The high incidence, mortality, and disability associated with ischemic stroke pose a significant threat to human health. The intestinal microbiota significantly influences the onset, progression, and prognosis of ischemic stroke. Gut flora plays a pivotal role in brain–gut interactions. The reflection of changes in the gut and brain caused by gut microbes facilitates the investigation of early warning biomarkers and potential therapeutic targets for ischemic stroke. In this narrative review of the relationship between gut microbiota and ischemic stroke, we primarily discuss three topics, grounded in real‐world human and animal studies. First, we examined the relationship between ischemic stroke and intestinal microbiota and its metabolites, delineate the overall characteristics of intestinal microbiota dysregulation in ischemic stroke, and assess the potential clinical value, prevailing research controversies, and unique phenomena of intestinal microbiota metabolites such as trimethylamine N‐oxide and short‐chain fatty acids in ischemic stroke. Second, we explored the potential communication pathways between intestinal flora and ischemic stroke based on the brain–gut axis, encompassing metabolic pathways, immune pathways, and neural pathways. Finally, we encapsulated the factors influencing the severity of ischemic stroke via intestinal flora, the pharmacological and nonpharmacological interventions that modulate intestinal flora in treating ischemic stroke, and the current research landscape of intestinal flora in the context of ischemic stroke sequelae.

Background: The 2023 American Heart Association/American Stroke Association guideline and Wessels et al’s 2024 randomized controlled trial highlight the potential benefits of intracranial nicardipine for aneurysmal subarachnoid hemorrhage (aSAH). This study aims to systematically identify the publication trends and research hotspots in this field through bibliometric analysis. Methods: Relevant publications were sourced from the Web of Science Core Collection (WoSCC). Bibliometric and visualization analyses were conducted using the online tools of the WoSCC database and CiteSpace 6.2.R6. Results: Analysis of 28 articles published by 158 researchers from 55 institutions across 8 countries revealed an intermittent small-scale growth in annual publication volume from 1994 to 2024, with a continuous rise in annual citation volume since 2005, indicating growing interest in the field. Japan, Germany, and the United States of America (USA) were the most prolific and influential countries. Institutions such as Tokyo Women’s Medical University showed particularly significant contributions. Kasuya Hidetoshi was the most prolific author. There was little global collaboration among countries, institutions, and authors, with distinct regional research characteristics: Japan and Germany focused on intracranial implants, while the USA concentrated on intrathecal injections. Major publishing and co-cited journals included Neurocritical Care, Acta Neurochirurgica, Journal of Neurosurgery, and Stroke. Popular keywords in 2024 included “preventing cerebral vasospasm”, “delayed cerebral ischemia”, “outcome events”, and “clinical trials”, revealing current research hotspots. Conclusion: This study maps the global clinical research landscape of intracranial application of nicardipine for aSAH from 1994 to 2024, providing valuable references and guidance for future research.

Background: In recent years, abnormal expression of collagen triple helix repeat containing 1 (CTHRC1) has been found in some tumors, closely related to the poor prognosis of cancer patients. However, the clinical significance of CTHRC1 in gliomas is not completely understood. Methods: We investigated the expression, prognostic value, and potential biological function of CTHRC1 in different types of gliomas through bioinformatics analysis and experimental verification. Results: Bioinformatics analysis revealed several key findings regarding the expression and clinical significance of CTHRC1 in gliomas. First, the analysis demonstrated a positive correlation between CTHRC1 expression and the World Health Organization (WHO) grading of gliomas, a relationship that was validated through immunohistochemistry experiments. In addition, a trend was observed in which CTHRC1 expression increased with the extent of glioma invasion, as supported by Western blot experiments. Subsequent bioinformatics analysis identified the mesenchymal subtype of gliomas as having the highest levels of CTHRC1 expression, a finding reinforced by immunohistochemical staining. Moreover, high CTHRC1 expression was associated with poor prognosis in gliomas and emerged as an independent prognostic factor, with varying impacts on prognosis between low-grade gliomas (LGGs) and glioblastoma (GBM) subgroups. Notably, comparative analysis unveiled distinct patterns of immune infiltration of CTHRC1 in LGG and GBM. Furthermore, alterations in copy number variations and DNA methylation were identified as potential mechanisms underlying elevated CTHRC1 levels in gliomas. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that CTHRC1 and its associated genes mainly function in the extracellular matrix and participate in tumor-related signaling pathways. Conclusions: The CTHRC1 has shown significant clinical utility as a prognostic marker and mesenchymal subtype marker of glioma.