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Dominant native plants are crucial for vegetation reconstruction and ecological restoration of mining areas, though their adaptation mechanisms in stressful environments are unclear. This study focuses on the interactions between dominant indigenous species in antimony (Sb) mining area, Artemisia lavandulaefolia and Betula luminifera, and the microbes in their rhizosphere. The rhizosphere microbial diversity and potential functions of both plants were analyzed through the utilization of 16S, ITS sequencing, and metabarcoding analysis. The results revealed that soil environmental factors, rather than plant species, had a more significant impact on the composition of the rhizosphere microbial community. Soil pH and moisture significantly affected microbial biomarkers and keystone species. Actinobacteria, Proteobacteria and Acidobacteriota, exhibited high resistance to Sb and As, and played a crucial role in the cycling of carbon, nitrogen (N), phosphorus (P), and sulfur (S). The genes participating in N, P, and S cycling exhibited metabolic coupling with those genes associated with Sb and As resistance, which might have enhanced the rhizosphere microbes’ capacity to endure environmental stressors. The enrichment of these rhizosphere functional microbes is the combined result of dispersal limitations and deterministic assembly processes. Notably, the genes related to quorum sensing, the type III secretion system, and chemotaxis systems were significantly enriched in the rhizosphere of plants, especially in B. luminifera, in the mining area. The phylogenetic tree derived from the evolutionary relationships among rhizosphere microbial and chloroplast whole-genome resequencing results, infers both species especially B. luminifera, may have undergone co-evolution with rhizosphere microorganisms in mining areas. These findings offer valuable insights into the dominant native rhizosphere microorganisms that facilitate plant adaptation to environmental stress in mining areas, thereby shedding light on potential strategies for ecological restoration in such environments.

Macrophages activation and inflammatory response play crucial roles in intracranial aneurysm (IA) formation and progression. The outcome of ruptured IA is considerably poor, and the mechanisms that trigger IA progression and rupture remain to be clarified, thereby developing effective therapy to prevent subarachnoid hemorrhage (SAH) become difficult. Recently, climbing evidences have been expanding our understanding of the macrophages relevant IA pathogenesis, such as immune cells population, inflammatory activation, intra-/inter-cellular signaling transductions and drug administration responses. Crosstalk between macrophages disorder, inflammation and cellular signaling transduction aggravates the devastating consequences of IA. Illustrating the pros and cons mechanisms of macrophages in IA progression are expected to achieve more efficient treatment interventions. In this review, we summarized the current advanced knowledge of macrophages activation, infiltration, polarization and inflammatory responses in IA occurrence and development, as well as the most relevant NF-κB, signal transducer and activator of transcription 1 (STAT1) and Toll-Like Receptor 4 (TLR4) regulatory signaling modulation. The understanding of macrophages regulatory mechanisms is important for IA patients’ clinical outcomes. Gaining insight into the macrophages regulation potentially contributes to more precise IA interventions and will also greatly facilitate the development of novel medical therapy.

BackgroundHyponatremia is a common electrolyte disturbance in patients with neurological disease; however, its predictive role for outcome in patients with supratentorial spontaneous intracerebral hemorrhage (sICH) is controversial. This study aims to explore the association between hyponatremia within 7 days after bleeding and 90-day mortality in patients with supratentorial sICH.MethodsA retrospective analysis was conducted at our institution. Patients with sICH meeting the inclusion criteria were enrolled in this study. Multivariate regression analyses were performed to determine the predictive value of hyponatremia (serum sodium

Intracranial aneurysm subarachnoid hemorrhage (SAH) is a cerebrovascular disorder associated with high overall mortality. Currently, the underlying mechanisms of pathological reaction after aneurysm rupture are still unclear, especially in the immune microenvironment, inflammation, and relevant signaling pathways. SAH-induced immune cell population alteration, immune inflammatory signaling pathway activation, and active substance generation are associated with pro-inflammatory cytokines, immunosuppression, and brain injury. Crosstalk between immune disorders and hyperactivation of inflammatory signals aggravated the devastating consequences of brain injury and cerebral vasospasm and increased the risk of infection. In this review, we discussed the role of inflammation and immune cell responses in the occurrence and development of aneurysm SAH, as well as the most relevant immune inflammatory signaling pathways [PI3K/Akt, extracellular signal-regulated kinase (ERK), hypoxia-inducible factor-1α (HIF-1α), STAT, SIRT, mammalian target of rapamycin (mTOR), NLRP3, TLR4/nuclear factor-κB (NF-κB), and Keap1/nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/ARE cascades] and biomarkers in aneurysm SAH. In addition, we also summarized potential therapeutic drugs targeting the aneurysm SAH immune inflammatory responses, such as nimodipine, dexmedetomidine (DEX), fingolimod, and genomic variation-related aneurysm prophylactic agent sunitinib. The intervention of immune inflammatory responses and immune microenvironment significantly reduces the secondary brain injury, thereby improving the prognosis of patients admitted to SAH. Future studies should focus on exploring potential immune inflammatory mechanisms and developing additional therapeutic strategies for precise aneurysm SAH immune inflammatory regulation and genomic variants associated with aneurysm formation.