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Microglia, as immune cells in the central nervous system, possess the ability to adapt morphologically and functionally to their environment. Glymphatic system, the principal waste clearance system in the brain, exhibits circadian rhythms. However, the impact of microglia on the glymphatic system function remains unknown. In this study, we explored the intricate relationship between microglia and the glymphatic system. Examining diurnal patterns, we identified synchronized behaviors in glymphatic activity and microglial morphology, peaking during sleep and exhibiting distinct changes in branching complexity. Depleting microglia using PLX5622 or in P2Y12 knockout mice enhanced glymphatic function. Chemogenetic manipulation of microglia demonstrated that activating HM3D improved glymphatic function, while inhibiting HM4D unexpectedly increased microglial complexity. These findings highlight the dynamic influence of microglia on the glymphatic system. [ABSTRACT FROM AUTHOR]

Donor‐specific HLA antibody (DSA) has been recognised as an independent risk factor for graft failure in patients undergoing haploidentical haematopoietic stem cell transplantation (HID HSCT). Therapeutic plasma exchange (TPE), as a first‐line strategy for DSA desensitisation, can promptly reduce serum DSA levels. This study aimed to investigate DSA characteristics and identify a biomarker predicting the efficacy of DSA desensitisation in patients proceeding to HID HSCT. We retrospectively enrolled 32 patients with DSA from April 2021 to January 2024, and analysed the mean fluorescence intensity (MFI) value of DSA at the different time points of desensitisation treatment. Compared with baseline DSA level before TPE, the median MFI of HLA class I DSA was reduced from 8178.6 to 795.3 (p < 0.001), and HLA class II DSA decreased from 6210.9 to 808.8 (p < 0.001) after TPE. The DSA level in 1:16 diluted pre‐TPE serum correlated well with DSA value in post‐TPE serum (class I, r = 0.85, p < 0.0001; class II, r = 0.94, p < 0.0001), predicting TPE efficacy in 84.4% of patients. Based on the degree of DSA reduction after TPE, patients were divided into complete responders (decreased by >70%), partial responders (decreased by 30 to 70%) and non‐responders (decreased by <30%) and the percentages were 43.8%, 25% and 31.2%, respectively. Non‐responders receiving aggressive immunotherapy had longer overall survival compared to those receiving standard strategies (p < 0.05). The 1:16 diluted pre‐TPE serum may predict the efficacy of TPE and allow for more rational immunotherapy strategy for patients with DSA proceeding to HID HSCT. [ABSTRACT FROM AUTHOR]

LiMnxFe1−xPO4-C cathode materials for lithium ion batteries were synthesized via solid-state method using Li2CO3, MnCO3, NH4H2PO4, FePO4 and sucrose as starting raw materials, followed by high-temperature reduction-annealing. A series of calcination experiments at different temperatures reveal that Mn2+-containing materials exhibit a lower temperature for olivine phase formation, for example LiMn0.5Fe0.5PO4 olivine phase forms at 275 °C, while manganese-free crystalline LiFePO4 generally forms at the required temperature of 350 °C. Increasing Mn2+ content is found to enhance crystallization degree of LiMnxFe1−xPO4 material prepared at lower calcination temperatures. X-ray photoelectron spectroscopy (XPS) results confirm that Mn valence state (+2) remains unchanged up to ~250 °C when calcined in ambient atmosphere. The above-mentioned beneficial effect of manganese on phase formation and crystallization of olivine can be well attributed to the stable nature of Mn2+ and its strong propensity to form olivine phases. [ABSTRACT FROM AUTHOR]

This article, titled "[Retracted] Effect of metformin on cell proliferation, apoptosis, migration and invasion in A172 glioma cells and its mechanisms," was published in Molecular Medicine Reports in 2019. However, it has since been retracted by the journal due to concerns about the authenticity of the data presented. A concerned reader pointed out that the data in Figures 2 and 6 were similar to data from other articles by different authors. The authors were asked for an explanation but did not respond. The journal apologizes for any inconvenience caused. [Extracted from the article]

Melanoma is a highly invasive malignant tumor originating from melanocytes, with increasing incidence in recent years. Ferroptosis is an iron-dependent and non-apoptotic form of programmed cell death characterized by the accumulation of lipid peroxides and reactive oxygen species. Morphologically, ferroptosis exhibits the alteration in cells, such as reduced mitochondrial volume, increased density of bilayer membrane, and a decrease or disappearance of mitochondrial cristae. Ferroptosis has shown tremendous potential and applicability in regulating the development of melanoma. As melanoma progresses, certain biomarkers associated with ferroptosis display characteristic patterns of expression. These changes not only reveal the sensitivity of tumor cells to ferroptosis but also provide potential targets for diagnosis and treatment. Besides, inducing ferroptosis has been well-documented to inhibit the growth of melanoma and enhance the efficacy of tumor immunotherapy. Hence, this review emphasizes the roles and regulatory mechanisms of ferroptosis in melanoma development, the involved immune regulation, as well as the potential for diagnosis and treatment of melanoma. The continuous explorations will endow novel strategies for developing ferroptosis-based therapies for melanoma., Competing Interests: Declaration of competing interest All the authors declare that there is no conflict of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Traditional Chinese medicine (TCM) offers the advantage of effectively relieving rheumatoid arthritis (RA) with minimal side effects. The Juanbi recipe is a commonly utilized TCM treatment for RA, yet its pharmacological mechanism remains unclear. Network pharmacology serves as an effective tool for identifying pharmaceutical ingredients and potential therapeutic targets of TCM, thereby uncovering its mechanisms. This study aimed to identify the core target genes and explore the mechanisms underlying the treatment of RA with the Juanbi recipe., Methods: This study adopted the method of network pharmacology to filter key gene targets of Juanbi recipe in RA treatment. Single-cell ribonucleic acid (RNA) sequencing data was used to screen the key genes to form the core genes of Juanbi recipe in RA treatment. The molecular docking technique was used to verify the core target genes and explore the mechanisms of Juanbi recipe in RA treatment. The RA model of mice was induced by the collagen-induced arthritis and the effect of Juanbi recipe was evaluated by intragastric administrating of extraction of Juanbi recipe. Enzyme linked immunosorbent assay was used to analysis serum inflammatory factors. Hematoxylin and eosin staining was used to evaluate inflammation and immunohistochemical (IHC) staining was used to evaluate core target genes and pathways in synovium of ankle., Results: This study screened out 281 active molecules in Juanbi recipe, found 105 key target genes of Juanbi recipe in RA treatment, and drew an "ingredient - molecule - gene" diagram. Juanbi recipe reduced the levels of serum interleukin (IL)-1 and IL-6, the inflammatory infiltration in synovium, demonstration that Juanbi recipe reduced both systemic and synovial inflammatory response. Single cell RNA sequencing data were used to select six core target genes and six core active molecules of Juanbi recipe in RA treatment. The pathways of Juanbi recipe in RA treatment involved in activator protein-1 ( AP-1 ) and nuclear factor kappa B ( NF-κB ) pathway. Results of western blot and IHC staining showed that Juanbi recipe decreased the expressions of c-jun and p65 , which demonstrated that Juanbi recipe inhibited the expression of AP-1 and NF-κB pathway in RA., Conclusions: The core active molecules of Juanbi recipe could inhibit key factors of AP-1 and NF-κB pathway to inhibit the inflammation, which played a protective role in RA., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aoj.amegroups.com/article/view/10.21037/aoj-23-72/coif). The authors have no conflicts of interest to declare., (2024 Annals of Joint. All rights reserved.)

Steroid-induced osteonecrosis of the femoral head (SONFH) is a progressive disease that leads to an increased disability rate. This study aimed to ascertain biomarkers, infiltrating immune cells, and therapeutic drugs for SONFH. The gene expression profile of the GSE123568 dataset was downloaded from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were identified using the NetworkAnalyst platform. Functional enrichment, protein-protein interaction network (PPI), and module analyses were performed using Metascape tools. An immune cell abundance identifier was used to explore immune cell infiltration. Furthermore, hub genes were identified based on maximal clique centrality (MCC) evaluation using cytoHubba application and confirmed by qRT-PCR using clinical samples. Finally, the L1000 platform was used to determine potential drugs for SONFH treatment. The SONFH mouse model was used to determine the therapeutic effects of aspirin. In total, 429 DEGs were identified in SONFH samples. Functional enrichment analysis showed that these DEGs were enriched in myeloid leukocyte activation and osteoclast differentiation processes. A set of nine immune cell types was confirmed to be markedly different between the SONFH and control samples. All 10 hub genes were significantly highly expressed in the serum of SONFH patients, as shown by qRT-PCR. Finally, the therapeutic effect of aspirin on SONFH was examined in animal experiments. Taken together, our data revealed the hub genes and infiltrating immune cells in SONFH, and we also screened potential drugs for use in SONFH treatment.