Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function. Additionally, we found that ferrostatin-1 reduced lipid reactive oxygen species production and attenuated the increased expression level of PTGS2 and its gene product cyclooxygenase-2 ex vivo and in vivo. Moreover, ferrostatin-1 in combination with other inhibitors that target different forms of cell death prevented hemoglobin-induced cell death in OHSCs and human induced pluripotent stem cell–derived neurons better than any inhibitor alone. These results indicate that ferroptosis contributes to neuronal death after ICH, that administration of ferrostatin-1 protects hemorrhagic brain, and that cyclooxygenase-2 could be a biomarker of ferroptosis. The insights gained from this study will advance our knowledge of the post-ICH cell death cascade and be essential for future preclinical studies.

Sequencing ribosomal DNA loci, such as ITS and LSU, are among the first steps to characterize and identify newly isolated fungal strains. Substantial doubt has recently been raised concerning the unequivocal suitability of using this sequence information for inferring inter- and intraspecific relationships, as especially the ITS locus was repeatedly shown to harbor high intragenomic plasticity. The evolutionary mechanisms leading to this phenomenon are poorly understood, but this is about to change, owing to the availability of third generation sequencing techniques. The current study attempts a comprehensive analysis of rDNA cistrons in the genomes of over 40 selected species of Hypoxylaceae (Xylariales), using a combination of 2nd generation (Illumina) and 3rd generation sequencing technologies (Oxford Nanopore), along with extensive usage of bioinformatic tools to obtain high-quality genomes. Our findings revealed high intragenomic polymorphisms in distinct Hypoxylaceae species, indicating the presence of deep rDNA paralogs. Phylogenetic inference of the ITS rDNA showed low support for the primary clades within Hypoxylaceae, while inference using the protein encoding gene RPB2 showed better support. We also found that proteinogenic genes are not prone to intraspecific and intragenomic polymorphisms as much as the rDNA loci. Our study highlights the limitations of solely relying on the rDNA cistron as a barcode for fungi. We propose TUB2 as a new primary barcoding marker for Hypoxylaceae and other Xylariales. Moreover, we demonstrate the feasibility to retrieve some DNA loci that had hitherto not been used for classical phylogenetic studies (such as TEF1) in Xylariales directly from genomes without the necessity to work with primers.

Background: Traumatic brain injury (TBI) and spinal cord injury (SCI) are acquired injuries to the central nervous system (CNS) caused by external forces that cause temporary or permanent sensory and motor impairments and the potential for long‐term disability or even death. These conditions currently lack effective treatments and impose substantial physical, social, and economic burdens on millions of people and families worldwide. TBI and SCI involve intricate pathological mechanisms, and the inflammatory response contributes significantly to secondary injury in TBI and SCI. It plays a crucial role in prolonging the post‐CNS trauma period and becomes a focal point for a potential therapeutic intervention. Previous research on the inflammatory response has traditionally concentrated on glial cells, such as astrocytes and microglia. However, increasing evidence highlights the crucial involvement of lymphocytes in the inflammatory response to CNS injury, particularly CD8⁺ T cells and NK cells, along with their downstream XCL1‐XCR1 axis.Objective: This review aims to provide an overview of the role of the XCL1‐XCR1 axis and the T‐cell response in inflammation caused by TBI and SCI and identify potential targets for therapy.Methods: We conducted a comprehensive search of PubMed and Web of Science using relevant keywords related to the XCL1‐XCR1 axis, T‐cell response, TBI, and SCI.Results: This study examines the upstream and downstream pathways involved in inflammation caused by TBI and SCI, including interleukin‐15 (IL‐15), interleukin‐12 (IL‐12), CD8⁺ T cells, CD4⁺ T cells, NK cells, XCL1, XCR1⁺ dendritic cells, interferon‐gamma (IFN‐γ), helper T0 cells (Th0 cells), helper T1 cells (Th1 cells), and helper T17 cells (Th17 cells). We describe their proinflammatory effect in TBI and SCI.Conclusions: The findings suggest that the XCL1‐XCR1 axis and the T‐cell response have great potential for preclinical investigations and treatments for TBI and SCI.

Low back pain (LBP) is quite common in clinical practice, which can lead to long-term bed rest or even disability. It is a worldwide health problem remains to be solved. LBP can be induced or exacerbated by abnormal structure and function of spinal tissue such as intervertebral disc (IVD), dorsal root ganglion (DRG) and muscle; IVD degeneration (IVDD) is considered as the most important among all the pathogenic factors. Inflammation, immune response, mechanical load, and hypoxia etc., can induce LBP by affecting the spinal tissue, among which inflammation and immune response are the key link. Inflammation and immune response play a double-edged sword role in LBP. As the main phagocytic cells in the body, macrophages are closely related to body homeostasis and various diseases. Recent studies have shown that macrophages are the only inflammatory cells that can penetrate the closed nucleus pulposus, expressed in various structures of the IVD, and the number is positively correlated with the degree of IVDD. Moreover, macrophages play a phagocytosis role or regulate the metabolism of DRG and muscle tissues through neuro-immune mechanism, while the imbalance of macrophages polarization will lead to more inflammatory factors to chemotaxis and aggregation, forming an “inflammatory waterfall” effect similar to “positive feedback,” which greatly aggravates LBP. Regulation of macrophages migration and polarization, inhibition of inflammation and continuous activation of immune response by molecular biological technology can markedly improve the inflammatory microenvironment, and thus effectively prevent and treat LBP. Studies on macrophages and LBP were mainly focused in the last 3–5 years, attracting more and more scholars’ attention. This paper summarizes the new research progress of macrophages in the pathogenesis and treatment of LBP, aiming to provide an important clinical prevention and treatment strategy for LBP.