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This review delves into the surface modification of MXenes, underscoring its pivotal role in improving their diverse physicochemical properties, including tailor MXenes’ electrical conductivity, mechanical strength, and wettability. It outlines various surface modification strategies and principles, highlighting their contributions to performance enhancements across diverse applications, including energy storage and conversion, materials mechanics, electronic devices, biomedical sciences, environmental monitoring, and fire-resistant materials. While significant advancements have been made, the review also identifies challenges and future research directions, emphasizing the continued development of innovative materials, methods, and applications to further expand MXenes’ utility and potential.

Background Damage in the ischemic core and penumbra after stroke affects patient prognosis. Microglia immediately respond to ischemic insult and initiate immune inflammation, playing an important role in the cellular injury after stroke. However, the microglial heterogeneity and the mechanisms involved remain unclear. Methods We first performed single-cell RNA-sequencing (scRNA-seq) and spatial transcriptomics (ST) on middle cerebral artery occlusion (MCAO) mice from three time points to determine stroke-associated microglial subclusters and their spatial distributions. Furthermore, the expression of microglial subcluster-specific marker genes and the localization of different microglial subclusters were verified on MCAO mice through RNAscope and immunofluorescence. Gene set variation analysis (GSVA) was performed to reveal functional characteristics of microglia sub-clusters. Additionally, ingenuity pathway analysis (IPA) was used to explore upstream regulators of microglial subclusters, which was confirmed by immunofluorescence, RT-qPCR, shRNA-mediated knockdown, and targeted metabolomics. Finally, the infarct size, neurological deficits, and neuronal apoptosis were evaluated in MCAO mice after manipulation of specific microglial subcluster. Results We discovered stroke-associated microglial subclusters in the brains of MCAO mice. We also identified novel marker genes of these microglial subclusters and defined these cells as ischemic core-associated (ICAM) and ischemic penumbra-associated (IPAM) microglia, according to their spatial distribution. ICAM, induced by damage-associated molecular patterns, are probably fueled by glycolysis, and exhibit increased pro-inflammatory cytokines and chemokines production. BACH1 is a key transcription factor driving ICAM generation. In contrast, glucocorticoids, which are enriched in the penumbra, likely trigger IPAM formation, which are presumably powered by the citrate cycle and oxidative phosphorylation and are characterized by moderate pro-inflammatory responses, inflammation-alleviating metabolic features, and myelinotrophic properties. Conclusions ICAM could induce excessive neuroinflammation, aggravating brain injury, whereas IPAM probably exhibit neuroprotective features, which could be essential for the homeostasis and survival of cells in the penumbra. Our findings provide a biological basis for targeting specific microglial subclusters as a potential therapeutic strategy for ischemic stroke.

Tantalum carbide MXenes, notably Ta4C3Tx and Ta2CTx, exhibit distinctive physicochemical properties that distinguish them from the well-studied Ti3C2Tx MXene. The combination of exceptional electrochemical properties, efficient photothermal conversion, and tunable surface terminations highlights the versatility of Ta-MXenes. These characteristics render them highly valuable for versatile applications. This minireview summarizes recent progress in tantalum carbide MXenes and their composites, focusing on applications in energy storage, conversion, sensing, and biomedicine. First, synthesis methods for tantalum carbide MXenes are summarized. Subsequently, their key properties are discussed, followed by a systematic review of diverse applications. Finally, this review offers a summary and outlook on the challenges and opportunities in the field of tantalum carbide MXenes research.

Inhibiting PD-1:PD-L1 signaling has transformed therapeutic immune restoration. CD4 + T cells sustain immunity in chronic infections and cancer, yet little is known about how PD-1 signaling modulates CD4 + helper T (T H ) cell responses or the ability to restore CD4 + T H -mediated immunity by checkpoint blockade. We demonstrate that PD-1:PD-L1 specifically suppressed CD4 + T H 1 cell amplification, prevents CD4 + T H 1 cytokine production and abolishes CD4 + cytotoxic killing capacity during chronic infection in mice. Inhibiting PD-L1 rapidly restored these functions, while simultaneously amplifying and activating T H 1-like T regulatory cells, demonstrating a system-wide CD4–T H 1 recalibration. This effect coincided with decreased T cell antigen receptor signaling, and re-directed type I interferon (IFN) signaling networks towards dominant IFN-γ-mediated responses. Mechanistically, PD-L1 blockade specifically targeted defined populations with pre-established, but actively suppressed proliferative potential, with limited impact on minimally cycling TCF-1 + follicular helper T cells, despite high PD-1 expression. Thus, CD4 + T cells require unique differentiation and functional states to be targets of PD-L1-directed suppression and therapeutic restoration. Snell et al. examine the heterogeneity of CD4 + T cells in chronic viral infection, showing that PD-L1 blockade enhances a cytotoxic gene program in antigen-specific T H 1 cells and can restore antiviral CD4 + T cell killer function.

Background This study aimed to assess the prognostic significance of serum lipoprotein(a) [Lp(a)] levels regarding overall survival (OS) and progression-free survival (PFS) among patients diagnosed with pancreatic cancer (PC). Methods A retrospective cohort of 364 pathologically confirmed PC patients treated at the Affiliated Hospital of Qingdao University between January 2019 and December 2022 was analyzed. The optimal cutoff for Lp(a) was identified using X-tile software, allowing categorization into high and low Lp(a) groups. To minimize selection bias, propensity score matching (PSM) was utilized. Survival outcomes were compared using Kaplan–Meier curves and log-rank tests. Cox proportional hazards models were applied to identify independent prognostic variables affecting OS and PFS. Results Patients with high Lp(a) had significantly shorter OS and PFS both before and after PSM (post-PSM OS: 12.28 vs. 27.67 months, P  = 0.003; PFS: 7.00 vs. 11.30 months, P  = 0.002). Multivariate Cox analysis confirmed high Lp(a) as an independent predictor of poor OS [HR = 2.11 (1.17–3.81), P  = 0.013] and PFS [HR = 2.14 (1.20–3.83), P  = 0.010]. In the surgical subgroup ( n  = 215), high Lp(a) was also associated with worse OS (16.43 vs. 35.47 months, P  = 0.02) and PFS (8.40 vs. 11.77 months, P  = 0.036). Multivariate analysis in this subgroup showed that high Lp(a) remained an independent risk factor for OS [HR = 2.82 (1.36–5.87), P  = 0.006] and PFS [HR = 2.01 (1.06–3.86), P  = 0.034]. Conclusion Elevated serum Lp(a) is an independent predictor of reduced OS and PFS in patients with pancreatic cancer. In contrast to conventional lipid profiles, the genetic stability of Lp(a) makes it a reliable baseline prognostic marker.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging hemorrhagic fever with a high mortality rate in humans, which is caused by SFTS virus (SFTSV), a novel phlebovirus in the family, is tick borne and endemic in Eastern Asia. Previous study found that SFTSV can infect and replicate in macrophages and . However, the role of macrophages in virus replication and the potential pathogenic mechanisms of SFTSV in macrophage remain unclear. In this study, we provided evidence that the SFTSV infection drove macrophage differentiation skewed to M2 phenotype, facilitated virus shedding, and resulted in viral spread. We showed evidence that miR-146a and b were significantly upregulated in macrophages during the SFTSV infection, driving the differentiation of macrophages into M2 cells by targeting STAT1. Further analysis revealed that the elevated miR-146b but not miR-146a was responsible for IL-10 stimulation. We also found that SFTSV increased endogenous miR-146b-induced differentiation of macrophages into M2 cells mediated by viral non-structural protein (NSs). The M2 skewed differentiation of macrophages may have important implication to the pathogenesis of SFTS.

Objective A lack of education among migrants remains an important but overlooked issue that indirectly contributes to HIV transmission. It is necessary to know who has received HIV education and who has a lower probability of being educated among migrants across different regions and age groups in China. Methods We used pooled data from the 2014 and 2015 Migrants Population Dynamic Monitoring Survey. The study population included 406,937 Chinese migrants. Participants were asked whether they had received any HIV education after migrating to the destination city. Regions were categorized into east-coast, central, northwest, southwest, west-Tibet, west-Uyghur, and northeast regions. Hierarchical logistic regression modeling was conducted to investigate the relationships between the independent variables and HIV education. Results Of 406,937 participants, half (50.6%) had reported receiving HIV education. Individuals in the west-Uyghur region had the highest proportion of receiving HIV education (73.0%), followed by the southwest region (67.9%) and the west-Tibet region (54.8%). Methods of receiving HIV education varied among different age groups. Individuals who were in a region with a higher prevalence of HIV, a lower density of medical professionals, and a higher density of migrants were more likely to receive HIV education. Conclusions The study showed significant regional disparities among migrants in China. More HIV resources need to be allocated to regions with large-scale floating populations, such as the east-coast region. Providing multiple options, including both new and traditional media, for both young and elderly migrants is essential. HIV education should be tailored to the age of migrants with low educational and income levels.

White matter hyperintensity (WMH) is widely observed in the elderly population and serves as a key indicator of cognitive impairment (CI). However, the underlying mechanism remains to be elucidated. Herein, we investigated the topological patterns of resting state functional networks in WMH subjects and the relationship between the topological measures and CI. A graph theory-based analysis was employed in the resting-state functional magnetic resonance scans of 112 subjects (38 WMH subjects with cognitive impairment without dementia (CIND), 36 WMH subjects with normal cognition and 38 healthy controls (HCs), and we found that WMH-CIND subjects displayed decreased global efficiency at the levels of the whole brain, specific subnetworks [fronto-parietal network (FPN) and cingulo-opercular network (CON)] and certain nodes located in the FPN and CON, as well as decreased local efficiency in subnetworks. Our results demonstrated that nodal global efficiency in frontal and parietal regions mediated the impairment of information processing speed related to periventricular WMH (PWMH). Additionally, we performed support vector machine (SVM) analysis and found that altered functional efficiency can identify WMH-CIND subjects with high accuracy, sensitivity and specificity. These findings suggest impaired functional networks in WMH-CIND individuals and that decreased functional efficiency may be a feature of CI in WMH subjects.

Chronic diseases have become serious threats to public health in China; the risk is particularly high for internal migrants. Chronic disease education is a key to the prevention and control of chronic diseases for such population. The national population-based Migrants Population Dynamic Monitoring Survey (MPSMA) was used to examine the current status and delivery methods of chronic disease education among internal migrants, from both provincial level and individual’s level. The study population included 402 587 internal migrants. Multilevel logistic regression was used to investigate factors that were related to chronic diseases education. In total, only 33.9% of the participants received chronic disease education. In the final model, parameter estimates on key variables from both individual and provincial level were significant (P < .001). Participants from provinces with higher level of health care resources and lower density of internal migrants were more likely to receive chronic disease education. The percentage and methods of receiving education varied across different age groups. This study suggests that future chronic disease education in China need to be more focused on areas with high density of internal migrants and younger internal migrants with low level of education and income. Attention should be paid to use tailored education methods to different populations.

Background Immune checkpoint inhibitors (ICIs) demonstrate unprecedented efficacy in multiple malignancies; however, the mechanisms of sensitivity and resistance are poorly understood and predictive biomarkers are scarce. INSPIRE is a phase 2 basket study to evaluate the genomic and immune landscapes of peripheral blood and tumors following pembrolizumab treatment. Methods Patients with incurable, locally advanced or metastatic solid tumors that have progressed on standard therapy, or for whom no standard therapy exists or standard therapy was not deemed appropriate, received 200 mg pembrolizumab intravenously every three weeks. Blood and tissue samples were collected at baseline, during treatment, and at progression. One core biopsy was used for immunohistochemistry and the remaining cores were pooled and divided for genomic and immune analyses. Univariable analysis of clinical, genomic, and immunophenotyping parameters was conducted to evaluate associations with treatment response in this exploratory analysis. Results Eighty patients were enrolled from March 21, 2016 to June 1, 2017, and 129 tumor and 382 blood samples were collected. Immune biomarkers were significantly different between the blood and tissue. T cell PD-1 was blocked (≥98%) in the blood of all patients by the third week of treatment. In the tumor, 5/11 (45%) and 11/14 (79%) patients had T cell surface PD-1 occupance at weeks six and nine, respectively. The proportion of genome copy number alterations and abundance of intratumoral 4-1BB+ PD-1+ CD8 T cells at baseline ( P  < 0.05), and fold-expansion of intratumoral CD8 T cells from baseline to cycle 2–3 ( P  < 0.05) were associated with treatment response. Conclusion This study provides technical feasibility data for correlative studies. Tissue biopsies provide distinct data from the blood and may predict response to pembrolizumab.