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Abstract Background Cervical and breast cancers are among the top 4 leading causes of cancer-related mortality in women. This study aimed to examine age-specific temporal trends in mortality for cervical and breast cancers in urban and rural areas of China from 2009 to 2021. Methods Age-specific mortality data for cervical and breast cancers among Chinese women aged 20–84 years were obtained from China’s National Disease Surveillance Points system spanning the years 2009 to 2021. Negative binomial regression models were utilized to assess urban–rural differences in mortality rate ratios, while Joinpoint models with estimated average annual percent changes (AAPC) and slopes were employed to compare temporal trends and the acceleration of mortality rates within different age groups. Results From 2009 to 2021, there was a relative increase in age-specific mortality associated with the two cancers observed in rural areas compared with urban areas. A rising trend in the screening age of 35–64 [AAPC: 4.0%, 95% confidence interval (CI) 0.5–7.6%, P = 0.026] for cervical cancer was noted in rural areas, while a stable trend (AAPC: − 0.7%, 95% CI − 5.8 to 4.6%, P = 0.78) was observed in urban areas. As for breast cancer, a stable trend (AAPC: 0.3%, 95% CI − 0.3 to 0.9%, P = 0.28) was observed in rural areas compared to a decreasing trend (AAPC: − 2.7%, 95% CI − 4.6 to − 0.7%, P = 0.007) in urban areas. Urban–rural differences in mortality rates increased over time for cervical cancer but decreased for breast cancer. Mortality trends for both cervical and breast cancers showed an increase with age across 4 segments, with the most significant surge in mortality observed among the 35–54 age group across urban and rural areas, periods, and regions in China. Conclusions Special attention should be given to women aged 35–54 years due to mortality trends and rural–urban disparities. Focusing on vulnerable age groups and addressing rural–urban differences in the delivery of cancer control programs can enhance resource efficiency and promote health equity.

Abstract Background Osteoporosis is a chronic bone disease characterized by bone loss and decreased bone strength. However, current anti‐resorptive drugs carry a risk of various complications. The deep learning‐based efficacy prediction system (DLEPS) is a forecasting tool that can effectively compete in drug screening and prediction based on gene expression changes. This study aimed to explore the protective effect and potential mechanisms of cinobufotalin (CB), a traditional Chinese medicine (TCM), on bone loss. Methods DLEPS was employed for screening anti‐osteoporotic agents according to gene profile changes in primary osteoporosis. Micro‐CT, histological and morphological analysis were applied for the bone protective detection of CB, and the osteogenic differentiation/function in human bone marrow mesenchymal stem cells (hBMMSCs) were also investigated. The underlying mechanism was verified using qRT‐PCR, Western blot (WB), immunofluorescence (IF), etc. Results A safe concentration (0.25 mg/kg in vivo, 0.05 μM in vitro) of CB could effectively preserve bone mass in estrogen deficiency‐induced bone loss and promote osteogenic differentiation/function of hBMMSCs. Both BMPs/SMAD and Wnt/β‐catenin signaling pathways participated in CB‐induced osteogenic differentiation, further regulating the expression of osteogenesis‐associated factors, and ultimately promoting osteogenesis. Conclusion Our study demonstrated that CB could significantly reverse estrogen deficiency‐induced bone loss, further promoting osteogenic differentiation/function of hBMMSCs, with BMPs/SMAD and Wnt/β‐catenin signaling pathways involved.

Purpose: Mannitol is one of the first-line drugs for reducing cerebral edema through increasing the extracellular osmotic pressure. However, long-term administration of mannitol in the treatment of cerebral edema triggers damage to neurons and astrocytes. Given that neural stem cell (NSC) is a subpopulation of main regenerative cells in the central nervous system after injury, the effect of mannitol on NSC is still elusive. The present study aims to elucidate the role of mannitol in NSC proliferation. Methods: C57 mice were derived from the animal house of Zunyi Medical University. A total of 15 pregnant mice were employed for the purpose of isolating NSCs in this investigation. Initially, mouse primary NSCs were isolated from the embryonic cortex of mice and subsequently identified through immunofluorescence staining. In order to investigate the impact of mannitol on NSC proliferation, both cell counting kit-8 assays and neurospheres formation assays were conducted. The in vitro effects of mannitol were examined at various doses and time points. In order to elucidate the role of Aquaporin 4 (AQP4) in the suppressive effect of mannitol on NSC proliferation, various assays including reverse transcription polymerase chain reaction, western blotting, and immunocytochemistry were conducted on control and mannitol-treated groups. Additionally, the phosphorylated p38 (p-p38) was examined to explore the potential mechanism underlying the inhibitory effect of mannitol on NSC proliferation. Finally, to further confirm the involvement of the p38 mitogen-activated protein kinase-dependent (MAPK) signaling pathway in the observed inhibition of NSC proliferation by mannitol, SB203580 was employed. All data were analyzed using SPSS 20.0 software (SPSS, Inc., Chicago, IL). The statistical analysis among multiple comparisons was performed using one-way analysis of variance (ANOVA), followed by Turkey's post hoc test in case of the data following a normal distribution using a Shapiro-Wilk normality test. Comparisons between 2 groups were determined using Student's t-test, if the data exhibited a normal distribution using a Shapiro-Wilk normality test. Meanwhile, data were shown as median and interquartile range and analyzed using the Mann-Whitney U test, if the data failed the normality test. A p

Personal protective equipment (PPE) has attracted more attention since the outbreak of the epidemic in 2019. Advanced nano techniques, such as electrospinning, can provide new routes for developing novel PPE. However, electrospun antibacterial PPE is not easily obtained. Fibers loaded with photosensitizers prepared using single-fluid electrospinning have a relatively low utilization rate due to the influence of embedding and their inadequate mechanical properties. For this study, monolithic nanofibers and core–shell nanofibers were prepared and compared. Monolithic F1 fibers comprising polyethylene oxide (PEO), poly(vinyl alcohol-co-ethylene) (PVA-co-PE), and the photo-antibacterial agent vitamin K3 (VK3) were created using a single-fluid blending process. Core–shell F2 nanofibers were prepared using coaxial electrospinning, in which the extensible material PEO was set as the core section, and a composite consisting of PEO, PVA-co-PE, and VK3 was set as the shell section. Both F1 and F2 fibers with the designed structural properties had an average diameter of approximately 1.0 μm, as determined using scanning electron microscopy and transmission electron microscopy. VK3 was amorphously dispersed within the polymeric matrices of F1 and F2 fibers in a compatible manner, as revealed using X-ray diffraction and Fourier transform infrared spectroscopy. Monolithic F1 fibers had a higher tensile strength of 2.917 ± 0.091 MPa, whereas the core–shell F2 fibers had a longer elongation with a break rate of 194.567 ± 0.091%. Photoreaction tests showed that, with their adjustment, core–shell F2 nanofibers could produce 0.222 μmol/L ·OH upon illumination. F2 fibers had slightly better antibacterial performance than F1 fibers, with inhibition zones of 1.361 ± 0.012 cm and 1.296 ± 0.022 cm for E. coli and S. aureus, respectively, but with less VK3. The intentional tailoring of the components and compositions of the core–shell nanostructures can improve the process–structure–performance relationship of electrospun nanofibers for potential sunlight-activated antibacterial PPE.