets have to be processed in the same way. The program exports results in standard CSV format. McDAPS runs in MATLAB, and is supported on MS Windows and MAC OS systems. The MATLAB source code is available at https://github.com/thuptimd/McDAPS.git.

Eriobotrya is an evergreen fruit tree native to South-West China and adjacent countries. There are more than 26 loquat species known in this genus, while E. japonica is the only species yet domesticated to produce fresh fruits from late spring to early summer. Fruits of cultivated loquat are usually orange colored, in contrast to the red color of fruits of wild E. henryi (EH). However, the mechanisms of fruit pigment formation during loquat evolution are yet to be elucidated. To understand these, targeted carotenoid and anthocyanin metabolomics as well as transcriptomics analyses were carried out in this study. The results showed that β-carotene, violaxanthin palmitate and rubixanthin laurate, totally accounted for over 60% of the colored carotenoids, were the major carotenoids in peel of the orange colored \'Jiefangzhong\' (JFZ) fruits. Total carotenoids content in JFZ is about 10 times to that of EH, and the expression levels of PSY, ZDS and ZEP in JFZ were 10.69 to 23.26 folds to that in EH at ripen stage. Cyanidin-3-O-galactoside and pelargonidin-3-O-galactoside were the predominant anthocyanins enriched in EH peel. On the contrary, both of them were almost undetectable in JFZ, and the transcript levels of F3H, F3\'H, ANS, CHS and CHI in EH were 4.39 to 73.12 folds higher than that in JFZ during fruit pigmentation. In summary, abundant carotenoid deposition in JFZ peel is well correlated with the strong expression of PSY, ZDS and ZEP, while the accumulation of anthocyanin metabolites in EH peel is tightly associated with the notably upregulated expressions of F3H, F3\'H, ANS, CHS and CHI. This study was the first to demonstrate the metabolic background of how fruit pigmentations evolved from wild to cultivated loquat species, and provided gene targets for further breeding of more colorful loquat fruits via manipulation of carotenoids and anthocyanin biosynthesis.

Physical activity (PA) in the form of aerobic exercise (AE) preserves and improves neurocognitive function across the lifespan. However, a mechanistic understanding of the pathways by which aerobic exercise impacts brain health is still lacking, particularly with respect to stress-related pathways. One mechanistic hypothesis is that AE improves neurocognitive health in part by modifying circulating levels of stress-related hormones and signaling factors associated with the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), as commonly measured by the biomarkers cortisol (CORT) and salivary α-amylase (sAA). Thus, this hypothesis predicts that changes in stress biomarkers, such as CORT and sAA, are possible explanatory pathways mediating the positive effects of AE on neurocognitive health. In the present review article, we provide a summary of available studies examining the possibility that exercise-induced changes to stress biomarkers could partly account for exercise-related improvements in neurocognitive health. Our review indicates that despite the intuitive appeal of this hypothesis, there is insufficient evidence available to conclude that chronic and habitual AE affects neurocognitive health by altering stress biomarker pathways. The cross-sectional nature of the majority of reviewed studies highlights the need for well-controlled studies to adequately test this hypothesis.

One approach to understanding how the human cognitive system stores and operates with quantifiers such as \"some,\" \"many,\" and \"all\" is to investigate their interaction with the cognitive mechanisms for estimating and comparing quantities from perceptual input (i.e., nonsymbolic quantities). While a potential link between quantifier processing and nonsymbolic quantity processing has been considered in the past, it has never been discussed extensively. Simultaneously, there is a long line of research within the field of numerical cognition on the relationship between processing exact number symbols (such as \"3\" or \"three\") and nonsymbolic quantity. This accumulated knowledge can potentially be harvested for research on quantifiers since quantifiers and number symbols are two different ways of referring to quantity information symbolically. The goal of the present review is to survey the research on the relationship between quantifiers and nonsymbolic quantity processing mechanisms and provide a set of research directions and specific questions for the investigation of quantifier processing.