Chia Nan University of Pharmacy and Science

Ensuring fast, reliable communication for emergency vehicles is vital in a smart-city vehicular ad hoc network. However, conventional technologies such as dedicated short-range communications and radio links often fail to meet strict low-latency, high-reliability requirements in congested, resource-limited environments. We developed a priority-based power allocation scheme that reserves sufficient transmission power and bandwidth for emergency vehicles while maintaining acceptable service for regular vehicles. Simulation and performance analysis show that the proposed method achieves lower outage probability and higher sum rate than existing resource allocation strategies under various channel conditions and signal-to-noise ratios, providing an effective communication solution for urban emergency services.

The mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in regulating a number of cellular processes, including proliferation, differentiation, apoptosis, and cellular responses to stress. In cancer, abnormal activation of some or all pathways of the MAPK cascade, particularly the RAS/RAF/MEK/ERK and p38/JNK signaling pathways, is common across many cancers as well as in an equal or disproportional measure in tumor initiation and progression. In the context of the tumor microenvironment (TME), the MAPK pathway facilitates complex interactions between cancer cells, stroma, and immune and endothelial cells. These interactions allow for elements of tumorigenesis, such as driving angiogenesis, immune suppression, and remodeling of the extracellular matrix, to all contribute to tumor survival and invasion. Additionally, MAPK signaling programs the response to cytokines and growth factor secretion by the TME beyond direct cellular responses, ultimately remodeling the TME in a favorable way for tumorigenesis. While targeting components of MAPK-related pathways has shown promise in the clinic, intrinsic and acquired resistance continues to develop in response to drug therapy composed of compensatory convoluted signaling, the activation of alternate signaling pathways, and TME-induced secondary feedback response. Recent data demonstrate that immune- and stroma-derived signals within the TME can sustain MAPK activity even under pharmacologic inhibition, providing the complexity of achieving durable therapeutic responses. As a result, it is crucial to gain consideration of the connections between MAPK signaling and the TME that may impart for sensitive strategies to elicit sustained drug-resistant treatment responses. Integrative therapies that incorporate MAPK inhibitors in conjunction with immunotherapy approaches, anti-angiogenic therapies, or metabolic modulators are also an important therapeutic strategy to elicit these adaptive pathways. This review will summarize our current understanding of the complex role of MAPK signaling in the TME, as well as propose broad ideas and potential future manipulation of MAPK-coordinated TME approaches for novel, durable cancer therapies.

Dementia is the most common neurodegenerative disease, but the risk factors associated with its progression remain incompletely understood. Identifying clinical and medication-related determinants of cognitive decline may inform patient management and guide treatment strategies. Individuals with dementia who underwent paired Mini-Mental State Examination (MMSE) assessments between 2013 and 2019 were identified from the Taipei Medical University Clinical Research Database. To ensure adequate follow-up, paired assessments were required to be at least 90 days apart, with an actual mean follow-up interval of 21.5 ± 18.0 months. Demographic data, comorbidities, medication prescriptions, and blood biochemistry results were extracted. Generalized estimating equations were applied to evaluate associations between these factors and MMSE changes. A total of 3,054 individuals with dementia were included (mean age 78.0 ± 9.2 years, 61.1% women). The mean baseline MMSE score was 18.5 ± 6.7 and it declined to 16.0 ± 7.5 at follow-up. Male sex was significantly associated with greater MMSE decline (estimate: -0.920, 95% CI: -1.552 to -0.289, p = 0.004). Antidementia medications were significantly associated with less decline in MMSE scores (estimate: 1.245, 95% CI: 0.676 to 1.815, p < 0.001). In contrast, non-aspirin antiplatelet agent use was associated with a greater decline among men (estimate: -1.346, 95% CI: -2.518 to -0.173, p = 0.025). These findings highlighted that both clinical and pharmacological factors influence cognitive decline in dementia. Antidementia medications were linked to slower deterioration, supporting their role in disease management. Conversely, the association of non-aspirin antiplatelet agents with faster decline in men suggested potential adverse effects that warrant further investigation. In this large real-world cohort, sex and medication use were key determinants of cognitive decline in dementia. Antidementia medications mitigated decline. Notably, only non-aspirin antiplatelet agents, but not aspirin, were associated with greater cognitive decline in men., underscoring the need for personalized treatment approaches.

Lung cancer (LC) represents a major and growing challenge in global healthcare, necessitating the exploration of innovative therapeutic strategies. In this context, nanoparticles (NPs) have emerged as promising platforms for enhancing treatment efficacy and improving patient outcomes. The present study investigated the cytotoxic effects of chitosan-functionalized mesoporous silica nanoparticles (MSNs) co-loaded with chrysin (Chr) and quercetin (Qur)—denoted as Chr–Qur@MSNs–Chi—on A549 lung cancer cells. Chr–Qur@MSNs–Chi NPs were synthesized and characterized using dynamic light scattering (DLS), Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy (SEM). Cell viability and apoptosis-related gene expression were evaluated using the MTT assay and quantitative real-time PCR (qRT-PCR), respectively.The synthesized NPs were spherical, with an average size range of 80–110 nm, and exhibited no detectable impurities. The DLS analysis indicated a particle size of approximately 110 nm and a zeta potential of − 36.5 mV. The MTT assay revealed IC₅₀ values of 1 µM and 2 µM after 24 and 48 h of treatment, respectively. Furthermore, Chr–Qur@MSNs–Chi induced greater cell cycle arrest at the G0/G1 phase compared to the free Chr–Qur combination. Gene expression analysis demonstrated significant upregulation of p53, Bax, and Fas (2.1-, 2.2-, and 2.4-fold, respectively), alongside downregulation of Cyclin D1, pRB, and Bcl-2 (0.6-, 0.8-, and 0.7-fold, respectively), indicating strong apoptotic effects (P < 0.001). These findings suggest that Chr–Qur@MSNs–Chi nanoparticles exhibit potent anticancer activity against A549 human lung cancer cells, likely through the induction of apoptosis and modulation of apoptosis-related gene expression pathways.