Development and Evaluation of a Novel Antibacterial Wound Dressing: A Powder Preparation Based on Cross-Linked Pullulan with Polyhexamethylene Biguanide for Hydrogel-Transition in Advanced Wound Management and Infection Control.

As antibiotic resistance increasingly undermines traditional infection management strategies, there is a critical demand for innovative wound care solutions that address these emerging challenges. This study introduces a novel antibacterial wound dressing based on Cross-Linked Pullulan (Pul) and Polyhexamethylene Biguanide (PHMB) for enhanced wound management and infection control. The dressing's adsorption rate reached 200% of its original weight within 30 min, exceeded 300% after 5 h, and exhibited significant non-Newtonian fluid properties. The dressings were able to release the loaded medication completely within 20 min; additionally, the dressing demonstrated significant antibacterial activity against a broad spectrum of bacteria. Significantly, the therapeutic effects of the Pul-PHMB/GP dressing were evaluated in a mouse model. Compared to untreated wounds, wounds treated with Pul-PHMB/GP exhibited a significant gelation process within 5 min post-treatment and showed a significant increase in wound healing rate within 12 days. This powder preparation overcomes the limitations associated with liquid and gel dressings, notably in storage and precise application, preventing the premature expansion or dissolution often caused by PHMB in high-humidity environments. The powder form can transform into a gel upon contact with wound exudate, ensuring accurate coverage of irregular wounds, such as those from burns or pressure sores, and offers excellent chemical and physical stability in a dry state, which facilitates storage and transport. This makes the dressing particularly suitable for emergency medical care and precision therapy, significantly improving the efficiency and adaptability of wound treatment and providing robust support for clinical treatments and emergency responses.

Yu-Ping-Feng-San alleviates inflammation in atopic dermatitis mice by TLR4/MyD88/NF-κB pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Yu-Ping-Feng-San (YPF) is a traditional Chinese medicine formula that has therapeutic effects on allergic diseases such as allergic rhinitis and asthma. However, its potential efficacy and mechanism in the treatment of atopic dermatitis (AD) has not been extensively illustrated. AIM OF THE STUDY: The purpose of this study was to investigate the efficacy and possible mechanisms of YPF in AD pathogenesis. METHODS: Network pharmacology and GEO data mining were adopted to firstly identify the potential mechanisms of YPF on AD. Then DNCB induced-AD murine model was established to test the efficacy of YPF and verify its effects on inflammatory cytokines and NF-κB pathway. In addition, molecular docking was performed to detect the binding affinity of YPF's active components with NF-κB pathway related molecules. RESULTS: Network pharmacology and human data mining suggested that YPF may act on the NF-κB pathway in AD pathogenesis. With DNCB mice model, we found that YPF significantly improved AD symptoms, reduced SCORAD scores, and alleviated skin tissue inflammation in mice. At the same time, the expression of inflammatory cytokines, TNF-α, sPLA2-IIA and IL-6, was down-regulated. Moreover, YPF suppressed TLR4/MyD88/NF-κB pathway in situ in a dose-dependent manner. Molecular docking further confirmed that seven compounds in YPF had exceptional binding properties with TNF-α, IL-6 and TLR4. CONCLUSION: YPF may help the recovery of AD by inhibiting the TLR4/MyD88/NF-κB pathway, which provides novel insights for the treatment of AD by YPF.

Global supply chains risks and COVID-19: Supply chain structure as a mitigating strategy for small and medium-sized enterprises.

After the COVID-19 pandemic, more research is needed to understand how the impacts of global events differ among alternative network structures in the presence of supply chain risks, and how relevant these potential risk mitigation strategies are for Small and Medium Enterprises(SMEs). Thus, our main motivation is to show how SMEs can configure their supply chains, and cost-effectively mitigate the risk created by major disruptions. We combined a case study with a simulation model. The results suggest the greater usefulness of certain network configuration strategies (e.g., collaboration, multi-sourcing) compared to others during catastrophic events. Our results indicate that SMEs can avoid suffering more harm than larger competitors by adopting strategies consisting of an adequate mix of proactive and reactive elements, and that an effective proactive strategy involves building flexibility by increasing the number of geographically spread supply chain partners, allowing for deeper discounts to preserve demand without hurting profits.

MiR-206 improves intervertebral disk degeneration by targeting GJA1.

BACKGROUND: A large amount of evidence suggested that miRNA was involved in the progression of intervertebral disk degeneration (IDD). The purpose of our study was to explore the function and potential mechanism of miR-206/GJA1 axis in IDD. METHODS: IDD nucleus pulposus (NP) cell model was established through treatment of LPS. IDD rat model was established by annulus fibrosus puncture. The expression of miR-206 and GJA1 was detected by RT-PCR, apoptosis was evaluated by flow cytometry or TUNEL, inflammatory factors were tested by ELISA, extracellular matrix related protein expression was detected by western blot, and HE and safranin-O staining were used to assess the pathological changes of IDD. RESULTS: GJA1 was found to be highly expressed in IDD tissues and LPS-induced NP cells. Down regulation of GJA1 reduced inflammatory factors, inhibited apoptosis and enhanced extracellular matrix in LPS-induced NP cells. MiR-206 was downregulated in IDD tissues and directly targeted GJA1, and the expression of miR-206 was negatively correlated with the expression of GJA1 in IDD tissues. Further, it was demonstrated that overexpression of miR-206 could attenuate LPS-induced NP cell injury by targeting GJA1. In vivo, the upregulation of miR-206 improved IDD and reduced NP cell apoptosis. CONCLUSION: Our study showed that miR-206 reduced the level of inflammatory factors, restrained NP cell apoptosis and increases extracellular matrix by targeting GJA1. These data suggested that miR-206/GJA1 might be potential therapeutic targets for IDD.