Selvaraj Vimalraj

Massive hemorrhage and impaired wound healing continue to pose critical clinical challenges, particularly due to the limitations of currently available commercial hemostatic dressings, which often exhibit delayed clot formation, poor regenerative potential, and incomplete biodegradation, leading to secondary inflammation. Here, we developed a hemostatic biosponge from aldehyde-functionalized Colocasia esculenta mucilage (OCO) to address these limitations. The introduction of reactive aldehyde groups forms Schiff's base interactions with amine groups present in blood components, facilitating efficient red blood cell entrapment and accelerated coagulation. In vitro studies demonstrated that the sponge effectively absorbs blood, exhibits blood-clotting ability, and is biocompatible. In vivo studies using a rat liver laceration model showed that the OCO sponge achieved hemostasis within 30 ± 2.4 s, significantly faster than the 102 ± 1.3 s required by a commercial gelatin sponge, highlighting its superior hemostatic performance. Furthermore, in vivo full-thickness skin wound studies confirmed enhanced wound healing, with the OCO-treated group exhibiting 1.10-fold greater wound closure by day 18 compared to the gelatin sponge group and showing gradual resorption without adverse tissue reaction, thereby minimizing the risk of chronic inflammation. Therefore, this engineered OCO biosponge represents a promising biomaterial for bleeding control and skin tissue repair in traumatic conditions.

Schematic illustration of the fabrication of the CHNF and its application in wound healing.

Breast cancer is one of the most prevalent cancers worldwide, with triple-negative breast cancer (TNBC) representing a particularly aggressive subtype, making it difficult to treat, and is associated with a poor prognosis. However, chemotherapy is associated with challenges such as drug resistance, off-target toxicity, and limited efficacy, highlighting the need for more effective therapies. Nanocarriers, including liposomes, micelles, and dendrimers, offer improved drug delivery efficacy and reduced toxicity but face challenges in terms of stability and scalability. Metal–organic frameworks (MOFs) have emerged as promising drug delivery systems, particularly for combination therapies to overcome resistance in TNBC. In this study, cobalt–nickel metal–organic frameworks (CNMs) were synthesized and loaded with a combination of cisplatin (Cis), doxorubicin (Dox), and 5-fluorouracil (5-Fu) (MD-CNM) to develop a novel multidrug delivery system. The MD-CNM exhibited high biocompatibility, an efficient drug loading capacity of 95.44 ± 4.05%, and sustained release over 96 h. Moreover, the MD-CNM demonstrated potent cytotoxicity against MDA-MB-231 breast cancer cells, with an IC₅₀ concentration of 461 nM, which is two- to five-fold less than the IC₅₀ value of individual drugs (Cis, Dox, and 5-Fu) loaded with the CNM, indicating enhanced therapeutic efficacy. Additionally, flow cytometry analysis revealed that the MD-CNM induced necrosis (77.59%) and late apoptosis (12.37%) with cell cycle arrest in the G₀/G₁ phase, further confirming its anticancer potential. Furthermore, the ex ovo chorioallantoic membrane (CAM) assay demonstrated that the MD-CNM significantly inhibited tumor angiogenesis by downregulating key pro-angiogenic factors, including vascular endothelial growth factor A (VEGFA), fibroblast growth factor 2 (FGF2), and angiopoietin 1 (ANG1) within the tumor microenvironment. These findings underscore the potential of CNMs as an innovative and efficient multidrug delivery platform for targeted cancer therapy, particularly for treating TNBC, offering a promising alternative to conventional chemotherapy with improved efficacy and reduced toxicity.

Air pollution poses significant risks to public health, with diesel exhaust particles (DEP) contributing to a variety of systemic effects, including potential impacts on bone metabolism. This study investigates DEP's osteogenic and bone toxic effects using both in vitro pre-osteoblast models and in vivo Zebrafish models under healthy and osteoporotic conditions. Pre-osteoblasts treated with DEP exhibited enhanced calcium deposition and upregulated osteogenic markers, including Runx2 and type I collagen, at 25–50 μg ml⁻¹ concentrations. Zebrafish larvae and adult models demonstrated similar concentration-dependent responses, with increased mineralization observed at lower DEP doses and reduced mineralization at higher concentrations (≥100 μg ml⁻¹). Notably, DEP exposure in osteoporotic Zebrafish consistently impaired bone regeneration and fracture healing, as evidenced by diminished calcium deposition, reduced alkaline phosphatase activity, and increased osteoclast activity. Mechanistically, DEP was shown to act through the aryl hydrocarbon receptor (AhR) pathway, disrupting the balance between osteoblast and osteoclast activity. At higher doses or under pathological conditions such as osteoporosis, DEP significantly impairs bone regeneration, delays fracture healing, and promotes bone resorption. The distinct responses elicited by these particles in healthy compared to osteoporotic bone highlight their dualistic nature and underscore the need for condition-specific investigation. This research underscores the importance of the risks associated with chronic DEP exposure in vulnerable populations. Future studies should focus on elucidating the molecular mechanisms underlying DEP's biphasic effects and exploring mitigation strategies for its adverse impacts on bone health.

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