Gelatin-based nanofiber membranes loaded with curcumin and borneol as a sustainable wound dressing.

Infection is a huge obstacle to wound healing. Thus, to enhance the healing of infected wounds, wound dressings that permit the dual delivery of antimicrobials and antioxidants are highly desirable. In this study, a series of gelatin-based nanofiber membranes with different curcumin contents were fabricated via solution electrospinning. The obtained membranes were characterized in terms of their morphologies, in addition to their physical, mechanical, and in vitro properties. The results showed that the membranes maintained an integrated morphology, excellent water absorption capability, satisfactory mechanical properties, and a high dissolution rate of curcumin. The addition of curcumin and borneol conferred the membranes the ability to inhibit Staphylococcus aureus and eliminate free radicals. Furthermore, cytocompatibility testing using the L929 cell line confirmed the excellent biocompatibility of the membranes. These gelatin-based nanofiber membranes loaded with curcumin and borneol can therefore be considered as promising materials for dressing wounds. Moreover, the use of biodegradable polymers and environmentally sustainable production techniques in this system render it suitable for the commercial manufacture of composite membranes.

Toward a better understanding of type I interferonopathies: a brief summary, update and beyond.

BACKGROUNDS: Type I interferonopathy is a group of autoinflammatory disorders associated with prominent enhanced type I interferon signaling. The mechanisms are complex, and the clinical phenotypes are diverse. This review briefly summarized the recent progresses of type I interferonopathy focusing on the clinical and molecular features, pathogeneses, diagnoses and potential therapies. DATA SOURCES: Original research articles and literature reviews published in PubMed-indexed journals. RESULTS: Type I interferonopathies include Aicardi-Goutières syndrome, spondyloenchondro-dysplasia with immune dysregulation, stimulator of interferon genes-associated vasculopathy with onset in infancy, X-linked reticulate pigmentary disorder, ubiquitin-specific peptidase 18 deficiency, chronic atypical neutrophilic dermatitis with lipodystrophy, and Singleton-Merten syndrome originally. Other disorders including interferon-stimulated gene 15 deficiency and DNAse II deficiency are believed to be interferonopathies as well. Intracranial calcification, skin vasculopathy, interstitial lung disease, failure to thrive, skeletal development problems and autoimmune features are common. Abnormal responses to nucleic acid stimuli and defective regulation of protein degradation are main mechanisms in disease pathogenesis. First generation Janus kinase inhibitors including baricitinib, tofacitinib and ruxolitinib are useful for disease control. Reverse transcriptase inhibitors seem to be another option for Aicardi-Goutières syndrome. CONCLUSIONS: Tremendous progress has been made for the discovery of type I interferonopathies and responsible genes. Janus kinase inhibitors and other agents have potential therapeutic roles. Future basic, translational and clinical studies towards disease monitoring and powerful therapies are warranted.