Since zinc oxide (ZnO) nanoparticles (NPs) have been widely applied, the nano community and the general public have paid great attention to the toxicity of ZnO NPs. We detected 20-nm ZnO NPs biotoxicity following nasal exposure utilizing the non-invasive and real-time magnetic resonance imaging (MRI) technique. MR images were scanned in the rat olfactory epithelium (OE) and olfactory bulb (OB) on a 4.7 T scanner following the treatment (as early as 1 day and up to 21 days after), and the histological changes were evaluated. The influence of the size of the ZnO NPs and chemical components was also investigated. Our study revealed that 20-nm ZnO NPs induced obvious structural disruption and inflammation in the OE and OB at the acute stage. The results suggest that the real-time and non-invasive advantages of MRI allow it to observe and assess, directly and dynamically, the potential toxicity of long-term exposure to ZnO NPs in the olfactory system. These findings indicate the size-dependent toxicity of ZnO NPs with respect to the olfactory bulb. Further study is needed to reveal the mechanism behind ZnO NPs’ toxicity.

It was controversial to operate on the primary site of breast cancer (BC) with bone metastasis only. We investigated the impact of surgery on BC patients with bone metastases via a SEER database retrospective analysis. A total of 2917 BC cases with bone metastasis, first diagnosed between 2010 and 2015 in the Surveillance, Epidemiology, and Results Database (SEER) of National Cancer Institute were selected. We assessed the effect of different surgical procedures on survival and prognosis. Compared with the non-surgical group, the primary tumor surgical group showed longer median survival time (χ² = 146.023, P < 0.001), and the breast-conserving subgroup showed the highest median survival time of 70 months (χ² = 157.117, P < 0.001). Compared with the non-surgery group, the median overall survival (OS) of primary surgery group was longer (HR = 0.525, 95%CI = 0.467–0.590, P < 0.001), and the breast-conserving subgroup showed the longest median operative OS (HR = 0.394, 95%CI = 0.325–0.478, P < 0.001). This study showed that primary surgery could improve the median survival time and OS of BC patients with bone metastasis. Moreover, under the condition of low tumor burden, breast conserving surgery was a better choice.

Lobelia nummularia Lam. is a traditional medicinal herb of which the anticancer mechanisms remain largely unexplored. Here, we demonstrated that its ethanolic extract (LNE) exerts potent anti-breast cancer activity by inducing ROS-dependent mitochondrial apoptosis in MDA-MB-231 cells, a mechanism confirmed via rescue experiments with the antioxidant N-acetylcysteine (NAC). This pro-apoptotic program is driven by a dual mechanism: potent suppression of the pro-survival EGFR/PI3K/AKT signaling pathway and simultaneous activation of the TP53-mediated apoptotic cascade, culminating in the cleavage of executor caspase-3. Phytochemical analysis identified numerous flavonoids, and quantitative HPLC confirmed that key bioactive compounds, including luteolin and apigenin, are substantially present in the extract. These mechanisms translated to significant in vivo efficacy, where LNE administration suppressed primary tumor growth and lung metastasis in a 4T1 orthotopic model in BALB/c mice. Furthermore, a validated molecular docking protocol provided a plausible structural basis for these multi-target interactions. Collectively, this study provides a comprehensive, multi-layered validation of LNE’s therapeutic potential, establishing it as a mechanistically well-defined candidate for natural product-based anticancer drug discovery.

Mosquito-borne arthritogenic alphaviruses, including chikungunya virus (CHIKV), Ross River virus (RRV), and Mayaro virus (MAYV), cause acute febrile polyarthralgia and can leave a substantial proportion of patients with persistent or relapsing musculoskeletal disease. In many cohorts, chronic arthritis continues after systemic viremia has declined, suggesting that late tissue pathology is sustained largely by host inflammatory programs rather than by ongoing productive viral replication. This Mini Review examines the NLRP3 inflammasome as a pathogenic node linking viral danger sensing to chronic joint and bone damage, and considers whether this pathway can be targeted to reduce tissue injury while preserving antiviral control. Across CHIKV, RRV, and MAYV models, pattern-recognition receptor signaling provides NF-κB-dependent priming of NLRP3, pro-IL-1β, and pro-IL-18, whereas K ⁺ efflux, mitochondrial stress, reactive oxygen species, and lysosomal disruption promote NLRP3–ASC–caspase-1 assembly in musculoskeletal niches. The resulting IL-1β and IL-18 release and, in selected contexts, pyroptosis-associated amplification propagate inflammatory signaling across monocytes/macrophages, fibroblast-like synoviocytes, osteoblasts, and osteoclast-lineage cells, thereby promoting synovitis, myositis, osteoclastogenesis, and bone loss. Pharmacological and genetic studies indicate partial phenotypic separation between tissue damage and viral control, as NLRP3 inhibition or IL-1 receptor blockade can attenuate musculoskeletal pathology with limited effects on viral burden in available preclinical models. We highlight three priorities for translation: defining post-acute therapeutic windows, stratifying patients using inflammasome and bone-turnover biomarkers, and incorporating bone-centered endpoints such as micro-computed tomography and osteoclast histomorphometry.