Maxillofacial bone defects can severely impact quality of life by impairing physiological functions such as chewing, breathing, swallowing, and pronunciation. Polyether ether ketone (PEEK) is commonly used for the repair of maxillofacial defects due to its mechanical adaptability, while its osteogenic properties still need refinement. Herein, we have utilized the piezoelectric effect exhibited by barium titanate (BTO) under low-intensity pulsed ultrasound (LIPUS) to develop an ultrasound responsive PEEK (PDA@BTO-SPEEK, PBSP) through the mediating effect of polydopamine (PDA), for repairing maxillofacial bone defects. After modification by PDA@BTO, PBSP possesses better hydrophilicity, which is conducive to cell growth and adhesion. Simultaneously, by virtue of the piezoelectric characteristics of BTO, PBSP obtains a piezoelectric coefficient that matches the bone cortex. Notably, when PBSP is stimulated by LIPUS, it can generate stable electricity and effectively accelerate the osteogenic differentiation of osteoblasts through the regulation of the Piezo1-induced calcium (Ca2+) influx and Akt/GSK3β/β-catenin pathway. In addition, PBSP presents satisfactory therapeutic effects in rat skull defect models, and its osteogenic efficiency can be further improved under LIPUS stimulation with high tissue penetration. Collectively, PBSP + LIPUS exhibits great potential as a promising alternative strategy for the repair of maxillofacial bone defects.

Background: High fasting plasma glucose (HFPG) is the leading risk factor contributing to the increase of stroke burden in the past three decades. However, the global distribution of stroke burden specifically attributable to HFPG was not studied in depth. Therefore, we analyzed the HFPG‐attributable burden in stroke and its subtypes in 204 countries and territories from 1990 to 2019.Methods: Detailed data on stroke burden attributable to HFPG were obtained from the Global Burden of Disease Study 2019. The numbers and age‐standardized rates of stroke disability‐adjusted life years (DALYs), deaths, years lived with disability, and years of life lost between 1990 and 2019 were estimated by age, sex, and region.Results: In 2019, the age‐standardized rate of DALYs (ASDR) of HFPG‐attributable stroke was 354.95 per 100 000 population, among which 49.0% was from ischemic stroke, 44.3% from intracerebral hemorrhage, and 6.6% from subarachnoid hemorrhage. The ASDRs of HFPG‐attributable stroke in lower sociodemographic index (SDI) regions surpassed those in higher SDI regions in the past three decades. Generally, the population aged over 50 years old accounted for 92% of stroke DALYs attributable to HFPG, and males are more susceptible to HFPG‐attributable stroke than females across their lifetime.Conclusions: Successful key population initiatives targeting HFPG may mitigate the stroke disease burden. Given the soaring population‐attributable fractions of HFPG for stroke burden worldwide, each country should assess its disease burden and determine targeted prevention and control strategies.

Elevated polyamine levels are required for tumor transformation and development; however, expression patterns of polyamines and their diagnostic potential have not been investigated in oral squamous cell carcinoma (OSCC), and its impact on prognosis has yet to be determined. A total of 440 OSCC samples and clinical data were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). Consensus clustering was conducted to classify OSCC patients into two subgroups based on the expression of the 17 polyamine regulators. Polyamine-related differentially expressed genes (PARDEGs) among distinct polyamine clusters were determined. To create a prognostic model, PARDEGs were examined in the training cohorts using univariate-Lasso-multivariate Cox regression analyses. Six prognostic genes, namely, “CKS2,” “RIMS3,” “TRAC,” “FMOD,” CALML5,” and “SPINK7,” were identified and applied to develop a predictive model for OSCC. According to the median risk score, the patients were split into high-risk and low-risk groups. The predictive performance of the six gene models was proven by the ROC curve analysis of the training and validation cohorts. Kaplan–Meier curves revealed that the high-risk group had poorer prognosis. Furthermore, the low-risk group was more susceptible to four chemotherapy drugs according to the IC50 of the samples computed by the “pRRophetic” package. The correlation between the risk scores and the proportion of immune cells was calculated. Meanwhile, the tumor mutational burden (TMB) value of the high-risk group was higher. Real-time quantitative polymerase chain reaction was applied to verify the genes constructing the model. The possible connections of the six genes with various immune cell infiltration and therapeutic markers were anticipated. In conclusion, we identified a polyamine-related prognostic signature, and six novel biomarkers in OSCC, which may provide insights to identify new treatment targets for OSCC.

A PVA-based soluble microneedle patch (Fe₃O₄ + VC-MNs) is constructed to consume excessive GSH in the tumor microenvironment and supply H₂O₂ for Fe₃O₄-induced Fenton reaction, thus promoting the production of lethal ˙OH for OSCC treatment.

Dysregulation of non‐coding RNAs (ncRNAs) has been proved to play important roles in oral squamous cell carcinoma (OSCC). This study aimed to determine the combined role of lncRNA TUG1, miR-593-3p, and MAPK signaling in oral squamous cell carcinoma (OSCC) development. Here, we found that TUG1 was up-regulated in OSCC tissues and cell lines. Silencing TUG1 suppressed proliferation migration, invasion and promoted apoptosis of OSCC cells. We also validated that knockdown of TUG1 suppressed MAPK signaling pathway and inhibited EMT process in OSCC cells. Then, a novel LncRNA TUG1/ miR-593-3p/MAPK axis was verified to rescue cell viability in OSCC cells. Mechanistically, miR-593-3p bound to lncRNA TUG1, and lncRNA TUG1 positively regulated MAPK related proteins through acting as RNA sponger for miR-593-3p. Further gain- and loss-of-function experiments evidenced that the protective effects of lncRNA TUG1 knock-down on OSCC cells were abrogated by silencing miRNA-593-3p. The OSCC nude mice model experiments demonstrated that depletion of TUG1 further inhibited tumor growth. In conclusion, appropriate diagnostic biomarkers and therapies for OSCC can be identified by targeting the TUG1/miR-593-3p/MAPK axis.