Thermal boundaries of survival: A case study in a marine invertebrate.

First-person perspective gesture observation in virtual reality: A novel approach for anomia rehabilitation in post-stroke aphasia.

Huang-Qi-Long-Dan Granule alleviates ischemic stroke injury by regulating the crosstalk between Nrf2 and NF-κB signaling.

Apathy, a reduction in self-initiated goal-directed behavior, is a quality-of-life diminishing characteristic of schizophrenia, which often goes underrecognized and undertreated. Actigraphy-derived motor activity measures provide potential objective markers for assessing apathy, but the value for assessing clinically relevant levels of apathy has yet to be determined in patients with schizophrenia. Patients with schizophrenia with (SZ+; n=42) and without (SZ-; n=40) severe apathy symptoms and a group of age and education matched non-affected individuals (NAC; n=40) were included. Activity indices derived from actigraphy recordings on two weekend days were compared between the three groups. Logistic regression analyses were conducted to examine whether actigraphy indices could predict presence of 1) a diagnosis of schizophrenia and 2) severe apathy. Lower levels and lower variability of activity and step counts during weekend days and the most active ten-hour period were associated with the presence of a schizophrenia diagnosis, and presence of severe apathy within patients. These associations were independent of sociodemographic, lifestyle status and clinical confounders. Backwards regression revealed that mean steps during the most active ten-hour period exhibited the strongest predictor of apathy severity. Results suggest that amount and variability of physical activity as measured with an actigraphy device can help to identify individuals with schizophrenia with high levels of apathy. Especially, the number of steps taken during the most active hours could be used to screen patients with a presence of severe apathy, therefore informing further diagnostics and treatment.

Genetic variants affecting the RNA polymerase II complex have been associated with various neurodevelopmental disorders (NDDs). SUPT6H, an RNA polymerase II-associated elongation factor and a histone chaperone, plays a critical role in transcriptional regulation. However, the contribution of SUPT6H variants to human NDDs and the phenotypic consequences of its loss-of-function in vivo remain unexplored. Here, we analyzed 18 published sporadic single-nucleotide variants (SNVs) of SUPT6H associated with human developmental disorders. Molecular modeling suggests that these variants are likely deleterious, leading to loss of function. Consistent with this, homozygous or heterozygous Supt6 null mice exhibit embryonic lethality, underscoring its essential role during development. To investigate the postnatal consequences of Supt6 deficiency, we generated conditional Supt6 knockout (KO) mice with targeted deletion in parvalbumin-expressing GABAergic interneurons (cKOPV). Homozygous Supt6 cKOPV mice displayed motor defects and behavioral seizures, whereas heterozygous counterparts exhibited behavioral phenotypes relevant to neuropsychiatric disorders despite normal motor activity. Notably, both heterozygous and homozygous Supt6 cKOPV mice showed a significant reduction in parvalbumin-expressing neurons compared to wild-type controls. These findings establish a direct link between Supt6 loss-of-function and neurodevelopmental phenotypes, highlighting its critical role in maintaining interneuron populations and neural circuit integrity. Altogether, our results suggest that deleterious SUPT6H variants may contribute to the etiology of NDDs, providing valuable insights into its function and potential as a therapeutic target.

Frankincense improves motor symptoms and attenuates the progression of Paraquat (PQ)-induced Parkinson's disease in mice by attenuating oxidative stress, inflammation, and apoptotic cell death and improving nerve growth factor gene expression.

Shared premotor resources underlie dual-task interference between speech and balance.

Background: Since their introduction in professional football, penalty shoot-outs represent key moments in matches. Motor imagery (MI) can improve soccer performance, but different MI modalities can be used to mentally simulate motor actions. This study aimed to evaluate whether the MI modality used by the players would influence their penalty shoot-out performance. Methods: Twenty youth skilled football players from the Elite Center of the French Regions of America (CERFA) voluntarily participated in this experiment (Mage ​= ​16.4 years). After an assessment of their MI ability, the participants completed 4 counterbalanced experimental sessions spread over 4 weeks, each including the completion of 5 penalty shoot-outs. The sessions consisted of a control condition (count-down and actual execution) and 3 MI conditions during which the players had to mentally imagine themselves performing a penalty shoot-out according to one of the MI modalities: Internal Visual Imagery (IVI), External Visual Imagery (EVI), or Kinesthetic Imagery (KI), before kicking. Number of goals scored, shooting accuracy and ball speed were measured and served as dependent variables. Results: The soccer players benefited from MI. Indeed, in both the IVI and KI conditions, their performances were significantly higher than in the no-MI (i.e., control) condition with respect to the total number of goals scored and shooting accuracy variables. Conclusions: Practically, we suggest skilled football players imagine, from an internal perspective, taking a successful penalty kick before shooting.

The phyB mutant exhibits robust salt tolerance via enhanced K⁺/Na⁺ homeostasis, proline accumulation, and membrane stability. Transcriptomics reveals PHYB coordinates a unique early-response network involving transcription factors, kinesins, and DNA metabolism. Integrated population eQTL analysis and transcriptional regulation prediction condense a core salt-tolerance module of four transcription factors, three kinesins, and six DNA metabolism genes. This study identifies actionable targets for genetic improvement of salt-tolerant varieties. Soil salinization poses a significant threat to global rice production, underscoring the urgent need to improve salt tolerance as a key strategy for ensuring food security. In this study, we report that the phytochrome B (phyB) mutant exhibits robust salt tolerance via enhanced K⁺/Na⁺ homeostasis, proline accumulation, and membrane stability. Transcriptomic profiling revealed that phyB modulates salt adaptation via transcription factor activity, DNA metabolism, and motor activity. Utilizing the salt-responsive expression quantitative trait loci (eQTL) data from global mini-core rice collection comprising 202 accessions, we systematically screened enriched Gene Ontology (GO) terms and predicted a set of core salt tolerance-related genes at genomic level in the phyB mutant. Transcriptional regulation analysis established a regulatory network in which four transcription factors potentially regulate three kinesin genes and six DNA metabolism-related genes. Luciferase (LUC) assays further confirmed that these transcription factors directly activate the promoters of downstream genes. Heterologous expression in yeast demonstrated that a representative transcription factor (Os10g0371100), a kinesin (Os05g0397900), and a DNA metabolism-related gene (Os01g0944900) significantly promoted yeast growth under salt stress conditions, indicating conserved functions. Collectively, these findings elucidate a novel molecular network through which PHYB deficiency enhances salt tolerance by integrating transcription factor activity, DNA metabolism, and motor activity, and provide a set of core candidate genes for the genetic improvement of salt tolerance in rice.

Performance during motor activities such as wheelchair riding, cycling, rowing and speed skating, depends critically on the average mechanical power output (AMPO) produced by the muscles. To maximise short-duration performance, limb movements should allow muscles to deliver maximal AMPO. However, it is unclear which movement maximises AMPO of human muscle. In this study, we employed a Hill-type muscle-tendon-complex (MTC) model to predict the maximally attainable AMPO of human m. quadriceps femoris for various imposed periodic knee joint movements. Based on these predictions, we selected one set of conditions predicted to yield identical maximally attainable AMPO despite substantial variations in knee joint movements and another set of conditions predicted to yield substantial variations in maximally attainable AMPO. In the experiment, periodic knee joint movements were fully imposed by a knee dynamometer. Participants were instructed to maximise AMPO and, to this end, received visual feedback on their cumulative mechanical work throughout each cycle. Experimental data closely matched predictions derived from the Hill-type MTC model, confirming the validity of the model. Model predictions showed a substantial influence of knee joint movement on the maximally attainable AMPO. Specifically, predictions revealed a strong interaction between cycle frequency and knee joint excursion: increasing one necessitates a decrease in the other to maximise AMPO. Even more interestingly, m. quadriceps femoris should spend about 80% of the cycle duration while shortening, independent of cycle frequency and/or knee joint excursion.

Transcutaneous spinal cord stimulation (tSCS) is an emerging treatment for motor recovery following spinal cord injury (SCI). However, the extent of motor recovery with tSCS and the reasons why some individuals with motor-complete SCI respond less effectively, despite having the same injury classification, remain unclear. Here, we demonstrate that lumbosacral tSCS can enable anti-gravity voluntary movement following motor-complete SCI, and identify markers that distinguish responders from non-responders. Ten individuals with chronic cervical and upper thoracic motor-complete SCI received 30Hz lumbosacral tSCS with a 10kHz carrier frequency for 60min, 2-5 times per week, for a minimum of 6 weeks (12-36 sessions). Post-intervention, volitional movement was measured using surface electromyography (EMG) over the quadriceps and tibialis anterior (TA), and knee and ankle joint range of motion. To identify markers of responsiveness, we assessed the integrity of the corticospinal tract (motor evoked potentials; MEPs), ascending sensory pathways (somatosensory evoked potentials; SEPs), spinal cord reflexes (H-reflex), and motor neurons (compound muscle action potential, CMAP), along with muscle morphology using ultrasound echo-intensity. This observational cohort study was reported in accordance with STROBE guidelines. Five of 10 individuals demonstrated voluntary anti-gravity knee extension and ankle dorsiflexion strength in the presence of tSCS. TA MEPs were observed in one responder only and tibial nerve SEPs were not observed in any participants. All participants showed poor TA muscle morphology. Four responders had a soleus H-reflex (compared to 2/5 non-responders) and a normal amplitude fibular CMAPs (compared to 2/5 non-responders). These results show that tSCS can enable volitional motor activity against gravity in people with motor-complete SCI, but there is variability in responsiveness. Using conventional neurophysiological techniques, we were unable to consistently demonstrate the pathways facilitating voluntary control or the factors differentiating responders versus non-responders, but trends were observed. Spinal cord reflex and peripheral motor nerve integrity may be important for responding to tSCS but may not distinguish responders from non-responders. Additional assessments are needed to develop biomarkers for stratifying motor responders to tSCS. Trial Registration on ClinicalTrials.gov NCT04726059 (registered: 2021-Jan-22), NCT04604951 (registered: 2020-Oct-25), NCT05369520 (registered: 2022-May-05).

ABSTRACT Across millennia and geographies, humans and dogs have lived, worked, and played together. While play between dogs and humans may be a hallmark of the dog–human bond, empirical research on dog–human play is relatively limited. This scoping review examined academic research on dog–human play, mapping (1) theoretical and methodological approaches to the study of dog–human play; (2) how play is defined by researchers; and (3) the primary aims of research studies focused on play. Four databases were searched: Web of Science (via OVID), Psych Info, Agricultural Sciences, and Family and Society Studies. One hundred and nine articles describing dog–human play were identified, with 28 articles primarily focusing on the dog–human play encounter. Most research was localized within European and American contexts to focus on companion or “pet” dogs, and most studies were rooted in scientific disciplines, such as ethology and comparative psychology. Less than half of the identified articles provided a definition of dog–human play, and the most common definitions focused on relational components of play and/or on specific motor activity involved within the play encounter. Almost all articles provided an example of play, which primarily focused on social object play (e.g., fetch, tug). Researchers highlighted specific functions of dog–human play behaviors or focused more generally on implications of the play relationship. This scoping review identifies a need for more diverse cultural, theoretical, and methodological contributions to the landscape of dog–human play and reiterates concerns that definitional ambiguity may devalue the important work of play research. Ultimately, dog–human play tends to center the “human” within the dyad and would benefit from more diverse considerations around what it means to play with our canine companions.

Background. Anterior Cruciate Ligament injuries represent a significant "epidemic" in sports medicine, disproportionately affecting female athletes. Women tear their ACL 2 to 10 times more often than men participating in the same sports. This disparity suggests that beyond anatomical and biomechanical differences, unique biological factors - specifically hormonal fluctuations and their impact on ligament structure - play a critical role in injury susceptibility. Aim. The aim of this study was to conduct an analysis of the publications from the last decade regarding the influence of the menstrual cycle, sex hormones and oral contraceptives on knee joint laxity and ACL injury risk. Material and methods. A comprehensive PubMed literature search (2014–2024) was conducted, only clinically relevant, English, free full-text articles were included, supplemented by foundational studies. Results. A total of 17 original studies were included, 4 review studies have been inspected for a better understanding of older research. The analysis confirms that the pre-ovulatory and ovulatory phases are associated with increased anterior knee laxity due to peak estrogen levels. However, recent evidence suggests that increased laxity does not always result in altered biomechanics in elite athletes due to neuromuscular compensation. Conclusions. Current evidence identifies the late follicular and ovulatory phases as the period of highest ACL injury risk, driven by a simultaneous decline in both passive joint stability and active motor control. Importantly, utilizing oral contraceptives does not offer a complete solution, as they only address passive laxity while leaving neuromuscular deficits unresolved and posing systemic risks. Future injury prevention must therefore adopt a multidimensional approach, utilizing individualized screening that integrates menstrual history, specific anatomical predispositions, and objective biomechanical assessments.

Animal learning can be analyzed on two timescales: task acquisition across training sessions and motivation fluctuations within training sessions. How do variations in motor and neurophysiologic activity relate to task performance over these timescales? Here, this question was examined in head-fixed mice performing a whisker-based sensory discrimination task. Male mice were trained for 12-14 daily sessions on a go/no-go task, each lasting approximately one hour to capture spontaneous performance fluctuations over minutes. Simultaneous to task performance, "non-performance variables" were tracked, including wheel running, pupil size, eyelid aperture and sensory cortical activity. First, motivation states were defined based on performance tendencies over minutes, leading to three state categories: persistent, disengaged, or attentive Non-performance variables were found to predict these states independent of task correctness. Then, when further parsing these states by the go/no-go outcomes of hit, miss, false alarm or correct rejection, learning-like changes were detected in wheel running, eye movements and brain activity. Thus, learning over days and motivation fluctuations over minutes form a continuum, as evidenced by changes in motor and physiologic activity variables not directly controlled by task contingencies, even during periods of suboptimal performance in well-trained subjects. These findings improve the understanding of performance variations and implicit learning, in addition to contributing a framework for the analysis of task performance indirectly from motor and neurophysiologic activity.Significance statement Task performance is typically measured by correctness percentages over daily training sessions but can also correlate with motivation state fluctuations within each session. Thus, while aggregating correctness percentages per session may reveal a learning curve, accounting for within-session state fluctuations can reveal variability in that curve, even among well-trained subjects. In this head-fixed mouse study, task acquisition across sessions and motivation fluctuations within sessions were categorized into three states: persistent, disengaged, or attentive Subsequently, metrics not directly controlled by the task, including locomotion, pupil dilation, eyelid aperture and brain activity, were found to predict both learning and state changes. Therefore, task performance can be tracked more comprehensively from brain and body activity metrics, adding nuance to correctness percentages.

Organisms must regulate metabolic resources such as oxygen (O2) and nutrients despite environmental variability and the energetic costs of their own actions1-3. Such regulation can occur reactively, through homeostatic corrections of recent imbalances, or predictively, through allostatic adjustments that anticipate future demand4,5. Predictive regulation is particularly important because metabolic resources often continue to be consumed for seconds to minutes after motor actions cease as tissues repay incurred costs, making it advantageous to prevent depletion before it occurs6. However, the cellular and circuit mechanisms for allostatic control remain largely unknown5,7,8. Using whole-brain neuronal and astroglial imaging and O2measurements in behaving zebrafish, we identified a noradrenergic-astroglial circuit that detects, anticipates, and prevents internal O2depletion. We found that swimming exacerbated internal hypoxia with a multi-second delay, but behavioral adaptations occurred before such self-generated hypoxia manifested, suggesting predictive control, confirmed using computational modeling. Noradrenergic neurons in the nucleus of the solitary tract directly detected brain hypoxia and received efference copies of swimming actions; these inputs summed at the level of membrane voltage to increase spiking and norepinephrine release when actions and resource scarcity co-occurred. Astroglia integrated noradrenergic input into prolonged Ca2+elevation that tracked the O2cost of recent actions and thereby predicted O2debt relative to O2availability, rising ~8 s before O2fell. This astroglial prediction reorganized brain-wide activity to suppress locomotion and promote respiration, preempting O2depletion. Silencing noradrenergic neurons or astroglial signaling abolished these hypoxia coping behaviors, whereas selective activation evoked them. This neuronal-astroglial mechanism constitutes a predictive control system that integrates physiological state with behavioral intent to avert metabolic crisis, revealing a cellular substrate for proactive energy management.

Tarsal tunnel syndrome is an entrapment neuropathy caused by the compression of the tibial nerve and its terminal branches in the tarsal tunnel. Electrophysiological examinations are often used to diagnose tarsal tunnel syndrome. Surgical decompression of the tibial nerve is performed in patients who are resistant to conservative treatment. However, the preoperative electrophysiological findings that predict surgical outcomes remain unknown. This study aimed to clarify the preoperative electrophysiological findings that predict the surgical outcomes of tarsal tunnel syndrome. We reviewed 28 feet of 23 patients who underwent preoperative electrophysiological examinations between November 2021 and October 2024, were diagnosed with tarsal tunnel syndrome, and subsequently underwent surgery. Electrophysiological examinations included nerve conduction study and needle electromyography. We reviewed patient characteristics and electrophysiological findings prior to surgery. Sensory plantar symptoms, such as numbness and pain, were evaluated using the Numerical Rating Scale before and after surgery. Patients were divided into the improvement and non-improvement groups based on the Numerical Rating Scale improvement rate after surgery. A comparative analysis of patient characteristics and preoperative electrophysiological findings was performed between the improvement and non-improvement groups. In a motor nerve conduction study of the tibial nerve, the amplitude of the compound motor action potential evoked by stimulation at the ankle was significantly lower in the non-improvement group than in the improvement group. In tarsal tunnel syndrome, a low compound motor action potential amplitude of the tibial nerve on preoperative motor nerve conduction study may indicate poor symptomatic improvement after surgery. Electrophysiological examinations may be useful for predicting the surgical outcomes of tarsal tunnel syndrome.

Infants help caregivers and unfamiliar others by their first birthday. Yet, developmental pathways leading to helping are largely unknown. This longitudinal study (6, 10, 14 months) investigated the association of caregiver-child interaction quality, motor development, action anticipation, and caregiver encouragement and modeling with helping (N = 118, 49 female, mostly White, European, data collection 2020-2022). Path models showed that helping the mother was related to motor development and maternal modeling, while helping the experimenter was related to motor development, action anticipation, and maternal interaction quality. This study provides novel evidence for a developmental systems approach to helping, emphasizing that early helping behavior is shaped by the caregiver-child interaction and interwoven with both motor and social development.

Respiration is governed by a widespread network of cortical and subcortical structures. This complex communication between the brain and lungs is altered in pathological conditions. Apnoea - the cessation of respiration - is a common condition in infants, particularly those born prematurely. Apnoea in infants is believed to relate to immaturity of brainstem respiratory centres; involvement of the cortex in respiration in infants has yet to be explored. We investigated if there was any evidence for cortical coupling with respiration in newborn humans and whether it relates to apnoea. Using simultaneous electroencephalography (EEG) and impedance pneumography, we investigated interactions between cortical and respiratory activity (known as cortico-respiratory coupling) using phase-amplitude coupling. We show that cortico-respiratory coupling is present in premature and term newborns (104 recordings from 68 infants; 34.5±2.6 weeks postmenstrual age), identifying an interplay between breathing phase and EEG amplitude. We further shed light on the biological meaning by revealing that the strongest coupling occurs during inspiration and that cortical activity precedes respiration, with coupling strongest over frontocentral regions. Whilst our study was limited in spatial resolution, and determining causality is challenging, we believe these findings support the notion that the cortico-respiratory coupling observed here constitutes communication between cortical motor areas and lung effectors. Moreover, we show that cortico-respiratory coupling is negatively correlated with the rate of apnoea, revealing novel insight into this common and potentially life-threatening neonatal pathology.

Diet-induced obesity (DIO) is associated with dysregulated adipoinsular axis and endocannabinoid system (eCBS) function. Acute cannabis consumption stimulates appetite; however, chronic consumption is paradoxically associated with lower prevalence of human obesity and type 2 diabetes. We investigated the impact of chronic exposure to Δ9 tetrahydrocannabinol (THC) and cannabis extracts on DIO and glucose homeostasis in mice. Male mice were fed a high-fat/sucrose diet or a low-fat/no-sucrose diet for 60days. At day 30, mice were administered THC (5mg/kg) or cannabis extracts matched for THC content daily for 30days. We assessed adipocyte biology, glucose tolerance, insulin sensitivity, eCBS expression, body weight, food intake and motor activity. Roles for the eCBS in cannabis-induced changes in metabolic processes, including cellular bioenergetics, were analysed in 3T3-L1 adipocytes. THC and extracts reduced body weight and fat mass in DIO mice, and reversed DIO-associated changes in expression of adipokines that regulate the adipoinsular axis. Extracts normalized expression of adipokines more effectively than THC. Notably, extracts - but not THC - normalized glucose clearance in DIO mice to levels found in lean mice. In addition, THC and extracts promoted anti-adipogenic effects and changes in energy metabolism in 3T3-L1 cells in a concentration-dependent manner. These studies suggest that chronic cannabinoid exposure improves metabolic function and dysregulated glucose homeostasis in DIO by a mechanism that includes restoring impaired adipoinsular axis function. KEY POINTS: Δ9 Tetrahydrocannabinol (Δ9THC) and cannabis extracts reduce body weight and fat mass in obese mice. Cannabis extracts, but not Δ9THC alone, improve glucose homeostasis in obese mice. Extracts more effectively normalize expression of components of the adipoinsular axis in obese mice. Δ9THC and extracts promote anti-adipogenic effects in 3T3-L1 cells. Δ9THC and extracts alter cellular bioenergetics in 3T3-L1 cells.

Converging evidence suggests that metabotropic glutamate receptor 7 (mGlu7) contributes to sleep-wake regulation and stress reactivity. We used the selective negative allosteric modulator (NAM) ADX71743 to examine the role of mGlu7 in sleep-wake control and in basal and stress-evoked neurotransmitter release in freely moving rats. Rats were implanted with electrodes and telemetry devices to record electroencephalogram (EEG), neck muscle electromyogram (EMG), motor activity (MA), and body temperature (BT) at baseline and for 9 h after subcutaneous (sc) administration of ADX71743 (50, 100, or 150 mg/kg) or vehicle (50% cyclodextrin in water), given 2 h after lights on. In a separate cohort, rats were implanted with microdialysis probes in the prefrontal cortex (PFC) and ventral hippocampus (vHipp). Samples were collected at baseline, followed by sc ADX71743 (100 mg/kg) or vehicle and 10 min of light handling 60 min later. Extracellular glutamate (Glu), GABA, glycine (Gly), serotonin (5-HT), norepinephrine (NE), and dopamine (DA) were quantified over the 180 min sampling period. ADX71743 increased wakefulness by up to 100% and reduced rapid-eye-movement (REM) sleep by up to 100% and non-REM (NREM) sleep by up to 75% (all p<0.05), with comparable effects across doses. ADX71743 also delayed NREM and REM sleep onset by nearly 2-fold (p<0.05) for 2 h after dosing, without altering MA or BT. Basal neurotransmitter concentrations were unchanged. However, ADX71743 attenuated stress-related changes in GABA and 5-HT, maintaining higher levels in the vHipp than in vehicle-treated controls. Stress-evoked NE and DA increases tended to be greater after ADX71743 than after vehicle. Neither treatment nor stress markedly affected Glu or Gly in the PFC or vHipp. These findings support an important role for mGlu7 in regulating sleep and wakefulness. The ADX71743-associated maintenance of higher vHipp 5-HT and GABA levels after stress may contribute to reduced stress- and anxiety-like reactivity produced by mGlu7 inhibition.