Hydrogel-based dressing materials offer significant potential in expediting skin wound healing. Nevertheless, they face several challenges: poor adhesion to wound tissues, difficulties in preservation under ambient conditions, and limited multifunctionality to support all wound healing stages. In this work, a dry patch is designed to address these persistent issues by featuring an solid-to-gel transformation and Janus wet tissue adhesiveness. The HGP patch integrates a wet adhesive layer combining dopamine-conjugated hyaluronic acid (HD) and poly(acrylic acid) (PAA), a drug-loading layer comprising gelatin (Gel), and a nonadhesive gelation layer of poly(vinyl alcohol) (PVA) and sodium alginate (SA). This hierarchical structural design confers exceptional wound adhesion, hemostatic capabilities, and antibacterial and antioxidant activities, as well as immune regulatory properties. These attributes collectively support accelerated skin wound healing, particularly in cases complicated by bacterial infections. This research charts an approach to engineer hydrogel-based wound dressings through on-site hydrogel formation, thus advancing the treatment of wounds afflicted with complex infections.
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http://dx.doi.org/10.1021/acsami.4c16041 | DOI Listing |
PLoS One
January 2025
Division of Neurosurgery, Department of Clinical Neuroscience, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom.
Introduction: Given its proximity to the central nervous system, surgical site infections (SSIs) after craniotomy (SSI-CRAN) represent a serious adverse event. SSI-CRAN are associated with substantial patient morbidity and mortality. Despite the recognition of SSI in other surgical fields, there is a paucity of evidence in the neurosurgical literature devoted to skin closure, specifically in patients with brain tumors.
View Article and Find Full Text PDFJ Dermatol
January 2025
Department of Dermatology and Allergology, EB House Austria, Research Program for Molecular Therapy of Genodermatoses, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Recessive dystrophic epidermolysis bullosa (RDEB) is caused by mutations in COL7A1, leading to loss or dysfunction of type-VII collagen (C7), a protein essential for skin stability. Clinically, patients suffer from severe skin blistering, chronic or recurrent wounds, and scarring, which predispose to early onset of aggressive squamous cell carcinoma. Previous studies showed that RDEB-keratinocytes (RDEB-KC) express high levels of matrix-metalloproteinase 9 (MMP-9), a molecule known to play a crucial role in wound chronification if dysregulated.
View Article and Find Full Text PDFArch Dermatol Res
January 2025
Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, 54538, South Korea.
Hair follicle growth depends on the intricate interaction of cells within the follicle and its vascular supply. Current FDA-approved treatments like minoxidil have limitations, including side effects and the need for continuous use. Moracin M, a compound from Moraceae family, was investigated for its effects on hair growth and vascular regeneration.
View Article and Find Full Text PDFAdv Wound Care (New Rochelle)
January 2025
Kenatha Scientific Consulting LLC, Fort Worth, Texas, USA.
SN514 is a thermolysin-like enzyme under development as a debrider. Preclinical and non-clinical studies supported a first in human healthy volunteer study to predict the need for protection of periwound skin. Pharmacologic activity testing compared digestion of collagen, fibrin, and elastin with relevant enzymes.
View Article and Find Full Text PDFAdv Wound Care (New Rochelle)
January 2025
Department of Plastic and Reconstructive Surgery, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Drugs regulating hypoxia-inducible factor (HIF)-1α have not been investigated for wound healing in lymphedema. Therefore, we examined the effects of drug modulation of HIF-1α activity for wound healing in our previously developed mouse model of nonirradiated hind limb lymphedema. Mouse hind limb lymphedema models ( = 17) and a sham group ( = 6) were created using 8- to 10-week-old male C57BL/6N mice.
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