Explore the vast range of titles available.

HighlightsThree-dimensional ordered mesoporous carbon spheres modified with ultrafine zinc oxide nanoparticles are successfully prepared.The microwave absorbing performance of zinc oxide/carbon nanocomposites can be controlled through regulating ratio of zinc oxide nanoparticles.Electromagnetic simulation of radar cross section on a complicated groove structure demonstrates the microwave absorbing ability of the carbon based nanocomposites.Currently, electromagnetic radiation and interference have a significant effect on the operation of electronic devices and human health systems. Thus, developing excellent microwave absorbers have a huge significance in the material research field. Herein, a kind of ultrafine zinc oxide (ZnO) nanoparticles (NPs) supported on three-dimensional (3D) ordered mesoporous carbon spheres (ZnO/OMCS) is prepared from silica inverse opal by using phenolic resol precursor as carbon source. The prepared lightweight ZnO/OMCS nanocomposites exhibit 3D ordered carbon sphere array and highly dispersed ultrafine ZnO NPs on the mesoporous cell walls of carbon spheres. ZnO/OMCS-30 shows microwave absorbing ability with a strong absorption (− 39.3 dB at 10.4 GHz with a small thickness of 2 mm) and a broad effective absorption bandwidth (9.1 GHz). The outstanding microwave absorbing ability benefits to the well-dispersed ultrafine ZnO NPs and the 3D ordered mesoporous carbon spheres structure. This work opened up a unique way for developing lightweight and high-efficient carbon-based microwave absorbing materials.

Glioma is the most common type of primary malignant tumor in the central nervous system with limited treatment satisfaction. Finding new therapeutic targets has remained a major challenge. Ferroptosis is a novel and distinct type of programmed cell death, playing a regulatory role in the progression of tumors. However, the role of ferroptosis or ferroptosis-related genes (FRGs) in glioma progression has not been extensively studied. In our study, a novel ferroptosis-related prognostic model, including 7 genes, was established, in which patients classified into the high-risk group had more immuno-suppressive status and worse prognosis. Among these 7 genes, we screened solute carrier family 1 member 5 (SLC1A5), an FRG, as a possible new target for glioma treatment. Our results showed that the expression of SLC1A5 was significantly upregulated in glioblastoma tissues compared with the low-grade gliomas. In addition, SLC1A5 knockdown could significantly inhibit glioma cell proliferation and invasion, and reduce the sensitivity of ferroptosis via the GPX4-dependent pathway. Furthermore, SLC1A5 was found to be related to immune response and SLC1A5 knockdown decreased the infiltration and M2 polarization of tumor-associated macrophages. Pharmacological inhibition of SLC1A5 by V9302 was confirmed to promote the efficacy of anti-PD-1 therapy. Overall, we developed a novel prognostic model for glioma based on the seven-FRGs signature, which could apply to glioma prognostic and immune status prediction. Besides, SLC1A5 in the model could regulate the proliferation, invasion, ferroptosis and immune state in glioma, and be applied as a prognostic biomarker and potential therapeutic target for glioma.

Although astrocytes undergo functional changes in response to brain injury and may be the driving force of subsequent neuronal death, the underlying mechanisms remain incompletely elucidated. Here, we showed that extracellular vesicle (EV)-shuttled miRNA-382-5p may serve as a biomarker for the severity of traumatic brain injury (TBI), as the circulating EV-miRNA-382-5p level was significantly increased in both human patients and TBI model mice. Mechanistically, astrocyte-derived EVs delivered the shuttled miRNA-382-5p to mediate astrocyte–neuron communication, which promoted neuronal mitochondrial dysfunction by inhibiting the expression of optic atrophy-1 (OPA1). Consistent with these findings, genetic ablation of neuronal OPA1 exacerbated mitochondrial damage and neuronal apoptosis in response to TBI. Moreover, engineered RVG-miRNA-382-5p inhibitor-EVs, which can selectively deliver a miRNA-382-5p inhibitor to neurons, significantly attenuated mitochondrial damage and improved neurological function after TBI. Taken together, our data suggest that EV-shuttled miRNA-382-5p may be a critical mediator of astrocyte-induced neurotoxicity under pathological conditions and that targeting miRNA-382-5p-OPA1 signaling has potential for clinical translation in the treatment of traumatic brain injury. Extracellular Vesicles Reveal Key Role in Brain Injury Traumatic brain injury often results in long-term disabilities. This study investigates how astrocytes contribute to nerve cell damage after TBI, focusing on extracellular vesicles and microRNAs, specifically miRNA-382-5p. The research involved blood samples from TBI patients and healthy people, and mouse experiments, to study the effects of astrocyte-derived EVs carrying miRNA-382-5p on nerve cells. The study found that after TBI, astrocytes release EVs with miRNA-382-5p, which disrupts mitochondrial function in nerve cells, causing damage. The study concludes that astrocyte-derived EVs carrying miRNA-382-5p significantly contribute to nerve cell damage after TBI. By inhibiting miRNA-382-5p, such damage can be reduced, offering a new TBI treatment approach. This research enhances our understanding of TBI and offers potential for targeted therapies. Future implications include using miRNA-382-5p as a diagnostic tool or treatment target to improve TBI outcomes. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Passage of systemically delivered pharmacological agents into the brain is largely blocked by the blood-brain-barrier (BBB), an organotypic specialization of brain endothelial cells (ECs). Tumor vessels in glioblastoma (GBM), the most common malignant brain tumor in humans, are abnormally permeable, but this phenotype is heterogeneous and may differ between the tumor's center and invasive front. Here, through single-cell RNA sequencing (scRNA-seq) of freshly isolated ECs from human glioblastoma and paired tumor peripheral tissues, we have constructed a molecular atlas of human brain ECs providing unprecedented molecular insight into the heterogeneity of the human BBB and its molecular alteration in glioblastoma. We identified 5 distinct EC phenotypes representing different states of EC activation and BBB impairment, and associated with different anatomical locations within and around the tumor. This unique data resource provides key information for designing rational therapeutic regimens and optimizing drug delivery.

Astrocytes are essential in maintaining normal brain functions such as blood-brain barrier (BBB) homeostasis and synapse formation as the most abundant cell type in the central nervous system. After the stroke, astrocytes are known as reactive astrocytes (RAs) because they are stimulated by various damage-associated molecular patterns and cytokines, resulting in significant changes in their reactivity, gene expression, and functional characteristics. RAs perform multiple functions after stroke. The inflammatory response of reactive astrocytes may aggravate neuro-inflammation and release toxic factors to exert neurological damage. However, RAs also reduce excitotoxicity and release neurotrophies to promote neuroprotection. Furthermore, RAs contribute to angiogenesis and axonal remodeling to promote neurological recovery. Therefore, reactive astrocytes' biphasic roles and mechanisms make them an effective target for functional recovery after stroke. In this review, we summarized the dynamic functional changes and internal molecular mechanisms of reactive astrocytes after stroke, as well as their therapeutic potential and strategies, in order to comprehensively understand the role of reactive astrocytes in the outcome of stroke disease and provide a new direction for the clinical treatment of stroke.

Due to the challenges in data acquisition, especially for developing countries and at local levels, spatiotemporal evaluation for SDG11 indicators was still lacking. The availability of big data and earth observation technology can play an important role to facilitate the monitoring of urban sustainable development. Taking Guilin, a sustainable development agenda innovation demonstration area in China as a case study, we developed an assessment framework for SDG indicators 11.2.1, 11.3.1, and 11.7.1 at the neighborhood level using high-resolution (HR) satellite images, gridded population data, and other geospatial big data (e.g., road network and point of interest data). The findings showed that the proportion of the population with convenient access to public transport in the functional urban area gradually improved from 42% in 2013 to 52% in 2020. The increase in built-up land was much faster than the increase in population. The areal proportion of public open space decreased from 56% in 2013 to 24% in 2020, and the proportion of the population within the 400 m service areas of open public space decreased from 73% to 59%. The township-level results indicated that low-density land sprawling should be strictly managed, and open space and transportation facilities should be improved in the three fast-growing towns, Lingui, Lingchuan, and Dingjiang. The evaluation results of this study confirmed the applicability of SDG11 indicators to neighborhood-level assessment and local urban governance and planning practices. The evaluation framework of the SDG11 indicators based on HR satellite images and geospatial big data showed great promise to apply to other cities for targeted planning and assessment.

The renovation of old residential quarters often faces challenges such as lack of spatio-temporal coordination and fragmented governance. Integrating theories of whole-cycle management, spatial production, and sustainable development, this study develops a spatio-temporal whole-cycle integrated framework comprising temporal, spatial, and governance dimensions, and delves into its underlying mechanisms and empirical validity. The analysis reveals that the spatio-temporal interaction mechanism maintains a dynamic balance between tasks at different stages and the allocation of spatial resources; the governance empowerment mechanism is underpinned by multi-stakeholder collaboration, institutional support, and digital enablement, while the feedback and optimization mechanism ensures closed-loop control and continuous improvement throughout the renovation process. Finally, a preliminary validation was conducted using the Jinniu Flower Garden project in Shanghai, with the aim of providing theoretical foundations and implementation pathways for the renewal of old residential quarters, thereby promoting a more sustainable governance model for urban regeneration.

Immune thrombocytopenia (ITP), an acquired autoimmune disease, is characterized by immune-mediated platelet destruction. A biomarker is a biological entity that contributes to disease pathogenesis and reflects disease activity. Metabolic alterations are reported to be associated with the occurrence of various diseases. As metabolic biomarkers for ITP have not been identified. This study aimed to identify metabolism-related differentially expressed genes as potential biomarkers for pathogenesis of ITP using bioinformatic analyses.The microarray expression data of the peripheral blood mononuclear cells were downloaded from the Gene Expression Omnibus database (GSE112278 download link: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE112278 ). Key module genes were intersected with metabolism-related genes to obtain the metabolism-related key candidate genes. The hub genes were screened based on the degree function in the coytoscape sofware. The key ITP-related genes were subjected to functional enrichment analysis. Immune infiltration analysis was performed using a single-sample gene set enrichment analysis algorithm to evaluate the differential infiltration levels of immune cell types between ITP patient and control. Molecular subtypes were identified based on the expression of hub genes. The expression of hub genes in the ITP patients was validated using quantitative real-time polymerase chain reaction analysis. This study identified five hub genes ( ADH4 , CYP7A1 , CYP1A2 , CYP8B1 , and NR1H4 ), which were be associated with the pathogenesis of ITP, and two molecular subtypes of ITP. Among these hub genes, CYP7A1 and CYP8B1 involved in cholesterol metabolism,were further verified in clinical samples.

Hemophilia B, an X‐linked recessive coagulation disorder, poses significant risks of life‐threatening intracranial hemorrhage (ICH). This case report details the multidisciplinary rehabilitation of a 41‐year‐old male with moderate hemophilia B (FIX activity: 3.9%) and ICH in a resource‐limited setting. Admitted to a high‐dependency unit postneurosurgical intervention, the patient received low‐dose prophylactic coagulation factor IX (maintained at 34.6%–66.2%) alongside real‐time coagulation monitoring. A stepwise rehabilitation protocol was implemented, including early passive joint mobilization, neuromuscular electrical stimulation, and progressive task‐oriented training, tailored to minimize bleeding risk. Over 7 weeks, the patient achieved marked functional improvement: Activity of Daily Living score increased from 0 to 80, modified Rankin Scale improved from 5 to 3, and Fugl‐Meyer Assessment (FMA) rose from 0 to 60, with no secondary bleeding. This case highlights the feasibility of integrating low‐dose prophylaxis with early rehabilitation in developing countries, offering a cost‐effective model to enhance functional recovery and reduce disability in hemophilia‐related ICH.