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Infections of central nervous system (ICNSs) are inflammatory diseases caused by infectious agents that can infiltrate the brain and spinal cord through various routes, including the bloodstream, peripheral nerves, or cranial nerves. Exosomes are found in plasma and have the capacity to cross the blood–brain barrier (BBB). Exosome constituents, including lipids, proteins, DNA, and RNA, change significantly over time and are correlated with the course of disease. Circular RNA (circRNA) has become a potential biomarker for various diseases, such as ICNSs. This study explores the diagnostic potential of circRNAs derived from brain‐derived exosomes in ICNSs. Our research shows that the brain‐derived exosomes from patients with CNS illnesses have different patterns of circRNA expression than those from healthy controls. Plasma samples from patients with bacterial ICNSs show significantly elevated levels of hsa_circ__0020840 and hsa_circ_0116108. In contrast, higher expression levels of hsa_circ_0056947 and hsa_circ_0021531 are observed in plasma samples from individuals with viral ICNSs compared to healthy subjects. These observations suggest their potential utility as sensitive and specific biomarkers for these diseases. Moreover, the capacity of circRNAs to be encapsulated within exosomes and released into circulation offers a noninvasive approach for diagnosing ICNSs. These findings highlight the promise of utilizing brain‐derived exosomal circRNAs as novel diagnostic markers for ICNSs, which may have implications for improving patient outcomes and disease management.

PTSD is considered the most common negative psychological reactions among survivors following an earthquake. The present study sought to find out the determinants of PTSD in earthquake survivors using a systematic meta-analysis. Four electronic databases (PubMed, Embase, Web of Science, and PsycInfo) were used to search for observational studies about PTSD following earthquakes. The literature search, study selection, and data extraction were conducted independently by two authors. 52 articles were included in the study. Summary estimates, subgroup analysis, and publication bias tests were performed on the data. The prevalence of PTSD after earthquakes ranged from 4.10% to 67.07% in adults and from 2.50% to 60.00% in children. For adults, the significant predictors were being female, low education level or socio-economic status, prior trauma; being trapped, experiencing fear, injury, or bereavement during the disaster. For children, the significant predictors were being older age, high education level; being trapped, experiencing fear, injury, or bereavement, witnessing injury/death during the earthquakes. Our study provides implications for the understanding of risk factors for PTSD among earthquake survivors. Post-disaster mental health recovery programs that include early identification, on-going monitoring, and sustained psychosocial support are needed for earthquake survivors.

Diabetic kidneys are particularly vulnerable to ischemia/reperfusion injury (I/RI). Although previous research has suggested that the circadian gene brain and muscle ARNT-like 1 (BMAL1) plays a role in regulating renal function, the exact functions and mechanisms of BMAL1 in diabetic renal I/RI remain elusive. In this study, bilateral renal artery ligation and release were performed in non-diabetic (db/+) and diabetic (db/db) mice. In diabetic kidneys, experimental findings demonstrated a significant decrease in BMAL1 expression, along with the inhibition of the HIF-1α/BNIP3 signaling pathway and compromised mitophagy. BMAL1 overexpression alleviated cell damage and apoptosis under high glucose and hypoxia/reoxygenation stimulation. Inhibition of the Hypoxia-inducible factor-1α (HIF-1α)/ B-cell lymphoma-2 interacting protein 3 (BNIP3) pathway by the HIF-1α inhibitor PX-478 intensified cellular damage and reduced the protective effect of BMAL1 overexpression in TCMK-1 cells. These results indicate that BMAL1 regulates mitophagy in diabetic renal I/RI through the HIF-1α/BNIP3 pathway, providing valuable insights for the development of targeted therapies for diabetic renal I/RI.

Diabetic nephropathy, a common and severe complication of diabetes, is the leading cause of end-stage renal disease, ultimately leading to renal failure and significantly affecting the prognosis and lives of diabetics worldwide. However, the complexity of its developmental mechanisms makes treating diabetic nephropathy a challenging task, necessitating the search for improved therapeutic targets. Intercellular communication underlies the direct and indirect influence and interaction among various cells within a tissue. Recently, studies have shown that beyond traditional communication methods, tunnel nanotubes, exosomes, filopodial tip vesicles, and the fibrogenic niche can influence pathophysiological changes in diabetic nephropathy by disrupting intercellular communication. Therefore, this paper aims to review the varied roles of intercellular communication in diabetic nephropathy, focusing on recent advances in this area.

Lipid metabolism and endoplasmic reticulum stress exhibit crosstalk in various cancer types, which are closely associated with the progression of colorectal cancer (CRC). This study constructs a prognostic signature based on lipid metabolism and endoplasmic reticulum stress-related genes (LERGs) for CRC patients, aiming to predict the prognosis and immune response. RNA sequencing and clinical data from the TCGA and GEO databases were analyzed to identify differentially expressed LERGs with prognostic relevance using univariate Cox regression. Subsequently, a risk model was developed using the LASSO regression. CRC patients were stratified into low-risk and high-risk groups based on risk scores, with the high-risk cohort demonstrating a poorer clinical prognosis in multiple databases. The risk model showed robust correlations with clinical features, gene mutations, and treatment sensitivity. Significant differences in immune cell infiltration and the expression of immune-related factors were also detected between risk groups, and elevated scores of cytokines and failure factors were detected in single-cell RNA sequencing analysis. This research indicates that lipid metabolism and endoplasmic reticulum stress in CRC are correlated with tumor progression, an immunosuppressive landscape, and alterations of drug sensitivity. The developed risk model can serve as a powerful prognostic tool, offering critical insights for refining clinical management and optimizing treatment in CRC patients.

Background Viral infections such as influenza have been shown to predispose hosts to increased colonization of the respiratory tract by pathogenic bacteria and secondary bacterial pneumonia. To examine how viral infections and host antiviral immune responses alter the upper respiratory microbiota, we analyzed nasal bacterial composition by 16S ribosomal RNA (rRNA) gene sequencing in healthy adults at baseline and at 1 to 2 weeks and 4 to 6 weeks following instillation of live attenuated influenza vaccine or intranasal sterile saline. A subset of these samples was submitted for microarray host gene expression profiling. Results We found that live attenuated influenza vaccination led to significant changes in microbial community structure, diversity, and core taxonomic membership as well as increases in the relative abundances of Staphylococcus and Bacteroides genera (both p  < 0.05). Hypergeometric testing for the enrichment of gene ontology terms in the vaccinated group reflected a robust up-regulation of type I and type II interferon-stimulated genes in the vaccinated group relative to controls. Translational murine studies showed that poly I:C administration did in fact permit greater nasal Staphylococcus aureus persistence, a response absent in interferon alpha/beta receptor deficient mice. Conclusions Collectively, our findings demonstrate that although the human nasal bacterial community is heterogeneous and typically individually robust, activation of a type I interferon (IFN)-mediated antiviral response may foster the disproportionate emergence of potentially pathogenic species such as S. aureus . Trial registration This study was registered with Clinicaltrials.gov on 11/3/15, NCT02597647 .

Sepsis is a syndrome of organ dysfunction caused by the invasion of pathogenic microorganisms. In clinical practice, patients with sepsis are prone to concurrent acute kidney injury, which has high morbidity and mortality rates. Thus, understanding the pathogenesis of sepsis-associated acute kidney injury is of significant clinical importance. Ferroptosis is an iron-dependent programmed cell death pathway, which is proved to play a critical role in the process of sepsis-associated acute kidney injury through various mechanisms. Epigenetic regulation modulates the content and function of nucleic acids and proteins within cells through various modifications. Its impact on ferroptosis has garnered increasing attention; however, the role of epigenetic regulation targeting ferroptosis in sepsis-associated acute kidney injury has not been fully elucidated. Growing evidence suggests that epigenetic regulation can modulate ferroptosis through complex pathway networks, thereby affecting the development and prognosis of sepsis-associated acute kidney injury. This paper summarizes the impact of ferroptosis on sepsis-associated acute kidney injury and the regulatory mechanisms of epigenetic regulation on ferroptosis, providing new insights for the targeted therapy of sepsis-associated acute kidney injury.

Type 2 diabetes mellitus (T2DM) is a common metabolic disease that is frequently accompanied by multiple complications, including diabetic myopathy, a muscle disorder that is mainly manifested as decreased muscle function and reduced muscle mass. Diabetic myopathy is a relatively common complication among patients with diabetes that is mainly attributed to mitochondrial dysfunction. Therefore, we investigated the mechanisms underlying diabetic myopathy development, focusing on the role of microRNAs (miRs). Zebrafish were fed a high-sugar diet for 8 weeks and immersed in a glucose solution to establish a model of T2DM. Notably, the fish exhibited impaired blood glucose homeostasis, increased lipid accumulation in the skeletal muscles, and decreased insulin levels in the skeletal muscle. Additionally, we observed various symptoms of diabetic myopathy, including a decreased cross-sectional area of skeletal muscle fibers, increased skeletal muscle fibrosis, a significant decline in exercise capacity, and a significant decrease in mitochondrial respiratory function. Mechanistically, bioinformatic analysis combined with various molecular analyses showed that the miR-139-5p/NAMPT pathway was involved in long-term high-glucose-induced mitochondrial dysfunction in the skeletal muscle, leading to diabetic myopathy. Conclusively, this study provides a basis for the development of novel strategies for the prevention and treatment of diabetic myopathy.

Recently, subjective cognitive decline (SCD) has been described as the earliest at-risk state of Alzheimer's disease (AD), and drawn attention of investigators. Studies suggested that SCD-community individuals may constitute a more vulnerable population than SCD-clinic patients, therefore, to investigate the early changes of the brain may provide guidance for treatment of the disease. We sought to investigate the changes of structure and functional connectivity alternation of the hippocampus in individuals with SCD recruited from the community using structural and resting-state functional MRI (fMRI). Thirty-five SCD patients and 32 healthy controls were recruited. Resting-state fMRI data and high-resolution T1-weighted images were collected. Whole-brain voxel-based morphometry was used to examine the brain structural changes. We also used the hippocampal tail and the whole hippocampus as seeds to investigate functional connectivity alternation in SCD. Individuals with SCD showed significant gray matter volume decreases in the bilateral hippocampal tails and enlargement of the bilateral paracentral lobules. We also found that individuals with SCD showed decreased hippocampal tail resting-state functional connectivity (rsFC) with the right medial prefrontal cortex (mPFC) and the left temporoparietal junction (TPJ), and decreased whole hippocampus rsFC with the bilateral mPFC and TPJ. These brain region and FC showing significant differences also showed significantly correlation with Montreal Cognitive Assessment (MoCA) scores. Individuals with SCD recruited from the community is associated with structural and functional changes of the hippocampus, and these changes may serve as potential biomarkers of SCD. The Declaration of Helsinki, and the study was registered in http://www.chictr.org.cn. The Clinical Trial Registration Number was ChiCTR-IPR-16009144.