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Soil amendments enhance phytoremediation utilizing trees, have attracted considerable attention because of their low cost, great benefits and huge potential. It’s demonstrated that amendments facilitate the metal immobilization via adjusting soil pH and metal availability, while the underlying mechanism on amendments improving phytoremediation efficiency remains unclear. In our previous studies, the phytoremediation efficiency of Quercus spp. for Cd and Zn was improved by application of soil amendments in a three-year field trial located in Hangzhou, China. Here, we collected the soil samples from the above mentioned experiment and further compared the characteristics of the rhizosphere bacterial community of Quercus texana and Quercus fabri amended with rice straw biochar, palygorskite, and a combination of rice straw biochar and palygorskite in Cd- and Zn-contaminated soils. There were no significant differences in bacterial diversity between the Q. texana and Q. fabri, which were characterized by a high and low accumulation of heavy metals. However, rhizosphere bacterial network of both species exhibited significant responses to the different soil amendments. Combined biochar increased the complexity and stability of bacterial networks, which was manifested mainly as an increase in network cohesion, negative:positive cohesion, and robustness. Partial least squares path modeling demonstrated that network stability was directly influenced by complexity (path coefficient = 0.551, p

Abstract Background and aim Conflicting results have been reported on the association between Parkinson's disease (PD) and cardiovascular disease (CVD) mortality in different populations. Therefore, studying the relationship between PD and CVD mortality is crucial to reduce mortality caused by the former. Methods In this cohort investigation, we enrolled 28,242 participants from the National Health and Nutrition Examination Survey spanning from 2003 to 2018. The 380 cases of PD in the cohort were identified by documenting ‘ANTIPARKINSON AGENTS’ in their reported prescription medications. Mortality outcomes were ascertained by cross-referencing the cohort database with the National Death Index, which was last updated on 31 December 2019. Cardiovascular disease mortality was categorised according to the 10th revision of the International Classification of Diseases by using a spectrum of diagnostic codes. Weighted multivariable Cox regression analysis was used to examine the association between PD and the risk of CVD mortality. Results A total of 28,242 adults were included in the study [mean age, 60.156 (12.55) years, 13,766 men (48.74%)], and the median follow-up period was 89 months. Individuals with PD had an adjusted HR of 1.82 (95% CI, 1.24–2.69; p = 0.002) for CVD mortality and 1.84 (95% CI, 1.44–2.33; p

Abstract Understanding how plant functional traits respond to mining activities and impact metal(loid)s accumulation in dominant species is crucial for exploring the driving mechanisms behind plant community succession and predicting the ecological restoration potential of these plants. In this study, we investigated four dominant herbaceous species (Artemisia argyi, Miscanthus sinensis, Ficus tikoua, and Ageratina adenophora) growing on antimony (Sb) mining sites (MS) with high Sb and arsenic (As) levels, as well as non‐mining sites (NMS). The aim was to analyze the variations in functional traits and their contribution to Sb and As concentrations in plants. Our results indicate that mining activities enhanced soil nitrogen (N) limitation and phosphorus (P) enrichment, while significantly reducing the plant height of three species, except for F. tikoua. The four species absorbed more calcium (Ca) to ensure higher tolerance to Sb and As levels, which is related to the activation of Ca signaling pathways and defense mechanisms. Furthermore, plant Sb and As concentrations were dependent on soil metal(loid) levels and plant element stoichiometry. Overall, these findings highlight the regulatory role of plant element traits in metal(loid) concentrations, warranting widespread attention and further study in the future.

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.

Malignant glioma is one of the most common primary brain tumors that develop via multiple pathways and gene deregulation. MicroRNAs are involved in human cancer development and progression, and their serum expression profiles of glioma patients may be useful for classifying cancers. However, the profile and molecular mechanism of serum microRNAs for human glioma are poorly understood. Thus, it is crucial to analyze microRNA expression in human glioma serum to identify molecular subclasses and early stage of glioma. In this study, we performed microRNA alteration that contributes to glioma profile via analysis of The Cancer Genome Atlas RNA sequencing data and other independent Gene Expression Omnibus microarray data. We identified the glioma-associated novel microRNA as a key regulator of human glioma development and progression. The putative novel miR-1825 was validated by real-time polymerase chain reaction and its expression was significantly decreased in the serum of glioma patients compared with healthy controls. Patients with high miR-1825 expression had a longer survival rate. Interestingly, we found that miR-1825 expression levels were dependent on tumor size and pathological grading in glioma patients, but not associated with other factors including age and T classification. MicroRNA–Gene Ontology network indicated that miR-1825 may play an important role in the development of human glioma including apoptosis, cell proliferation, and invasion. In vitro assays of miR-1825 inhibit U87 cell proliferation and invasion and induce apoptosis. Furthermore, we provide evidence that the tumor-suppressive microRNA miR-1825 controls KLF2 expression. Reporter gene analyses revealed that both microRNAs directly targeted the 3′-untranslated region of KLF2 messenger RNA. These data demonstrated that miR-1825 expression in serum of human glioma was associated with tumorigenesis and miR-1825 may be used as a biomarker for identification of the pathological grade of glioma.

Organised stroke care has become a keystone in delivering efficient and effective treatment to patients with stroke with improved outcomes. Delivering timely acute reperfusion therapy to those with acute ischaemic strokes is key to good recovery. Emergency stroke unit (ESU) is a novel organised stroke care system developed in China. It centralises all necessary procedures for the diagnosis and treatment of acute stroke into one unit that can perform clinical assessment, imaging examination and acute treatments. In ESU, artificial intelligence algorithms are used to aid in reading brain images and making clinical decisions. Therefore, ESU can significantly enhance the efficiency of emergent stroke care. In this guideline, we aim to clarify the concept, construction standards and personnel requirements of an ESU, standardise ESU-based acute stroke triage and treatment workflow, establish metrics of quality control, facilitate the construction and promotion of ESU and continue the improvement of the quality of stroke care.