Twenty-five years of research on resting-state fMRI of major depressive disorder: A bibliometric analysis of hotspots, nodes, bursts, and trends.

Major depressive disorder (MDD) is a debilitating mental health condition that poses significant risks and burdens. Resting-state functional magnetic resonance imaging (fMRI) has emerged as a promising tool in investigating the neural mechanisms underlying MDD. However, a comprehensive bibliometric analysis of resting-state fMRI in MDD is currently lacking. Here, we aimed to thoroughly explore the trends and frontiers of resting-state fMRI in MDD research. The relevant publications were retrieved from the Web of Science database for the period between 1998 and 2022, and the CiteSpace software was employed to identify the influence of authors, institutions, countries/regions, and the latest research trends. A total of 1501 publications met the search criteria, revealing a gradual increase in the number of annual publications over the years. China contributed the largest publication output, accounting for the highest percentage among all countries. Particularly, the University of Electronic Science and Technology of China, Capital Medical University, and Harvard Medical School were identified as key institutions that have made substantial contributions to this growth. Neuroimage, Biological Psychiatry, Journal of Affective Disorders, and Proceedings of the National Academy of Sciences of the United States of America are among the influential journals in the field of resting-state fMRI research in MDD. Burst keywords analysis suggest the emerging research frontiers in this field are characterized by prominent keywords such as dynamic functional connectivity, cognitive control network, transcranial brain stimulation, and childhood trauma. Overall, our study provides a systematic overview into the historical development, current status, and future trends of resting-state fMRI in MDD, thus offering a useful guide for researchers to plan their future research.

Neural substrates of predicting anhedonia symptoms in major depressive disorder via connectome-based modeling.

MAIN PROBLEM: Anhedonia is a critical diagnostic symptom of major depressive disorder (MDD), being associated with poor prognosis. Understanding the neural mechanisms underlying anhedonia is of great significance for individuals with MDD, and it encourages the search for objective indicators that can reliably identify anhedonia. METHODS: A predictive model used connectome-based predictive modeling (CPM) for anhedonia symptoms was developed by utilizing pre-treatment functional connectivity (FC) data from 59 patients with MDD. Node-based FC analysis was employed to compare differences in FC patterns between melancholic and non-melancholic MDD patients. The support vector machines (SVM) method was then applied for classifying these two subtypes of MDD patients. RESULTS: CPM could successfully predict anhedonia symptoms in MDD patients (positive network: r = 0.4719, p < 0.0020, mean squared error = 23.5125, 5000 iterations). Compared to non-melancholic MDD patients, melancholic MDD patients showed decreased FC between the left cingulate gyrus and the right parahippocampus gyrus (p_bonferroni = 0.0303). This distinct FC pattern effectively discriminated between melancholic and non-melancholic MDD patients, achieving a sensitivity of 93.54%, specificity of 67.86%, and an overall accuracy of 81.36% using the SVM method. CONCLUSIONS: This study successfully established a network model for predicting anhedonia symptoms in MDD based on FC, as well as a classification model to differentiate between melancholic and non-melancholic MDD patients. These findings provide guidance for clinical treatment.

Potential correlations between abnormal homogeneity of default mode network and personality or lipid level in major depressive disorder.

BACKGROUND: Default mode network (DMN) is one of the most recognized resting-state networks in major depressive disorder (MDD). However, the homogeneity of this network in MDD remains incompletely explored. Therefore, this study aims to determine whether there is abnormal network homogeneity (NH) of the DMN in MDD patients. At the same time, correlations between clinical variables and brain functional connectivity are examined. METHODS: We enrolled 42 patients diagnosed with MDD and 42 HCs. A variety of clinical variables were collected, and data analysis was conducted using the NH and independent component analysis methods. RESULTS: The study shows that MDD patients have higher NH values in the left superior medial prefrontal cortex (MPFC) and left posterior cingulate cortex (PCC) compared to HCs. Additionally, there is a positive correlation between NH values of the left superior MPFC and Eysenck Personality Questionnaire values. NH values of the left PCC are positively linked to CHOL levels, LDL levels, and utilization scores. However, these correlations lose significance after the Bonferroni correction. CONCLUSION: Our findings indicate the presence of abnormal DMN homogeneity in MDD, underscoring the significance of DMN in the pathophysiology of MDD. Simultaneously, the study provides preliminary evidence for the correlation between clinical variables and brain functional connectivity.

Cerebellar functional connectivity and its associated genes: A longitudinal study in drug-naive patients with obsessive-compulsive disorder.

The role of cerebellar-cerebral functional connectivity (CC-FC) in obsessive-compulsive disorder (OCD), its trajectory post-pharmacotherapy, and its potential as a prognostic biomarker and genetic mechanism remain uncertain. To address these gaps, this study included 37 drug-naive OCD patients and 37 healthy controls (HCs). Participants underwent baseline functional magnetic resonance imaging (fMRI), followed by four weeks of paroxetine treatment for patients with OCD, and another fMRI scan post-treatment. We examined seed-based CC-FC differences between the patients and HCs, and pre- and post-treatment patients. Support vector regression (SVR) based on CC-FC was performed to predict treatment response. Correlation analysis explored associations between CC-FC and clinical features, as well as gene profiles. Compared to HCs, drug-naive OCD patients exhibited reduced CC-FC in executive, affective-limbic, and sensorimotor networks, with specific genetic profiles associated with altered CC-FC. Gene enrichment analyses highlighted the involvement of these genes in various biological processes, molecular functions, and pathways. Post-treatment, the patients showed partial clinical improvement and partial restoration of the previously decreased CC-FC. Abnormal CC-FC at baseline correlated negatively with compulsions severity and social functional impairment, while changes in CC-FC correlated with cognitive function changes post-treatment. CC-FC emerged as a potential predictor of symptom severity in patients following paroxetine treatment. This longitudinal resting-state fMRI study underscores the crucial role of CC-FC in the neuropsychological mechanisms of OCD and its pharmacological treatment. Transcriptome-neuroimaging spatial correlation analyses provide insight into the neurobiological mechanisms underlying OCD pathology. Furthermore, SVR analyses hold promise for advancing precision medicine approaches in treating patients with OCD.

Chronic intranasal oxytocin alleviates cognitive impairment and reverses oxytocin signaling upregulation in MK801-induced mice.

OBJECTIVE: Cognitive impairment, especially impaired social cognition, is largely responsible for the deterioration of the social life of patients with schizophrenia (SZ). Oxytocin (OT) is a neuropeptide that offers promising therapy for SZ. This study aimed to explore whether OT could affect dizocilpine (MK801)-induced cognitive impairment and to investigate the effect of exogenous OT on the endogenous OT system in the hippocampus. METHODS: The SZ mouse model was established by repeated administration of dizocilpine [MK801, 0.6 mg/kg, intraperitoneal (i.p.)], and then OT (6-60 µg/kg, intranasal) or risperidone (0.3 mg/kg, i.p.) was administered to explore the effect of OT on cognitive impairment. RESULTS: OT at a dose of 6 µg/kg alleviated MK801-induced hyperactivity, sociability impairment, and spatial memory impairment. OT at a dose of 20 or 60 µg/kg attenuated the hyperactivity and social novelty impairment. In MK801-injected mice, the compensatory upregulation of OT mRNA in the hippocampus was reversed by three OT doses, whereas 60 µg/kg OT reversed the compensatory upregulation of CD38 protein expression. CONCLUSION: OT alleviated cognitive impairment in the SZ mouse model to varying degrees, reversing the compensatory upregulation of OT signaling in the hippocampus.

Association Between Geriatric Nutrition Risk Index and 90-Day Mortality in Older Adults with Chronic Obstructive Pulmonary Disease: a Retrospective Cohort Study.

Background: Malnutrition adversely affects prognosis in various medical conditions, but its implications in older adults with Chronic Obstructive Pulmonary Disease (COPD) in the ICU are underexplored. The geriatric nutritional risk index (GNRI) is a novel tool for assessing malnutrition risk. This study investigates the association between GNRI and 90-day mortality in this population. Methods: We selected older adults with COPD admitted to the ICU from Medical Information Mart for Intensive Care (MIMIC)-IV 2.2 database. A total of 666 patients were categorized into four groups based on their GNRI score: normal nutrition (>98), mild malnutrition (92-98), moderate malnutrition (82-91), and severe malnutrition (≤81) groups. We employed a restricted cubic spline (RCS) analysis to assess the presence of a curved relationship between them and to investigate any potential threshold saturation effect. Results: In multivariate Cox regression analyses, compared with individuals had normal nutrition (GNRI in Q4 >98), the adjusted HR values for GNRI in Q3 (92-98), Q2 (82-91), and Q1 (≤81) were 1.81 (95% CI: 1.27-2.58, p=0.001), 1.23 (95% CI: 0.84-1.79, p=0.296), 2.27 (95% CI: 1.57-3.29, p<0.001), respectively. The relationship between GNRI and 90-day mortality demonstrates an L-shaped curve (p=0.016), with an approximate inflection point at 101.5. Conclusion: These findings imply that GNRI is a useful prognostic tool in older adults with COPD in the ICU. An L-shaped relationship was observed between GNRI and 90-day mortality in these patients.

A Quantitative Trait Locus with a Major Effect on Root-Lesion Nematode Resistance in Barley.

Although the root-lesion nematode Pratylenchus thornei is known to affect barley (Hordeum vulgare L.), there have been no reports on the genetic control of P. thornei resistance in barley. In this research, P. thornei resistance was assessed for a panel of 46 barley mapping parents and for two mapping populations (Arapiles/Franklin and Denar/Baudin). With both populations, a highly significant quantitative trait locus (QTL) was mapped at the same position on the long arm of chromosome 7H. Single-nucleotide polymorphisms (SNPs) in this region were anchored to an RGT Planet pan-genome assembly and assayed on the mapping parents and other barley varieties. The results indicate that Arapiles, Denar, RGT Planet and several other varieties likely have the same resistance gene on chromosome 7H. Marker assays reported here could be used to select for P. thornei resistance in barley breeding. Analysis of existing barley pan-genomic and pan-transcriptomic data provided a list of candidate genes along with information on the expression and differential expression of some of those genes in barley root tissue. Further research is required to identify a specific barley gene that affects root-lesion nematode resistance.

High-pressure synthesis of A-site ordered perovskite PbMn3(CrMn3)O12 with long-range antiferromagnetic ordering and a spin glass transition.

An AA'3B4O12-type perovskite oxide PbMn3(CrMn3)O12 was synthesized by high-pressure solid-state reactions at 8 GPa and 1373 K. Synchrotron X-ray diffraction shows a cubic crystal structure with the space group Im3̄. The charge states are verified by X-ray photoelectron spectroscopy to be PbMn3+3(Cr3+Mn3+2Mn4+)O12, where the Pb2+ and Mn3+ are 1 : 3 ordered respectively at A and A' sites, while the Cr3+, Mn3+ and Mn4+ are disorderly distributed at the B site. PbMn3(CrMn3)O12 features a long-range antiferromagnetic order of A'-site Mn3+ spins at about 66 K and a subsequent spin glass transition around 36 K due to the randomly distributed Cr3+, Mn3+, and Mn4+ cations at the B site. This unique stepwise order of A' and B-site spins indicates weak A'-B site spin interactions, which are dominated by the difference in the B-site Mn3+/Ni2+ and Mn4+ number in the quadruple perovskites AMn3B4O12.

Uncovering the crystallography and formation mechanism of nanoscale clusters in Sb-rich SPPs of a p-type (Bi, Sb)2Te3 alloy.

Considering that the crystallographic characteristics of the Sb-rich secondary phase particles (SPPs) greatly affect the thermoelectric properties of Bi2Te3 based materials, it is of great significance to explore the mechanism behind the Sb-rich SPPs in the p-type (Bi, Sb)2Te3 material. Here a conventional TEM technique was used to characterize the composition, size and distribution of Sb-rich SPPs in a spark plasma sintered p-type (Bi, Sb)2Te3 alloy. The results indicated that two different morphologies of Sb-rich SPPs including elongated and circular Sb-rich SPPs were frequently observed. Combined with high-resolution transmission electron microscopy, this work provides atomic-scale evidence for the formation mechanism behind the Sb-rich SPPs in the (Bi, Sb)2Te3 material.

Generation of allogeneic CAR-NKT cells from hematopoietic stem and progenitor cells using a clinically guided culture method.

Cancer immunotherapy with autologous chimeric antigen receptor (CAR) T cells faces challenges in manufacturing and patient selection that could be avoided by using 'off-the-shelf' products, such as allogeneic CAR natural killer T (AlloCAR-NKT) cells. Previously, we reported a system for differentiating human hematopoietic stem and progenitor cells into AlloCAR-NKT cells, but the use of three-dimensional culture and xenogeneic feeders precluded its clinical application. Here we describe a clinically guided method to differentiate and expand IL-15-enhanced AlloCAR-NKT cells with high yield and purity. We generated AlloCAR-NKT cells targeting seven cancers and, in a multiple myeloma model, demonstrated their antitumor efficacy, expansion and persistence. The cells also selectively depleted immunosuppressive cells in the tumor microenviroment and antagonized tumor immune evasion via triple targeting of CAR, TCR and NK receptors. They exhibited a stable hypoimmunogenic phenotype associated with epigenetic and signaling regulation and did not induce detectable graft versus host disease or cytokine release syndrome. These properties of AlloCAR-NKT cells support their potential for clinical translation.

Potential correlations between asymmetric disruption of functional connectivity and metabolism in major depressive disorder.

OBJECTIVE: Previous research has suggested a connection between major depressive disorder (MDD) and certain comorbidities, including gastrointestinal issues, thyroid dysfunctions, and glycolipid metabolism abnormalities. However, the relationships between these factors and asymmetrical alterations in functional connectivity (FC) in adults with MDD remain unclear. METHOD: We conducted a study on a cohort of 42 MDD patients and 42 healthy controls (HCs). Participants underwent comprehensive clinical assessments, including evaluations of blood lipids and thyroid hormone levels, as well as resting-state functional magnetic resonance imaging (Rs-fMRI) scans. Data analysis involved correlation analysis to compute the parameter of asymmetry (PAS) for the entire brain's functional connectome. We then examined the interrelationships between abnormal PAS regions in the brain, thyroid hormone levels, and blood lipid levels. RESULTS: The third-generation ultra-sensitive thyroid stimulating hormone (TSH3UL) level was found to be significantly lower in MDD patients compared to HCs. The PAS score of the left inferior frontal gyrus (IFG) decreased, while the bilateral posterior cingulate cortex (Bi-PCC) PAS increased in MDD patients relative to HCs. Notably, the PAS score of the left IFG negatively correlated with both TSH and total cholesterol (CHOL) levels. However, these correlations lose significance after the Bonferroni correction. CONCLUSION: MDD patients demonstrated abnormal asymmetry in resting-state FC (Rs-FC) within the fronto-limbic system, which may be associated with CHOL and thyroid hormone levels.

Fractional amplitude of low-frequency fluctuations in sensory-motor networks and limbic system as a potential predictor of treatment response in patients with schizophrenia.

BACKGROUND: Previous investigations have revealed substantial differences in neuroimaging characteristics between healthy controls (HCs) and individuals diagnosed with schizophrenia (SCZ). However, we are not entirely sure how brain activity links to symptoms in schizophrenia, and there is a need for reliable brain imaging markers for treatment prediction. METHODS: In this longitudinal study, we examined 56 individuals diagnosed with 56 SCZ and 51 HCs. The SCZ patients underwent a three-month course of antipsychotic treatment. We employed resting-state functional magnetic resonance imaging (fMRI) along with fractional Amplitude of Low Frequency Fluctuations (fALFF) and support vector regression (SVR) methods for data acquisition and subsequent analysis. RESULTS: In this study, we initially noted lower fALFF values in the right postcentral/precentral gyrus and left postcentral gyrus, coupled with higher fALFF values in the left hippocampus and right putamen in SCZ patients compared to the HCs at baseline. However, when comparing fALFF values in brain regions with abnormal baseline fALFF values for SCZ patients who completed the follow-up, no significant differences in fALFF values were observed after 3 months of treatment compared to baseline data. The fALFF values in the right postcentral/precentral gyrus and left postcentral gyrus, and the left postcentral gyrus were useful in predicting treatment effects. CONCLUSION: Our findings suggest that reduced fALFF values in the sensory-motor networks and increased fALFF values in the limbic system may constitute distinctive neurobiological features in SCZ patients. These findings may serve as potential neuroimaging markers for the prognosis of SCZ patients.

Combination of UGT1A1 polymorphism and baseline plasma bilirubin levels in predicting the risk of antipsychotic-induced dyslipidemia in schizophrenia patients.

The prolonged usage of atypical antipsychotic drugs (AAPD) among individuals with schizophrenia often leads to metabolic side effects such as dyslipidemia. These effects not only limit one's selection of AAPD but also significantly reduce compliance and quality of life of patients. Recent studies suggest that bilirubin plays a crucial role in maintaining lipid homeostasis and may be a potential pre-treatment biomarker for individuals with dyslipidemia. The present study included 644 schizophrenia patients from two centers. Demographic and clinical characteristics were collected at baseline and 4 weeks after admission to investigate the correlation between metabolites, episodes, usage of AAPDs, and occurrence of dyslipidemia. Besides, we explored the combined predictive value of genotypes and baseline bilirubin for dyslipidemia by employing multiple PCR targeted capture techniques to sequence two pathways: bilirubin metabolism-related genes and lipid metabolism-related genes. Our results indicated that there existed a negative correlation between the changes in bilirubin levels and triglyceride (TG) levels in patients with schizophrenia. Among three types of bilirubin, direct bilirubin in the baseline (DBIL-bl) proved to be the most effective in predicting dyslipidemia in the ROC analysis (AUC = 0.627, p < 0.001). Furthermore, the odds ratio from multinomial logistic regression analysis showed that UGT1A1*6 was a protective factor for dyslipidemia (ß = -12.868, p < 0.001). The combination of baseline DBIL and UGT1A1*6 significantly improved the performance in predicting dyslipidemia (AUC = 0.939, p < 0.001). Schizophrenia patients with UGT1A1*6 mutation and a certain level of baseline bilirubin may be more resistant to dyslipidemia and have more selections for AAPD than other patients.

Two imprinted genes primed by DEMETER in the central cell and activated by WRKY10 in the endosperm.

The early development of the endosperm is crucial for balancing the allocation of maternal nutrients to offspring. This process is believed to be evolutionarily associated with genomic imprinting, resulting in parentally biased allelic gene expression. Beyond FertilizationIndependentSeed (FIS) genes, the number of imprinted genes involved in early endosperm development and seed size determination remains limited. This study introduces early endosperm-expressed HAIKU (IKU) downstream Candidate F-box 1 (ICF1) and ICF2 as maternally expressed imprinted genes (MEGs) in Arabidopsis thaliana. Although these genes are also demethylated by DEMETER (DME) in the central cell, their activation differs from the direct DME-mediated activation seen in classical MEGs such as the FIS genes. Instead, ICF maternal alleles carry pre-established hypomethylation in their promoters, priming them for activation by the WRKY10 transcription factor in the endosperm. On the contrary, paternal alleles are predominantly suppressed by CG methylation. Furthermore, we find that ICF genes partially contribute to the small seed size observed in iku mutants. Our discovery reveals a two-step regulatory mechanism that highlights the important role of conventional transcription factors in the activation of imprinted genes, which was previously not fully recognized. Therefore, the mechanism provides a new dimension to understand the transcriptional regulation of imprinting in plant reproduction and development.

Similar imaging changes and their relations to genetic profiles in bipolar disorder across different clinical stages.

Bipolar disorder (BD) across different clinical stages may present shared and distinct changes in brain activity. We aimed to reveal the neuroimaging homogeneity and heterogeneity of BD and its relationship with clinical variables and genetic variations. In present study, we conducted fractional amplitude of low-frequency fluctuations (fALFF), functional connectivity (FC) and genetic neuroimaging association analyses with 32 depressed, 26 manic, 35 euthymic BD patients and 87 healthy controls (HCs). Significant differences were found in the bilateral pre/subgenual anterior cingulate cortex (ACC) across the four groups, and all bipolar patients exhibited decreased fALFF values in the ACC when compared to HCs. Furthermore, positive associations were significantly observed between fALFF values in the pre/subgenual ACC and participants' cognitive functioning. No significant changes were found in ACC-based FC. We identified fALFF-alteration-related genes in BD, with enrichment in biological progress including synaptic and ion transmission. Taken together, abnormal activity in ACC is a characteristic change associated with BD, regardless of specific mood stages, serving as a potential neuroimaging feature in BD patients. Our genetic neuroimaging association analysis highlights possible heterogeneity in biological processes that could be responsible for different clinical stages in BD.

Association between abnormal default mode network homogeneity and sleep disturbances in major depressive disorder.

Background: Sleep disturbance is a common comorbidity of major depressive disorder (MDD). However, network homogeneity (NH) changes of the default mode network (DMN) in MDD with sleep disturbances are unclear. Aims: The purpose of this study was to probe the abnormal NH in the DMN in MDD with sleep disturbances and to reveal the differences between MDD with or without sleep disturbances. Methods: Twenty-four patients with MDD and sleep disturbances (Pa_s), 33 patients with MDD without sleep disturbances (Pa_ns) and 32 healthy controls (HCs) were recruited in this study. Resting-state functional imaging data were analysed using NH. Results: Compared with Pa_ns and HCs, Pa_s showed decreased NH in the left superior medial prefrontal cortex and increased NH in the right precuneus. There was a negative correlation between NH in the left superior medial prefrontal cortex and sleep disturbances (r=-0.42, p=0.001) as well as a positive correlation between NH in the right precuneus and sleep disturbances (r=0.41, p=0.002) in patients with MDD. Conclusions: MDD with sleep disturbances is associated with abnormal NH in the DMN, which could differentiate pa_s from pa_ns. The DMN may play a crucial role in the neurobiological mechanisms of MDD with sleep disturbances.

BMSC-Derived Exosomes Carrying miR-26a-5p Ameliorate Spinal Cord Injury via Negatively Regulating EZH2 and Activating the BDNF-TrkB-CREB Signaling.

BACKGROUND: Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes show great therapeutic potential for SCI. Exosomes derived from miR-26a-modified MSCs promote axonal regeneration following SCI. Our study aims to uncover the mechanisms by which BMSC-derived exosomes carrying miR-26a-5p regulate SCI. METHODS: BMSCs and BMSC-derived exosomes were isolated and characterized by Oil Red O and alizarin red staining, transmission electron microscopy, flow cytometry, nanoparticle tracking analysis and Western blotting. PC12 cells were treated with lipopolysaccharides (LPS), and SCI was established through laminectomy with contusion injury in rats. Annexin-V staining, CCK-8 and EdU incorporation were applied to determine cell apoptosis, viability, and proliferation. Hematoxylin and Eosin, Nissl and TUNEL staining was used to evaluate SCI injury and apoptosis in the spinal cord. Luciferase and chromatin immunoprecipitation assays were applied to evaluate gene interaction. RESULTS: BMSC-derived exosomes facilitated LPS-treated PC12 cell proliferation and inhibited apoptosis by delivering miR-26a-5p. Moreover, BMSC-derived exosomal miR-26a-5p alleviated SCI. Furthermore, miR-26a-5p inhibited EZH2 expression by directly binding to EZH2, and EZH2 inhibited BDNF expression via promoting H3K27me3. Increased phosphorylated CREB enhanced KCC2 transcription and expression by binding to its promoter. Knockdown of miR-26a-5p abrogated BMSC-derived exosome-mediated protection in LPS-treated PC12 cells, but it was reversed by KCC2 overexpression. CONCLUSION: BMSC-derived exosomes carrying miR-26a-5p repressed EZH2 expression to promote BDNF and TrkB expression and CREB phosphorylation and subsequently increase KCC2 expression, thus protecting PC12 cells and ameliorating SCI.

Research and application of deep learning-based sleep staging: Data, modeling, validation, and clinical practice.

Over the past few decades, researchers have attempted to simplify and accelerate the process of sleep stage classification through various approaches; however, only a few such approaches have gained widespread acceptance. Artificial intelligence technology, particularly deep learning, is promising for earning the trust of the sleep medicine community in automated sleep-staging systems, thus facilitating its application in clinical practice and integration into daily life. We aimed to comprehensively review the latest methods that are applying deep learning for enhancing sleep staging efficiency and accuracy. Starting from the requisite "data" for constructing deep learning algorithms, we elucidated the current landscape of this domain and summarized the fundamental modeling process, encompassing signal selection, data pre-processing, model architecture, classification tasks, and performance metrics. Furthermore, we reviewed the applications of automated sleep staging in scenarios such as sleep-disorder screening, diagnostic procedures, and health monitoring and management. Finally, we conducted an in-depth analysis and discussion of the challenges and future in intelligent sleep staging, particularly focusing on large-scale sleep datasets, interdisciplinary collaborations, and human-computer interactions.

Metagenomic insights into the mechanism for the rapid enrichment and high stability of Candidatus Brocadia facilitated by Fe(â ¢).

The rapid enrichment of anammox bacteria and its fragile resistance to adverse environment are the critical problems facing of anammox processes. As an abundant component in anammox bacteria, iron has been proved to promote the activity and growth of anammox bacteria in the mature anammox systems, but the functional and metabolic profiles in Fe(III) enhanced emerging anammox systems have not been evaluated. Results indicated that the relative abundance of functional genes involved in oxidative phosphorylation, nitrogen metabolism, cofactors synthesis, and extracellular polymers synthesis pathways was significantly promoted in the system added with 5 mg/L Fe(III) (R5). These enhanced pathways were crucial to energy generation, nitrogen removal, cell activity and proliferation, and microbial self-defense, thereby accelerating the enrichment of anammox bacteria Ca. Brocadia and facilitating their resistance to adverse environments. Microbial community analysis showed that the proportion of Ca. Brocadia in R5 also increased to 64.42 %. Hence, R5 could adapt rapidly to the increased nitrogen loading rate and increase the nitrogen removal rate by 108 % compared to the system without Fe(III) addition. However, the addition of 10 and 20 mg/L Fe(III) showed inhibitory effects on the growth and activity of anammox bacteria, which exhibited the lower relative abundance of Ca. Brocadia and unstable or even collapsed nitrogen removal performance. This study not only clarified the concentration range of Fe(III) that promoted and inhibited the enrichment of anammox bacteria, but also deepened our understanding of the functional and metabolic mechanisms underlying enhanced enrichment of anammox bacteria by Fe(III), providing a potential strategy to hasten the start-up of anammox from conventional activated sludge.

Reduced functional connectivity of the right dorsolateral prefrontal cortex at rest in obsessive-compulsive disorder.

BACKGROUND: Neuroimaging studies have revealed the role of the right dorsolateral prefrontal cortex (DLPFC) in the neurobiological mechanism of obsessive-compulsive disorder (OCD). However, only a few studies have examined the functional connectivity (FC) pattern of the right DLPFC at rest in OCD. OBJECTIVE: The aim of this research is to examine the FC patterns of the right DLPFC at rest in OCD. METHODS: Twenty-eight medication-free patients with OCD and 20 healthy controls underwent resting-state functional magnetic resonance imaging. Seed-based FC and support vector machine (SVM) were used to analyze the imaging data. RESULTS: The patients with OCD showed reduced FC values in the right middle temporal gyrus (MTG), right superior temporal gyrus, right ventral anterior cingulate cortex (vACC), and left Crus II. No brain regions showed a remarkable difference in FC values in patients with OCD after 8 weeks of medication treatment. The reduced right DLPFC-right MTG and right DLPFC-right vACC connectivities were correlated with the clinical symptoms of OCD. SVM results showed that reduced right DLPFC-right MTG connectivity at rest could predict the therapeutic response to OCD medication. CONCLUSIONS: The findings highlight the important role of the right DLPFC in the pathophysiological mechanism of OCD.