In everyday interactions, our perceptions of a partner's personality traits, such as extraversion and agreeableness, significantly influence how we engage with them. However, joint action research has largely overlooked the impact of these perceived partner traits on the co-representation of partners' task performance in a joint action setup. To address this, we conducted three experiments where participants first learned about their partner's personality through a trait learning task and then performed a joint Simon task with their perceived (not real) partner. Experiment 1 showed that perceived differences in partner extraversion and agreeableness significantly modulated the joint Simon effect (JSE), with a significantly larger JSE observed for partners perceived as extraverted or agreeable compared to those perceived as introverted or disagreeable. In contrast, perceived differences in partner conscientiousness did not exhibit such a modulation effect. Experiment 2 revealed that this modulation effect disappeared when these traits were perceived as peripheral to the partner's personality. Experiment 3 demonstrated similar modulation effects on the JSE as those observed in Experiment 1, while controlling for potential influences of valence. Overall, these results suggest that perceived partner traits, particularly extraversion and agreeableness, can modulate task co-representation. However, this effect occurs only when these traits are central to the partner. These findings highlight the influence of perceived socially relevant traits on shaping task co-representation in a joint action setup.

Iron accumulation in the substantia nigra is a hallmark of Parkinson's disease (PD), but its cellular drivers remain unclear. Oligodendrocytes, the most iron-rich cells in the brain, have been implicated in PD pathology. Our previous studies showed that 6-hydroxydopamine (6-OHDA) promotes iron accumulation in neurons and astrocytes by increasing iron influx and decreasing efflux. However, its effects on oligodendrocyte iron metabolism remain unknown. In this study, we examined how 6-OHDA affects iron homeostasis and inflammatory gene expression in MO3.13 oligodendrocytes. Using MTT, calcein-AM fluorescence assays, RT-PCR, and Western blotting, we compared undifferentiated and differentiated cells. In undifferentiated oligodendrocytes, 6-OHDA increased transferrin receptor 1 (TfR1) and iron regulatory protein 1 (IRP1) while reducing ferroportin 1 (FPN1), resulting in enhanced iron uptake and reduced export. In contrast, differentiated cells showed decreased TfR1 and IRP1 and increased FPN1, promoting iron efflux. 6-OHDA also induced stage-specific inflammatory responses. In undifferentiated cells, IL-1β and TNF-α mRNA levels rose in a dose-dependent manner, whereas differentiated cells selectively upregulated IL-1β. These results suggest that undifferentiated oligodendrocytes undergo iron-related inflammation that may promote differentiation, while differentiated cells respond with a more restricted cytokine profile. This study is the first to demonstrate that 6-OHDA promotes iron accumulation in undifferentiated oligodendrocytes by disrupting the IRP1-mediated balance between TfR1 and FPN1. Moreover, 6-OHDA induces distinct inflammatory responses depending on the stage of oligodendrocyte differentiation. These findings highlight the dual role of oligodendrocytes as both iron reservoirs and modulators of the neuroinflammatory microenvironment, providing new insights into the cellular mechanisms underlying nigral iron accumulation in PD, and suggesting that oligodendrocytes play a critical regulatory role in PD pathogenesis.

The pedunculopontine nucleus (PPN) is a heterogeneous cluster within the dorsolateral pontomesencephalic tegmentum, functioning as a critical neuromodulatory hub. A key organizing principle is its rostrocaudal functional gradient rostral glutamatergic Chx10 + neurons mediate global motor arrest, while caudal Vglut2 + neurons drive locomotor initiation and maintenance. This model, emphasizing topographically organized microcircuits, provides a coherent framework for reconciling heterogeneous outcomes of PPN stimulation across experimental and clinical settings. This review comprehensively analyzes the PPN's anatomical organization, neuronal composition, and connectivity, which collectively support its roles in locomotion, arousal, and reward processing. Particular focus is placed on its pathophysiological alterations in Parkinson's disease (PD), wherein selective degeneration of caudal cholinergic and Vglut2 + neurons contributes to treatment-resistant axial symptoms. The nucleus exhibits considerable neurochemical heterogeneity, encompassing cholinergic, glutamatergic, and GABAergic populations; this diversity underpins its broad functional roles and selective vulnerability in PD, with distinct implications for disease subtypes. We further examine disease-associated shifts in oscillatory activity, highlighting abnormal dynamics characteristic of the parkinsonian state. The therapeutic promise of PPN deep brain stimulation for alleviating gait freezing and falls in advanced PD is critically assessed, acknowledging challenges related to target localization, stimulation parameters, and patient selection. By integrating neuroanatomical, electrophysiological, and clinical evidence, this review offers a unified perspective on the PPN's central importance in PD pathophysiology and its growing relevance as a neuromodulation target.

Joint statistical learning enables interacting individuals to form shared representations, but prior research has primarily focused on homogeneous dyads with equivalent expertise. Real-world interactions often involve knowledge asymmetries, yet it remains unclear how novices implicitly acquire statistical regularities from expert partners via sensorimotor signals. This study investigated whether novices can implicitly extract sequence regularities to enhance joint statistical learning and compared two candidate mechanisms, action feedback versus action visibility. Using a modified serial reaction time task across three experiments, we found that novices paired with trained experts exhibited significantly steeper declines in reaction time compared to those paired with pseudo-experts. Moreover, expert-paired novices demonstrated a pronounced quadratic trajectory, indicating sequence-specific learning. Experiment 2 revealed that the absence of immediate action feedback eliminated this sequence-specific interference effect in novices, highlighting the critical role of shared perceptual outcomes in the implicit transmission of task regularities. Conversely, Experiment 3 showed that the absence of visual access to the expert’s physical movements attenuated neither the novices’ general sequence acquisition nor their sequence-specific interference effect. These findings extend the Theory of Event Coding framework to asymmetric social contexts by demonstrating that effect-based coding, rather than direct kinematic observation, drives implicit behavioral facilitation in joint action.

Asthma is a reversible condition characterized by airflow limitation and chronic airway inflammation. Previous neuroimaging studies have confirmed brain structural and functional abnormalities associated with asthma, primarily occurring in regions such as the anterior cingulate cortex, superior frontal gyrus, occipital lobe, postcentral gyrus, and corpus callosum. These changes may be attributable to asthma-related systemic inflammation. This study investigates modifications in the topological organization of functional brain networks in individuals with asthma using functional magnetic resonance imaging (fMRI) and graph theory techniques. Thirty-one asthma patients and thirty-one healthy controls participated, with resting-state fMRI data collected through MRI scanning. Data preprocessing was conducted using DPABI and SPM12 software, and functional brain networks were constructed and analyzed using the GRETNA toolbox. We computed global and nodal indices to evaluate network characteristics, identifying significant connectivity changes through network-based statistics (NBS). Results revealed notable differences in global network efficiency and small-world properties between individuals with asthma and controls, as well as significant distinctions in specific brain regions related to visual processing and cognitive functions. NBS analysis indicated that asthma patients exhibited substantial alterations in connectivity across various essential brain networks, suggesting effects on cognitive and emotional processing. Overall, the findings emphasize the significant impact of asthma on brain functional connectivity, influencing both global and nodal network properties, with potential implications for patients’ cognitive and emotional well-being. Further research is required to understand the clinical implications of these alterations and to develop targeted interventions.

Emotion-induced blindness (EIB) refers to the impaired perception of a target due to attentional capture by emotional distractors. While prior research indicates that EIB can be attenuated by enhancing target priority or by regulating emotional distractors through proactive inhibition or passive habituation, it remains unclear whether the intrinsic motivational value of self-relevance can effectively counteract such emotional capture. Grounded in the self-categorization framework, three experiments investigated whether enhancing target self-relevance mitigates EIB across individual, relational, and collective levels. In a two-phase paradigm, neutral images were endowed with high or low self-relevance via associative learning and subsequently presented as targets following emotional distractors in a rapid serial visual presentation (RSVP) task. Results demonstrated that individual (Experiment 1) and relational (Experiment 2) self-relevance significantly reduced EIB, yielding higher accuracy for highly self-relevant targets following negative distractors. For the collective self (Experiment 3), modulation of EIB depended on identity concreteness. Concrete-identity self-relevance (university) effectively buffered against EIB, whereas abstract-identity self-relevance (gender) did not. These findings suggest that target self-relevance may function as a protective buffer that helps reduce emotional interference in EIB across multiple self-levels, potentially offering practical ways to enhance psychological resilience during adverse experiences in real-world settings.

BACKGROUND:Depression is one of the most common non-motor disorders and neuropsychiatric comorbidities in Parkinson's disease (PD). The pathophysiology of depression in PD patients remains unclear and has been largely unexplored. METHOD:In this study, we employed chemogenetics and pharmacology to modulate the lateral habenula (LHb) and its downstream brain regions, the rostromedial tegmental nucleus (RMTg) and the ventral tegmental area (VTA) in wild type (WT) and 6-hydroxydopamine (6-OHDA) mice, to investigate the potential mechanisms underlying the improvement of PD-related depression. RESULTS:Inhibition of LHb glutamatergic neurons, as well as disruption of the LHb-RMTg pathway, along with inhibition of RMTg GABAergic neurons ameliorates depressive-like behavior in 6-OHDA mice. Conversely, activation of LHb glutamatergic neurons, the LHb-RMTg pathway, and activation of RMTg GABAergic neurons exacerbated depressive-like behavior in WT and 6-OHDA mice. Notably, either inhibition or activation of the LHb-VTA pathway did not produce any significant changes in depressive-like behavior in WT and 6-OHDA mice. Additionally, activation of VTA DAergic neurons effectively ameliorating depressive-like behavior in 6-OHDA mice. CONCLUSIONS:Inhibition of the LHb glutamatergic pathway ameliorates depressive-like behaviors in 6-OHDA PD mice model. These findings offer new insights for advancing research and developing novel treatments for PD-related depression.

OBJECTIVES:To investigate the mechanism through which N-acetylneuraminic acid (Neu5Ac) exacerbates hypoxia/reoxygenation (H/R) injury in rat cardiomyocytes (H9C2 cells). METHODS:H9C2 cells were cultured in hypoxia and glucose deprivation for 8 h followed by reoxygenation for different durations to determine the optimal reoxygenation time. Under the optimal H/R protocol, the cells were treated with 0, 5, 10, 20, 30, 40, 50, and 60 mmol/L Neu5Ac during reoxygenation to explore the optimal drug concentration. The cells were then subjected to H/R injury followed by treatment with Neu5Ac, Fer-1 (a ferroptosis inhibitor), or both. The changes in SOD activity, intracellular Fe2+ and lipid ROS levels in the cells were evaluated, and the cellular expressions of Nrf2, GPX4, HO-1, FSP1, and xCT proteins were detected using Western blotting. RESULTS:Following hypoxia and glucose deprivation for 8 h, the cells with reoxygenation for 6 h, as compared with other time lengths of reoxygenation except for 9 h, showed the lowest expression levels of Nrf2, GPX4, HO-1, and FSP1 proteins (P<0.001). Neu5Ac treatment of dose-dependently decreased the viability of the cells with H/R injury with an IC50 of 30.07 mmol/L. Reoxygenation for 3 h with normal glucose supplementation and a Neu5Ac concentration of 30 mmol/L were selected as the optimal conditions in the subsequent experiments. The results showed that Neu5Ac could significantly increase SOD activity, Fe2+ and lipid ROS levels and reduce Nrf2, GPX4, HO-1, and FSP1 protein expressions in H9C2 cells with H/R injury, but its effects were significantly attenuated by treatment with Fer-1. CONCLUSIONS:Neu5Ac exacerbates ferroptosis of myocardial cells with H/R injury by inhibiting the Nrf2 axis to promote the production of ROS and lipid ROS.

The tip-of-the-tongue (TOT) phenomenon is characterized by a temporary inability to retrieve a word despite a strong sense of familiarity. While extensive research has linked phonological processing to TOT, the exact nature of this relationship remains debated. The “blocking hypothesis” suggests that the retrieval of target words is interfered with by phonological neighbors, whereas the “transmission deficit hypothesis” posits that TOT arises from insufficient phonological activation of the target words. This study revisited this issue by examining the relationship between the microstructural integrity of the phonological processing brain network and TOT, utilizing graph-theoretical analyses of neuroimaging data from the Cambridge Centre for Ageing and Neuroscience (Cam-CAN), which included diffusion tensor imaging (DTI) data from 576 participants aged 18–87. The results revealed that global efficiency and mean degree centrality of the phonological processing network positively predicted TOT rates. At the nodal level, the nodal efficiency of the bilateral posterior superior temporal gyrus and the clustering coefficient of the left premotor cortex positively predicted TOT rates, while the degree centrality of the left dorsal superior temporal gyrus (dSTG) and the clustering coefficient of the left posterior supramarginal gyrus (pSMG) negatively predicted TOT rates. Overall, these findings suggest that individuals with a more enriched network of phonological representations tend to experience more TOTs, supporting the blocking hypothesis. Additionally, this study highlights the roles of the left dSTG and pSMG in facilitating word retrieval, potentially reducing the occurrence of TOTs.

The study aimed to investigate whether actors can go beyond individual-level statistical learning in social statistical learning and encode irrelevant information in their own tasks.By manipulating the attention pat-terns of two co-actors to their sequences,and distin-guishing relevant and irrelevant stimuli,the study found that co-actors could process irrelevant stimuli in their own tasks and also represent task-irrelevant information in their co-actors' tasks.The findings suggest that social context could widen the scope of attention and promote the representation of task-ir-relevant information in sequence learning.

Asthma is a reversible disease characterized by airflow limitation and chronic airway inflammation. Previous neuroimaging studies have shown structural and functional abnormalities in the brains of individuals with asthma. However, earlier research has primarily focused on static changes in brain activity, neglecting the effects of asthma on the dynamic characteristics of functional brain networks. This study included 31 asthma patients and 31 healthy controls (HCs). Independent component analysis (ICA) was employed to extract changes in static functional network connectivity (sFNC) and dynamic functional network connectivity (dFNC) from the acquired data. Compared to the HC group, the overall functional connectivity (FC) within the visual network (VN) in asthma patients declined, whereas the FC in the auditory network (AN) and cerebellar network (CN) increased. Additionally, functional network connectivity (FNC) analysis revealed enhanced connectivity between the VN and AN, as well as between the VN and executive control network (ECN), while AN-AN functional connectivity was reduced. The dFNC was primarily characterized by abnormal connections among the default mode network (DMN), AN, and other brain regions. The support vector machine (SVM) model based on FC and FNC demonstrates excellent performance in distinguishing asthma patients from HCs. Our findings highlight significant alterations in functional connectivity within the sFNC and dFNC of asthma patients. These results enhance our understanding of the potential neurobiological mechanisms underlying emotional deficits and cognitive impairments in asthma patients. Furthermore, they provide additional neuroimaging evidence that may be helpful for researchers in identifying potential neurobiological markers to differentiate asthma patients from HCs.

Previous studies have primarily focused on exploring the sources of time perception bias at an individual level, but few studies have investigated the mechanisms behind time perception bias in social contexts. To address this gap, the present study combined joint action and time perception paradigms with the goal of investigating time perception in social contexts and further examining the mechanisms of co-representation and/or social facilitation in joint temporal perception through three experiments.This study used a between-subject 2 x 2 experimental design, with the factors of context (individual vs. joint) and duration distribution (short intervals vs. long intervals). The stimulus durations were 400 ms or 1000 ms for the short interval group, and 1000 ms or 1600 ms for the long interval group. The varying intervals were indicated by yellow or green circles. Participants initially completed a learning task alone and were then randomly assigned to either an individual or joint context to complete a practice task. In the joint context, two participants who were unfamiliar with each other practiced with different temporal intervals and completed the experiment together. In the individual context, one participant sat alone on the left or right side of the screen to complete the experiment. During the learning phase, participants became familiar with the short- and long-interval stimuli. In the practice phase, solid orange circles of varying durations (from 400 ms to 1000 ms, in 100 ms increments) or solid green circles (from 1000 ms to 1600 ms, in 100 ms increments) were randomly shown on the screen. Participants then judged whether the duration of the stimulus was "short" or "long" based on criteria presented during the learning phase. In Experiment 1, we found that individuals' subjective equivalence points were significantly altered, and their sensitivity to time perception was notably reduced in joint situations compared to individual situations. In Experiment 2, we stimulated co-representation by manipulating participants' beliefs, and the absence of peers reduced the influence of social inhibition. Individuals had similar shifts in subjective equivalence points as observed in joint situations, but there was no significant change in temporal perceptual sensitivity. In Experiment 3, co-representation was attenuated by giving the peer a non-temporal estimation task, while the presence of peers elicited social inhibition. These findings demonstrated a significant decrease in individuals' time-perception sensitivity compared to the individual situation, but no significant shift in subjective equivalence points was observed. In summary, the present study suggests that individuals in joint action contexts represent their peers' task information through the mechanism of co-representation, which introduces bias in time estimation. Additionally, the presence of others creates competition for attentional resources, leading to a reduction in individuals' sensitivity to time perception in joint action contexts.

The lateral habenula (LHb) and the rostromedial tegmental nucleus (RMTg) are critical brain structures involved in reward processing, aversive signaling, and mood regulation. Recent research has uncovered significant progress in understanding their physiological functions, neural circuits, and implications in neuropsychiatric disorders. By integrating signals from the limbic system and projecting into the midbrain monoaminergic system, the LHb encodes negative reward prediction error and mediates behaviors associated with depressive as well as stress response. Its overactivation can inhibit dopamine release, resulting in anhedonia. As the main downstream target of LHb, the RMTg exerts inhibitory control over dopaminergic neurons in the ventral tegmental area (VTA) via γ-aminobutyric acid (GABA), and participates in reward inhibition, addiction withdrawal and hyperalgesia regulation. The LHb activates GABAergic neurons within the RMTg through glutaminergic projection, thereby inhibiting dopamine release in the VTA neurons. This neuronal circuitry is critically involved in the pathophysiological mechanisms of depression, addiction and other neuropsychiatric disorders‌. Here, we reviewed the anatomical features and molecular markers of both LHb and RMTg along with their inputs, outputs and physiological functions of LHb and RMTg. This research is of great significance for understanding the neural mechanisms underlying neuropsychiatric diseases.

Previous research suggests that statistical learning enhances memory for self-related information at the individual level and that individuals exhibit better memory for partner-related items than they do for irrelevant items in joint contexts (i.e., the joint memory effect, JME). However, whether statistical learning improves memory for partner-related information in joint contexts remains unclear. This study investigated memory performance for partner-related words when higher level statistical regularities were embedded in word streams during a joint memory task. Participants performed a word categorization task, followed by a surprise free recall task across four experiments. Experiment 1 replicated the JME, revealing improved memory for partner-related items than for irrelevant items when using Chinese words with increased repetition. Experiment 2 embedded semantic regularities within partners' word streams; Experiment 3a employed regularities based on non-adjacent fixed temporal positions; and Experiment 3b employed regularities based on adjacent fixed temporal positions. Results showed that the JME was enhanced only when semantic regularities were present (Experiment 2) and not with temporal positional rules (Experiments 3a and 3b). These findings suggest a hierarchical structure of co-representation and show that co-represented statistical regularities facilitate the processing of partner-related words, but only when the regularities align with partners' intentions. This study advances our understanding of co-representation in joint action by highlighting its hierarchical nature, and the top-down interaction between structural levels.

Selective loss of dopaminergic neurons in the substantia nigra (SN) is the main pathological feature of Parkinson's disease (PD), and nigral iron deposition is a key factor in the pathogenesis of PD. Excessive iron can lead to increased production of reactive oxygen species (ROS) in cells and cause cell damage. The abnormal synthesis and metabolism of cholesterol in the brain are closely related to the occurrence of central nervous system diseases, but the mechanisms remain unclear. This experiment investigates the effects and mechanisms of cholesterol and 24S-hydroxycholesterol (24S-OHC) on SH-SY5Y neurons and primary cultured ventral mesencephalon neurons. The viability of SH-SY5Y neurons and primary cultured ventral mesencephalon (VM) neurons was detected by cell counting kit-8 (CCK-8) assay. The intracellular ROS levels were detected by flow cytometry. The expressions of proteins related to ferroptosis, apoptosis, and necroptosis were detected by western blot. The mRNA expression of pro-inflammatory cytokines was detected by real-time PCR. In neurons treated with cholesterol or 24S-OHC, the protein expressions of iron regulatory protein 1 (IRP1), transferrin receptor 1 (TfR1), divalent metal transporter 1 (DMT1), and ferritin were increased, while the expression of ferroportin 1 (FPN1) was decreased, thus leading to increased intracellular iron levels. However, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11; also called x-CT), ferroptosis suppressor protein 1 (FSP1), and malondialdehyde (MDA), the indicators of ferroptosis, showed no obvious alterations. Cholesterol induced the increased expressions of pro-inflammatory cytokines interleukin-1 beta (IL-1β) and IL-6 in neurons, and the Erk-NF-κB pathway changed accordingly. Moreover, the expressions of cleaved caspase-3, the ratio of Bax/Bcl-2, receptor-interacting protein kinase 1 (RIPK1), RIPK3, and phosphorylated mixed lineage kinase domain-like (p-MLKL) in neurons were also elevated by 24S-OHC treatment. Morphologically, we found nuclear membrane breakdown, chromatin condensation, organelle expansion, cytoplasmic vacuolization, and contents outflow in neurons, which were further signs of neuronal apoptosis and necroptosis. Additionally, co-treatment with deferoxamine (DFO) can partially reduce cleaved caspase-3 expression but cannot reduce p-MLKL expression. Our findings suggest that both cholesterol and 24S-OHC can raise the level of reactive oxygen species (ROS) and activate IRP1 to increase iron influx and decrease iron outflow in neurons. Despite the increase in iron content, ferroptosis is not observed. Cholesterol also increases the expressions of IL-1β and IL-6, which may be related to the Erk-NF-κB pathway, while 24S-OHC can cause both apoptosis and necroptosis. DFO can only partially reduce apoptosis but cannot prevent necroptosis in neurons.

By observing dynamically changing facial expressions, humans can use a specialized capacity known as ensemble coding to effortlessly obtain a summary representation of an individual’s emotional state. However, few studies have examined whether the missing expression informed by the statistical regularity in the changing facial expressions can be sampled and then influence the perceptual averaging process. In Experiment 1a and 1b, we manipulated the amount of prior information from local regularity by varying the position of the missing expression in the temporal sequence (1a: Neutral to Disgust and/or Disgust to Neutral,1b: Neutral to Happy and/or Happy to Neutral) within a trial. Results showed that ensemble estimates were towards the mean of expressions including both the presented and the missing faces, only when sufficient predictability (e.g. a missing expression in the late position) informed by local regularity. In Experiment 2, we added prior information from global regularities to help boost the predictability of an early missing expression by keeping the emotional direction consistent in a block. However, estimates were not towards the mean of expressions including both the presented and the missing expressions as expected. Although the generalizability may be limited, these findings suggest that prior information at different levels of hierarchical predictive coding may exert qualitatively different influences on the perceptual averaging of temporally ordered facial expressions with missing items.

The present case report investigated the clinicopathological features and potential mechanisms underlying the transformation to peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), following treatment for classical Hodgkin lymphoma (CHL) in a 73-year-old man. The patient was admitted to hospital in 2012 and underwent a left cervical lymph node biopsy, which confirmed CHL of the nodular sclerosing type, with evident bone marrow involvement. The patient received four cycles of doxorubicin, bleomycin, vinblastine and dacarbazine chemotherapy, after which they achieved complete remission. However, after 3 years, the patient presented with enlarged left inguinal lymph nodes and a biopsy revealed PTCL-NOS. Molecular studies indicated a T-cell receptor-γ gene rearrangement. A literature review, together with the current case, identified 11 patients with CHL that transformed into PTCL-NOS. Among these, nine patients (81.82%) were middle-aged or elderly (>45 years old), and eight (72.73%) experienced transformation within 3 years post-treatment of CHL. Among these eight patients, seven (87.50%) predominantly exhibited the nodular sclerosis subtype, with a median recurrence time of 26 months. Five (45.45%) patients died of the disease. The rare transformation of CHL to PTCL-NOS, primarily among men, underscores its clinical significance. Notably, nodular sclerosing-type CHL appears to be particularly prone to transformation into PTCL-NOS. The poor prognosis in such cases may be attributed to the complex tumor microenvironment of CHL.

ObjectiveBronchial Asthma (BA) is a common chronic respiratory disease worldwide. Earlier research has demonstrated abnormal functional connectivity (FC) in multiple cognition-related cortices in asthma patients. The thalamus (Thal) serves as a relay center for transmitting sensory signals, yet the modifications in the thalamic FC among individuals with asthma remain uncertain. This research employed the resting-state functional connectivity (rsFC) approach to explore alterations in thalamic functional connectivity among individuals with BA.Patients and methodsAfter excluding participants who did not meet the criteria, this study finally included 31 patients with BA, with a gender distribution of 16 males and 15 females. Subsequently, we recruited 31 healthy control participants (HC) matched for age, gender, and educational background. All participants underwent the Montreal Cognitive Assessment (MoCA) and the Hamilton Depression Rating Scale (HAMD) assessment. Following this, both groups underwent head magnetic resonance imaging scans, and resting-state functional magnetic resonance imaging (rs-fMRI) data was collected. Based on the AAL (Automated Anatomical Labeling) template, the bilateral thalamic regions were used as seed points (ROI) for subsequent rsFC research. Pearson correlation analysis was used to explore the relationship between thalamic functional connectivity and neuropsychological scales in both groups. After controlling for potential confounding factors such as age, gender, intelligence, and emotional level, a two-sample t-test was further used to explore differences in thalamic functional connectivity between the two groups of participants.ResultCompared to the HC group, the BA group demonstrated heightened functional connectivity (FC) between the left thalamus and the left cerebellar posterior lobe (CPL), left postcentral gyrus (PCG), and right superior frontal gyrus (SFG). Concurrently, there was a decrease in FC with both the Lentiform Nucleus (LN) and the left corpus callosum (CC). Performing FC analysis with the right thalamus as the Region of Interest (ROI) revealed an increase in FC between the right thalamus and the right SFG as well as the left CPL. Conversely, a decrease in FC was observed between the right thalamus and the right LN as well as the left CC.ConclusionIn our study, we have verified the presence of aberrant FC patterns in the thalamus of BA patients. When compared to HCs, BA patients exhibit aberrant alterations in FC between the thalamus and various brain areas connected to vision, hearing, emotional regulation, cognitive control, somatic sensations, and wakefulness. This provides further confirmation of the substantial role played by the thalamus in the advancement of BA.

Observers can rapidly extract the mean emotion from a set of faces with remarkable precision, known as ensemble coding. Previous studies have demonstrated that matched physical backgrounds improve the precision of ongoing ensemble tasks. However, it remains unknown whether this facilitation effect still occurs when matched social information is perceived from the backgrounds. In two experiments, participants decided whether the test face in the retrieving phase appeared more disgusted or neutral than the mean emotion of the face set in the encoding phase. Both phases were paired with task-irrelevant animated backgrounds, which included either the forward movement trajectory carrying the "cooperatively chasing" information, or the backward movement trajectory conveying no such chasing information. The backgrounds in the encoding and retrieving phases were either mismatched (i.e., forward and backward replays of the same trajectory), or matched (i.e., two identical forward movement trajectories in Experiment 1, or two different forward movement trajectories in Experiment 2). Participants in both experiments showed higher ensemble precisions and better discrimination sensitivities when backgrounds matched. The findings suggest that consistent social information perceived from memory-related context exerts a context-matching facilitation effect on ensemble coding and, more importantly, this effect is independent of consistent physical information.