Therapeutic dressings to enhance burn wound repair and regeneration are required. Silk fibroin (SF), a natural protein, induces cell migration and serves as a biomaterial in various dressings. SF dressings usually contain α-helices and β-sheets. The former has been confirmed to improve cell proliferation and migration, but the wound healing effect and related mechanisms of β-sheet SF remain unclear. We investigated the effects of β-sheet SF in vivo and in vitro. Alcohol-treated α-helix SF transformed into the β-sheet form, which promoted granulation formation and re-epithelialization when applied as lyophilized SF dressing (LSFD) in a rat burn model. Our in vitro results showed that β-sheet SF increased human dermal fibroblast (HDF) migration and promoted the expression of extracellular matrix (ECM) proteins (fibronectin and type III collagen), matrix metalloproteinase-12, and the cell adhesion molecule, integrin β1, in rat granulation tissue and HDFs. This confirms the role of crosstalk between integrin β1 and ECM proteins in cell migration. In summary, we demonstrated that β-sheet SF facilitates tissue regeneration by modulating cell adhesion molecules in dermal fibroblasts. LSFD could find clinical application for burn wound regeneration. Moreover, β-sheet SF could be combined with anti-inflammatory materials, growth factors, or antibiotics to develop novel dressings.

To clarify the predictive factors of significant platelet count improvement in thrombocytopenic chronic hepatitis C (CHC) patients. CHC patients with baseline platelet counts of <150 × 10³/μL receiving direct-acting antiviral (DAA) therapy with at least 12-weeks post-treatment follow-up (PTW12) were enrolled. Significant platelet count improvement was defined as a ≥10% increase in platelet counts at PTW12 from baseline. Platelet count evolution at treatment week 4, end-of-treatment, PTW12, and PTW48 was evaluated. This study included 4922 patients. Sustained virologic response after 12 weeks post-treatment was achieved in 98.7% of patients. Platelet counts from baseline, treatment week 4, and end-of-treatment to PTW12 were 108.8 ± 30.2, 121.9 ± 41.1, 123.1 ± 43.0, and 121.1 ± 40.8 × 10³/μL, respectively. Overall, 2230 patients (45.3%) showed significant platelet count improvement. Multivariable analysis revealed that age (odds ratio (OR) = 0.99, 95% confidence interval (CI): 0.99–1.00, p = 0.01), diabetes mellitus (DM) (OR = 1.20, 95% CI: 1.06–1.38, p = 0.007), cirrhosis (OR = 0.66, 95% CI: 0.58–0.75, p < 0.0001), baseline platelet counts (OR = 0.99, 95% CI: 0.98–0.99, p < 0.0001), and baseline total bilirubin level (OR = 0.80, 95% CI: 0.71–0.91, p = 0.0003) were independent predictive factors of significant platelet count improvement. Subgroup analyses showed that patients with significant platelet count improvement and sustained virologic responses, regardless of advanced fibrosis, had a significant increase in platelet counts from baseline to treatment week 4, end-of-treatment, PTW12, and PTW48. Young age, presence of DM, absence of cirrhosis, reduced baseline platelet counts, and reduced baseline total bilirubin levels were associated with significant platelet count improvement after DAA therapy in thrombocytopenic CHC patients.

Severe burn injuries are often associated with excessive and prolonged inflammation, resulting in delayed wound healing and poor tissue regeneration. Accordingly, the development of effective skin substitutes capable of modulating inflammation and promoting tissue repair remains a critical challenge in regenerative medicine. Gelatin methacryloyl (GelMA) has emerged as a promising biomaterial for tissue engineering applications. Moreover, dihydrolipoic acid-modified gold nanoclusters (AuNC@DHLA) have demonstrated anti-inflammatory and regenerative-promoting effects. In this study, we fabricated a bioactive tissue-engineered skin construct by incorporating AuNC@DHLA, fibroblasts, and keratinocytes into a 3D-bioprinted GelMA hydrogel scaffold. The therapeutic efficacy of the cell-laden AuNC@DHLA/GelMA scaffold was evaluated using a murine burn wound model. Furthermore, RNA sequencing was further conducted to explore the molecular mechanisms underlying wound repair, and the findings were subsequently validated by immunohistochemistry. The results demonstrated that the scaffold significantly attenuated local inflammatory responses and accelerated burn wound closure compared with control treatments. Transcriptomic analysis revealed the modulation of inflammation-related and tissue regeneration-associated pathways, which was further confirmed by immunohistochemical analyses. Collectively, these findings indicate that the AuNC@DHLA/GelMA bioengineered skin substitute promotes burn wound healing by regulating the inflammatory microenvironment and enhancing tissue regeneration. This strategy represents a promising therapeutic approach for the treatment of severe burn injuries.