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Mental disorders and neurological diseases are becoming a rapidly increasing medical burden. Although extensive studies have been conducted, the progress in developing effective therapies for these diseases has still been slow. The current dilemma reminds us that the human being is a superorganism. Only when we take the human self and its partner microbiota into consideration at the same time, can we better understand these diseases. Over the last few centuries, the partner microbiota has experienced tremendous change, much more than human genes, because of the modern transformations in diet, lifestyle, medical care, and so on, parallel to the modern epidemiological transition. Existing research indicates that gut microbiota plays an important role in this transition. According to gut-brain psychology, the gut microbiota is a crucial part of the gut-brain network, and it communicates with the brain via the microbiota-gut-brain axis. The gut microbiota almost develops synchronously with the gut-brain, brain, and mind. The gut microbiota influences various normal mental processes and mental phenomena, and is involved in the pathophysiology of numerous mental and neurological diseases. Targeting the microbiota in therapy for these diseases is a promising approach that is supported by three theories: the gut microbiota hypothesis, the \"old friend\" hypothesis, and the leaky gut theory. The effects of gut microbiota on the brain and behavior are fulfilled by the microbiota-gut-brain axis, which is mainly composed of the nervous pathway, endocrine pathway, and immune pathway. Undoubtedly, gut-brain psychology will bring great enhancement to psychology, neuroscience, and psychiatry. Various microbiota-improving methods including fecal microbiota transplantation, probiotics, prebiotics, a healthy diet, and healthy lifestyle have shown the capability to promote the function of the gut-brain, microbiota-gut-brain axis, and brain. It will be possible to harness the gut microbiota to improve brain and mental health and prevent and treat related diseases in the future.

This study narrows its focus to the Yangtze River Delta, an important region in China known for its advancements in both digital economy and low-carbon technology. In contrast to previous studies, we also examine the heterogeneous effects between central and non-central cities, as well as the role of local financial development, when analyzing the impact of the digital economy on low-carbon innovation. Based on the data of 41 cities from 2011 to 2019, we find a significant direct promoting effect of the digital economy on low-carbon innovation. Furthermore, the development of the digital economy indirectly enhances low-carbon innovation through local financial development. The heterogeneous analysis reveals a positive impact of the digital economy on low-carbon innovation in both central and non-central cities, with a stronger effect observed in non-central cities. These findings suggest several policy recommendations, including promoting digital economy and finance, green finance, and fostering regional integration in the Yangtze River Delta.

Major depression is one of the leading causes of disability, morbidity, and mortality worldwide. The brain–gut axis functions are disturbed, revealed by a dysfunction of the brain, immune system, endocrine system, and gut. Traditional depression treatments all target the brain, with different drugs and/or psychotherapy. Unfortunately, most of the patients have never received any treatment. Studies indicate that gut microbiota could be a direct cause for the disorder. Abnormal microbiota and the microbiota–gut–brain dysfunction may cause mental disorders, while correcting these disturbance could alleviate depression. Nowadays, the gut microbiota modulation has become a hot topic in treatment research of mental disorders. Depression is closely related with the health condition of the brain–gut axis, and maintaining/restoring the normal condition of gut microbiota helps in the prevention/therapy of mental disorders.

Tuft cells are a rare chemosensory lineage that coordinates immune and neural responses to foreign pathogens in mucosal tissues 1 . Recent studies have also revealed tuft-cell-like human tumours 2 , 3 , particularly as a variant of small-cell lung cancer. Both normal and neoplastic tuft cells share a genetic requirement for the transcription factor POU2F3 (refs.  2 , 4 ), although the transcriptional mechanisms that generate this cell type are poorly understood. Here we show that binding of POU2F3 to the uncharacterized proteins C11orf53 and COLCA2 (renamed here OCA-T1/ POU2AF2 and OCA-T2/ POU2AF3 , respectively) is critical in the tuft cell lineage. OCA-T1 and OCA-T2 are paralogues of the B-cell-specific coactivator OCA-B; all three proteins are encoded in a gene cluster and contain a conserved peptide that binds to class II POU transcription factors and a DNA octamer motif in a bivalent manner. We demonstrate that binding between POU2F3 and OCA-T1 or OCA-T2 is essential in tuft-cell-like small-cell lung cancer. Moreover, we generated OCA-T1-deficient mice, which are viable but lack tuft cells in several mucosal tissues. These findings reveal that the POU2F3–OCA-T complex is the master regulator of tuft cell identity and a molecular vulnerability of tuft-cell-like small-cell lung cancer. The POU2F3–OCA-T complex is the master regulator of tuft cell identity and a prominent molecular vulnerability of tuft-cell-like small-cell lung cancer.

Hypoxia is a common feature of solid tumors. It is closely related to tumor progression. Exosomal microRNAs derived from cancers are considered to be mediators between cancer cells and the tumor microenvironment. In addition, the number of tumor-associated macrophages (TAMs) in the tumor microenvironment has also been demonstrated to correlate with tumor development. However, the relationship between tumor-secreted exosomes and TAM polarization under hypoxic conditions during tumor progression is not clear. Herein, we demonstrated that hypoxia induces the high expression of microRNA-940 (miR-940) in exosomes derived from epithelial ovarian cancer (EOC). We also found that miR-940 is highly expressed in exosomes isolated from ascites of EOC patients. Moreover, the overexpression of miR-940 in macrophages delivered by exosomes stimulated M2 phenotype polarization, while the M2 subtype macrophages promoted EOC proliferation and migration. These results highlight the function of hypoxia in enhancing the high level of expression of miR-940 in tumor exosomes taken up by macrophages. We also showed that the tumor-promoting function of miR-940 is mediated by TAM polarization in EOC. These findings show that tumor-derived exosomal miR-940 induced by hypoxia plays an important role in stimulating TAM polarization in the progression of EOC.

Background Studies investigating salivary cortisol level as susceptibility marker for post-traumatic stress disorder (PTSD) produced inconsistent results. The aim of this study was to compare salivary cortisol concentration levels in PTSD patients with those in controls by synthesizing published data. Methods We did a systematic review, meta-analysis and meta-regression of studies comparing concentrations of salivary cortisol between patients with PTSD and controls. The electronic databases of PubMed, Embase, Web of Science and Psyc-ARTICLES were searched for relevant articles. A random-effects model with restricted maximum-likelihood estimator is used to synthesize the effect size (assessed by standardized mean difference). Results A total of 784 articles were identified of which 22 were included in the final analysis. A trend of lower salivary cortisol levels was found in PTSD patients when compared with the controls (SMD = − 0.28, 95% CI-0.53;-0.04, p  = 0.022). Subgroup analysis showed that the salivary cortisol levels were lower in patients with PTSD than in controls in studies conducted after 2007 or in studies using saliva samples collected in the morning. Conclusions The evidence from this meta-analysis supports that salivary samples collected in the morning consistently showed a lower salivary cortisol level in patients with PTSD than in controls, although whether salivary cortisol could be used as a diagnostic tool requires further research.

The present study utilizes the significant differences in θ, α, and β band power spectra observed in electroencephalograms (EEGs) during distracted versus focused driving. Three subtasks, visual distraction, auditory distraction, and cognitive distraction, were designed to appear randomly during driving simulations. The θ, α, and β band power spectra of the EEG signals of the four driving attention states were extracted, and SVM, EEGNet, and GRU-EEGNet models were employed for the detection of the driving attention states, respectively. Online experiments were conducted. The extraction of the θ, α, and β band power spectrum features of the EEG signals was found to be a more effective method than the extraction of the power spectrum features of the whole EEG signals for the detection of driving attention states. The driving attention state detection accuracy of the proposed GRU-EEGNet model is improved by 6.3% and 12.8% over the EEGNet model and PSD_SVM method, respectively. The EEG decoding method combining EEG features and an improved deep learning algorithm, which effectively improves the driving attention state detection accuracy, was manually and preliminarily selected based on the results of existing studies.

Mitophagy is a highly conserved cellular process that maintains the mitochondrial quantity by eliminating dysfunctional or superfluous mitochondria through autophagy machinery. The mitochondrial outer membrane protein BNIP3L/Nix serves as a mitophagy receptor by recognizing autophagosomes. BNIP3L is initially known to clear the mitochondria during the development of reticulocytes. Recent studies indicated it also engages in a variety of physiological and pathological processes. In this review, we provide an overview of how BNIP3L induces mitophagy and discuss the biological functions of BNIP3L and its regulation at the molecular level. We further discuss current evidence indicating the involvement of BNIP3L-mediated mitophagy in human disease, particularly in cancer and neurological disorders.

In this study, effects of continuous cropping on soil properties, enzyme activities, and relative abundance, community composition and diversity of fungal taxa were investigated. Rhizosphere soil from field continuously cropped for one-year, three-year and five-year by Coptis chinensis Franch. was collected and analyzed. Illumina high-throughput sequencing analysis showed that continuous cropping of C. chinensis resulted in a significant and continuous decline in the richness and diversity of soil fungal population. Ascomycota, Zygomycota, Basidiomycota, and Glomeromycota were the dominant phyla of fungi detected in rhizosphere soil. Fungal genera such as Phoma, Volutella, Pachycudonia, Heterodermia, Gibberella, Cladosporium, Trichocladium, and Sporothrix, were more dominant in continuously cropped samples for three-year and five-year compared to that for one-year. By contrast, genera, such as Zygosaccharomyces, Pseudotaeniolina, Hydnum, Umbelopsis, Humicola, Crustoderma, Psilocybe, Coralloidiomyces, Mortierella, Polyporus, Pyrenula, and Monographella showed higher relative abundance in one-year samples than that in three-year and five-year samples. Cluster analysis of the fungal communities from three samples of rhizosphere soil from C. chinensis field revealed that the fungal community composition, diversity, and structure were significantly affected by the continuous cropping. Continuous cropping of C. chinensis also led to significant declines in soil pH, urease, and catalase activities. Redundancy analysis showed that the soil pH had the most significant effect on soil fungal population under continuous cropping of C. chinensis.

Background Improving medical resource utilization is a significant global challenge. In China, the hospital grading system serves as a key policy to promote collaboration and division of labor among institutions of different grades, with the goal of enhancing the overall performance. However, the medical resource utilization in China remains suboptimal. This study examines the relationship between the hospital grading system and medical resource utilization, offering insights for advancing the healthcare system. Methods Using data from 31 provinces in China spanning 2010 to 2019, this study applies a dynamic panel data model to analyze the relationship between the hospital grading system and medical resource utilization. In addition, a mechanism analysis explores how the hospital grading system may influence utilization through the structure of resource allocation. Results The hospital grading system demonstrates a significant negative association with the utilization of both outpatient and inpatient medical resources, with the impact varying across regions and levels of resource endowment. Furthermore, disparities in the allocation of resources between hospitals and primary healthcare institutions constitute a key mechanism through which the hospital grading system undermines overall utilization. Conclusions This study finds that the hospital grading system is associated with a reduction in medical resource utilization in China. The results provide evidence to inform reforms aimed at revising hospital grading system standards, optimizing medical resource allocation and improving overall system performance in China, while also offering potential lessons for other countries facing similar healthcare challenges.