Cutaneous Wound Research Articles

Histone demethylase JARID1C/KDM5C regulates Th17 cells by increasing IL-6 expression in diabetic plasmacytoid dendritic cells.

Plasmacytoid dendritic cells (pDCs) are first responders to tissue injury, where they prime naive T cells. The role of pDCs in physiologic wound repair has been examined, but little is known about pDCs in diabetic wound tissue and their interactions with naive CD4+ T cells. Diabetic wounds are characterized by increased levels of inflammatory IL-17A cytokine, partly due to increased Th17 CD4+ cells. This increased IL-17A cytokine, in excess, impairs tissue repair. Here, using human tissue and murine wound healing models, we found that diabetic wound pDCs produced excess IL-6 and TGF-β and that these cytokines skewed naive CD4+ T cells toward a Th17 inflammatory phenotype following cutaneous injury. Further, we identified that increased IL-6 cytokine production by diabetic wound pDCs is regulated by a histone demethylase, Jumonji AT-rich interactive domain 1C histone demethylase (JARID1C). Decreased JARID1C increased IL-6 transcription in diabetic pDCs, and this process was regulated upstream by an IFN-I/TYK2/JAK1,3 signaling pathway. When inhibited in nondiabetic wound pDCs, JARID1C skewed naive CD4+ T cells toward a Th17 phenotype and increased IL-17A production. Together, this suggests that diabetic wound pDCs are epigenetically altered to increase IL-6 expression that then affects T cell phenotype. These findings identify a therapeutically manipulable pathway in diabetic wounds.

Neohesperidin-loaded microemulsion for improved healing of Acinetobacter baumannii-infected wound

A wound is a complicated process that eventually induces marked tissue destruction, frequently complicated by a secondary bacterial infection. The chief goal of this investigation was to evaluate the plausible wound-healing action of neohesperidin. This was extended to explore the potential of microemulsion systems to boost its wound-healing activity. Two microemulsion systems of wheat germ oil were prepared and characterized. The nominated systems employed tween 80 as surfactant and capryol 90 as co-surfactant at weight ratios of 2:1 and 1:1. The cutaneous wound healing potential of the selected systems in the presence and absence of neohesperidin load were assessed in vivo employing experimentally induced wound model in rats. The induced dorsal skin wounds were additionally infected with Acinetobacter baumannii bacteria. The results reflected a promising wound healing potential of neohesperidin-loaded microemulsion systems and a significant reduction in the infected wound's bacterial count. The selected systems induced significant up-regulation of transforming growth factor (TGF-β), basic fibroblast growth factor (b-FGF), collagen-I, and cytokeratin-14 (K14), while metalloproteinase-1 (MMP-1), interleukin-6 (IL-6), and nuclear factor kabba B (NF-ĸB) levels were reduced. The wound-healing impact of neohesperidin could be confirmed via its angiogenesis, re-epithelization, collagen deposition, and antibacterial, and anti-inflammatory effects.

Modification of mesenchymal stromal cells with silibinin-loaded PLGA nanoparticles improves their therapeutic efficacy for cutaneous wound repair

The use of mesenchymal stromal cells (MSCs) for treating chronic inflammatory disorders, wounds, and ischemia-reperfusion injuries has shown improved healing efficacy. However, the poor survival rate of transplanted cells due to oxidative stress in injured or inflamed tissue remains a significant concern for MSC-based therapies. In this study, we developed a new approach to protect MSCs from oxidative stress, thereby improving their survival in a wound microenvironment and enhancing their therapeutic effect. We produced PLGA nanoparticles loaded with the cytoprotective phytochemical silibinin (SBN), and used them to modify MSCs. Upon internalization, these nanoformulations released SBN, activating the Nrf2/ARE signaling pathway, resulting in threefold reduction in intracellular ROS content and improved cell survival under oxidative stress conditions. Modification of MSCs with SBN-loaded PLGA nanoparticles increased their survival upon transplantation to full-thickness cutaneous wounds and improved wound healing. This study suggests that MSC modification with cytoprotective nanoparticles could be a promising approach for improving wound healing.

SKIN MICROBIOTA AND ITS INTERPLAY WITH WOUND AND BURN HEALING: IMPACT OF EPITHELIAL BIOREGENERATOR

The skin microbiota is intimately coupled with cutaneous health and disease. Interactions between commensal microbiota and the multiple cell types involved in cutaneous wound healing regulate the immune response and promote barrier restoration. This dialog between host cells and the microbiome is dysregulated in chronic wounds and burns. To investigate whether changes in composition were present in the skin microbiome of individuals at risk of developing these lesions. Colonization of the wound and burn with commensal bacteria may promote wound and burn healing by inducing antimicrobial proteins such as Perforin-2, thus stimulating a protective immune response against pathogenic bacteria. Wound and burn infection with pathogenic bacteria results in Perforin-2 suppression in both hematopoietic and nonhematopoietic cells and inhibition of healing. A new study now shows that, in most cases, the causative agents of these infections are bacteria from the patient's own skin. For this reason, authors investigated the impact of Epithelial Bioregenerator to eliminate microorganisms from the chronic wounds and burns.

Emu oil enhances cutaneous wound healing by modulating inflammation through promoting macrophage M2 polarization via MAPK signaling pathway

Persistent inflammation impedes wound healing due to the excessive infiltration of inflammatory cells and the accumulation of pro-inflammatory cytokines. Emu oil (EO) exhibits strong anti-inflammatory properties, but the molecular mechanisms underlying the anti-inflammatory effects on wound healing remain largely unknown. Emu oil promotes wound healing by accelerating the wound closure rate, re-epithelialization, and collagen formation. In vivo, emu oil enhanced the secretion of IL-10 while suppressing IL-1β secretion, promoting the M2 macrophage polarization, and significantly reducing the phosphorylation of JNK and p38. In vitro, emu oil decreased the expression of IL-1β and TNF-α in the RAW264.7 inflammation model while inhibiting the activation of p-JNK and p-p38. The immunomodulatory effect of emu oil was found to be mediated via the suppression of JNK signaling, leading to enhanced anti-inflammatory responses and pro-polarization of M2 macrophages. These findings provide valuable and innovative insights into the therapeutic potential of emu oil in wound healing.

Carbon monoxide-releasing Vehicle CO@TPyP-FeMOFs modulating macrophages phenotype in inflammatory wound healing

Healing of chronic wounds has been critically limited by prolonged inflammation. Carbon monoxide (CO) is a biologically active molecule with high potential based on its efficacy in modulating inflammation, promoting wound healing and tissue remodeling. Strategies to use CO as a gaseous drug to chronic wounds have emerged, but controlling the sustained release of CO at the wound site remains a major challenge. In this work, a porphyrin-Fe based metal organic frameworks, TPyP-FeMOFs was prepared. The synthesized TPyP-FeMOFs was high-temperature vacuum activated (AcTPyP-FeMOFs) and AcTPyP-FeMOFs had a relatively high Fe (II) content. CO sorption isotherms showed that AcTPyP-FeMOFs chemisorbed CO and thus CO release was sustained and prolonged. In vitro evaluation results showed that CO@TPyP-FeMOFs reduced the inflammatory level of lipopolysaccharide (LPS) activated macrophages, polarized macrophages to M2 anti-inflammatory phenotype, and promoted the proliferation of fibroblasts by altering the pathological microenvironment. In vivo study confirmed CO@TPyP-FeMOFs promoted healing in a LPS model of delayed cutaneous wound repair and reduced macrophages and neutrophils recruitment. Both in vitro and in vivo studies verified that CO@TPyP-FeMOFs acted on macrophages by modulating phenotype and inflammatory factor expression. Thus, CO release targeting macrophages and pathological microenvironment modulation presented a promising strategy for wound healing.

Tropoelastin modulates systemic and local tissue responses to enhance wound healing

Wound healing is facilitated by biomaterials-based grafts and substantially impacted by orchestrated inflammatory responses that are essential to the normal repair process. Tropoelastin (TE) based materials are known to shorten the period for wound repair but the mechanism of anti-inflammatory performance is not known. To explore this, we compared the performance of the gold standard Integra Dermal Regeneration Template (Integra), polyglycerol sebacate (PGS), and TE blended with PGS, in a murine full-thickness cutaneous wound healing study. Systemically, blending with TE favorably increased the F4/80+ macrophage population by day 7 in the spleen and contemporaneously induced elevated plasma levels of anti-inflammatory IL-10. In contrast, the PGS graft without TE prompted prolonged inflammation, as evidenced by splenomegaly and greater splenic granulocyte and monocyte fractions at day 14. Locally, the inclusion of TE in the graft led to increased anti-inflammatory M2 macrophages and CD4+T cells at the wound site, and a rise in Foxp3+ regulatory T cells in the wound bed by day 7. We conclude that the TE-incorporated skin graft delivers a pro-healing environment by modulating systemic and local tissue responses. Statement of significanceTropoelastin (TE) has shown significant benefits in promoting the repair and regeneration of damaged human tissues. In this study, we show that TE promotes an anti-inflammatory environment that facilitates cutaneous wound healing. In a mouse model, we find that inserting a TE-containing material into a full-thickness wound results in defined, pro-healing local and systemic tissue responses. These findings advance our understanding of TE's restorative value in tissue engineering and regenerative medicine, and pave the way for clinical applications.

Advances in Quantitative and Qualitative Assessment of Collagen in Cutaneous Wound Healing

Advances in Quantitative and Qualitative Assessment of Collagen in Cutaneous Wound Healing

Cutaneous wound healing in castrated and uncastrated rabbits: Comparative study

Cutaneous wound healing in castrated and uncastrated rabbits: Comparative study

Repurposing of Nano-Engineered Piroxicam as an Approach for Cutaneous Wound Healing

Drug repurposing is a potential strategy to overcome the huge economic expenses of wound healing products. This work aims to develop a topical gel of piroxicam encapsulated into a nanospanlastics vesicular system as an effective, dermal wound dressing. Firstly, piroxicam was entrapped into nanospanlastics formulations and optimized utilizing 23 full factorial experimental designs. The scrutinized factors were Span 60: Edge activator ratio, edge activator type, and permeation enhancer type. The measured responses were vesicle size (VS), polydispersity index (PDI), and% entrapment efficiency (EE). The optimized formula was further adopted into an alginate-pectin gel matrix to maximize adherence to the skin. The rheology and in-vitro release were studied for the developed nanospanlastics gel. Cytotoxicity and wound healing potential using scratch assay were assessed on human adult dermal fibroblast cells. The optimal piroxicam nanospanlastics formula demonstrated a VS of 124.1 ± 1.3 nm, PDI of 0.21 ± 0.01, and EE% of 97.27±0.21%. About 70.0 ± 0.9% and 57.4 ± 0.1% of piroxicam were released from nanospanlastics dispersion and gel within 24 h, respectively. Nanospanlastics gel of piroxicam flowed in a non-Newtonian pseudoplastic shear thinning pattern. It was also biocompatible with the human dermal fibroblast cells and significantly promoted their migration rate which suggests an auspicious cutaneous wound healing aptitude.

Topical Clonidine Accelerates Cutaneous Wound Healing in Diabetic Rats by Regulating the Expression of Related Cytokine Signaling.

Based on the analgesic and anti-inflammatory effects of clonidine in previous studies, we hypothesized that clonidine could accelerate wound healing in rats by regulating the expression of related cytokines. In this study, the wound healing effect of clonidine was evaluated using an excision wound model in diabetic rats and a HaCaT cell model. The wounds were treated daily with topical clonidine. The results analyzed by ImageJ2 software show that the wounds of the rats that were treated with 15 ng/mL clonidine recovered faster, and the wound size was also significantly reduced compared to the control group. Western blot assays determined that clonidine induced an increase in the expression of vascular growth factors, namely, Ang-1, Ang-2, and VEGF. Moreover, clonidine demonstrated a rescuing effect on JAK2 within the JAK/STAT pathway by inhibiting SOCS3 expression, leading to decreased SOCS3 levels and increased expression of JAK2 and phospho-STAT3. Histopathological analysis revealed that clonidine promoted complete epithelial repair and minimized inflammation in skin tissue. Additionally, clonidine stimulated HaCaT cell proliferation in vitro and enhanced cellular energy levels in the presence of AGEs. In conclusion, clonidine promoted vascular growth and wound healing by stimulating the expression of cytokines that are beneficial for wound healing.

Circ-Erbb2ip from adipose-derived mesenchymal stem cell-derived exosomes promotes wound healing in diabetic mice by inducing the miR-670-5p/Nrf1 axis

BackgroundTo investigate the mechanism of exosomes (Exo) secretion by hypoxic pretreated adipose-derived mesenchymal stem cells (ADSCs) promoting skin wound healing in diabetic (DM) mice. MethodsHigh-throughput sequencing was used to investigate abnormal expression of circRNA in hypoxic pretreatment ADSCs exosome (HExo) and ADSCs exosome (Exo). Bioinformatics analysis and luciferase reporting analysis were used to clarify the interacted relationship among circRNA, miRNA and mRNA. EPCs cells were employ to analysis the ROS, inflammatory cytokines expression, angiogenic differentiation function under hypoxic condition by using immunofluorescence, ELISA detection and tube forming experiment. DM ulceration mice model were constructed and the therapeutic effect of Exo were detected using immunohistochemistry, immunofluorescence. ResultsThe result show that HExo have more treatment effect than Exo in promotes cutaneous wound healing of DM mice. High-throughput sequencing found that circ-Erbb2ip play a role in HExo mediated tissues repair. Downregulation circ-Erbb2ip decreased the therapeutic effect of HExo to wound healing in diabetic mice. Bioinformatics analysis and luciferase reporting analysis confirmed that both miR-670-5p and Nrf1 were downstream targets of circ-Erbb2ip. Downregulation of Nrf1 or overexpression of miR-670-5p reversed the protective effect of circ-Erbb2ip to EPCs after exposure to high glucose microenvironment. Upregulation circ-Erbb2ip increased the therapeutic effect of Exo to wound healing in diabetic mice by increased angiogenesis and decreased ROS, inflammatory cytokines expression. ConclusionIn conclusion, ADSC-Exos containing circ-Erbb2ip promotes wound healing by targeting miR-670-5p/Nrf1 pathway, and their effects in promoting soft tissue wound healing warrant further study.

Advanced age worsens respiratory function and pulmonary inflammation after burn injury and this correlates with changes in the fecal microbiome in mice.

Cutaneous burn injury in the elderly is associated with poor clinical outcomes and increased pulmonary-related complications. We and others have shown that burn injury triggers a cascade of inflammatory mediators which increase gut permeability and dysbiosis of the fecal microbiota and this is more dramatic in the aged. Since cross-talk between intestinal microbes and the lung, termed the "gut-lung axis," impacts immunity and homeostasis in the airway, we hypothesized that the increased intestinal dysbiosis in age and burn injury may contribute to excessive pulmonary inflammation and poor prognosis after injury. To explore this hypothesis, we used a clinically relevant murine model of burn injury in which young and aged mice are subjected to a 12% total body surface area dorsal scald burn or sham injury. 24 hours after injury, lung function was assessed and lungs and feces were collected for analysis of inflammatory mediators and fecal microbial species. The results show that, when compared to younger mice, burn injury in aged mice triggers a decline in respiratory function and exacerbates pulmonary inflammation. In addition to heightened levels of the neutrophil recruiting chemokine CXCL1, aged mice displayed a profound increase in the pro-inflammatory protein, calprotectin, in the lung after burn injury. Comparison of the fecal microbiome and inflammatory markers in the lung revealed unique, age-dependent, correlation patterns between individual taxa and pulmonary inflammation. Taken together, these findings suggest that the post-burn dysbiosis of the gut flora in aged mice may contribute to the changes in pulmonary inflammatory profiles.

AT2R Activation Improves Wound Healing in a Preclinical Mouse Model.

Abnormal skin healing resulting in chronic wounds or hypertrophic scarring remains a major healthcare burden. Here, the antifibrotic angiotensin II type 2 receptor (AT2R) signaling pathway was modulated to determine its impact on cutaneous wound healing. Balb/c mice received two splinted full-thickness wounds. Topical treatments with the selective AT2R agonist compound 21 (C21) and/or selective antagonist PD123319 or saline vehicle were administered until sacrifice on post-wounding days 7 or 10. The rate of wound re-epithelialization was accelerated by PD123319 and combination treatments. In vitro, C21 significantly reduced human fibroblast migration. C21 increased both collagen and vascular densities at days 7 and 10 post-wounding and collagen I:III ratio at day 10, while PD123319 and combination treatments decreased them. Genes associated with regeneration and repair were upregulated by C21, while PD123319 treatment increased the expression of genes associated with inflammation and immune cell chemotaxis. C21 treatment reduced wound total leukocyte and neutrophil staining densities, while PD123319 increased these and macrophage densities. Overall, AT2R activation with C21 yields wounds that mature more quickly with structural, cellular, and gene expression profiles more closely approximating unwounded skin. These findings support AT2R signal modulation as a potential therapeutic target to improve skin quality during wound healing.

Analysis of Enhanced Wound Closure Potential of ADSC-Derived Secretome Compared to Aquacel Extra in Diabetic Rats

Background: Diabetes Mellitus (DM) can lead to serious complications, such as Diabetic Foot Ulcers (DFUs). Currently, Aquacel Extra is one of the standard therapies for DFUs, but its efficacy has some limitations that may be overcome by alternative treatments, such as the secretome derived from Adipose-Derived Stem Cells (ADSCs). ADSC secretome has shown promising results in promoting wound healing by enhancing cell proliferation, collagen synthesis, and migration of fibroblasts. Aims: This study aims to compare the effect of the adipose-derived stem cell (ADSC) secretome to Aquacel Extra, a hydrofiber dressing containing gel-forming agents, on wound healing in a diabetic rat model. Aquacel Extra has sodium carboxymethylcellulose fibers, which contribute to its unique properties. Objective: The objective of this study is to compare the wound healing outcome of ADSC secretome and Aquacel Extra in streptozotocin-induced diabetic rats. Methods: Sprague Dawley rats received a single intravenous administration of streptozotocin to induce diabetes mellitus (DM). A full-thickness excisional circular wound was created at the dorsum aspect of the rats two weeks after diabetic induction. Rats were randomly divided into two groups: the Aquacel Extra group, which received the hydrofiber dressing Aquacel Extra containing gel-forming agents, and the secretome group, which received the ADSC secretome on days 0, 3, and 7. The gross examination was performed on days 0, 3, 7, and 14. On day 14, the rats were euthanized, and full-thickness skin biopsies of the wounds were taken for histological and immunohistochemical analysis. Results: The secretome group demonstrated accelerated cutaneous wound healing compared to the Aquacel Extra group, as indicated by faster wound closure (p < 0.05). Hematoxylin and eosin staining revealed a thicker epidermal layer in the secretome group than in the Aquacel Extra group (p < 0.05). The mean histological score of the secretome group was higher at 10 ± 1.73 compared to the score of 8.33 ± 1.52 in the Aquacel Extra group, indicating a more mature tissue architecture. Immunohistochemical analysis showed lower expression of α-smooth muscle actin (α-sma) in the secretome group than in the Aquacel Extra group, which correlated with reduced collagen secretion and deposition in the secretome group, as indicated by Masson’s trichrome staining. Conclusion: The ADSC secretome accelerated the healing of diabetic wounds compared to Aquacel Extra. However, as this study is preliminary, future studies should be conducted similar to this study with a larger sample and wound size. In addition, the optimal dosage of ADSC secretome and the components of the secretome that promoted wound healing should be determined to fully elucidate the clinical potential of ADSC secretome.

Stimulated Full-Thickness Cutaneous Wound Healing with Bioactive Dressings of Zinc and Cobalt Ion-Doped Bioactive Glass-Coated Eggshell Membranes in a Diabetic Rabbit Model.

Eggshell membrane-based biomedical applications have recently received great attention for their wound-healing properties. However, there are limited studies on diabetic wound healing. In this regard, we devised four types of composite eggshell membrane mats with nanoscale coatings of bioactive glass/Zn/Co-doped bioactive glass (ESM + BAG, ESM + ZnBAG, ESM + CoBAG, and ESM + ZnCoBAG) as wound-dressing materials for chronic nonhealing diabetic wounds. A detailed study of the physicochemical properties of the mats was conducted. In vitro studies demonstrated cytocompatibility and viability of human dermal fibroblasts on all four types of mats. The cells also attached finely on the mats with the help of cellular extensions, as evident from scanning electron microscopy (SEM) and rhodamine-phalloidin and Hoechst 33342 staining of cellular components. Endowed with bioactive properties, these mats influenced all aspects of full-thickness skin wound healing in diabetic animal model studies. All of the mats, especially the ESM + ZnCoBAG mat, showed the earliest wound closure, effective renewal, and restructuring of the extracellular matrix in terms of an accurate and timely accumulation of collagen, elastin, and reticulin fibers. Hydroxyproline and sulfated glycosaminoglycans were significantly (p < 0.01, p < 0.05) higher in ESM-ZnCoBAG-treated wounds in comparison to ESM-BAG-treated wounds, which suggests that these newly developed mats have potential as an affordable diabetic wound care solution in biomedical research.

The role of circulating metabolites and gut microbiome in hypertrophic scar: a two-sample Mendelian randomization study.

Hypertrophic scarring is a fibro-proliferative disorder caused by abnormal cutaneous wound healing. Circulating metabolites and the gut microbiome may be involved in the formation of these scars, but high-quality evidence of causality is lacking. To assess whether circulating metabolites and the gut microbiome contain genetically predicted modifiable risk factors for hypertrophic scar formation. Two-sample Mendelian randomization (MR) was performed using MR-Egger, inverse-variance weighting (IVW), Mendelian Randomization Pleiotropy RESidual Sum and Outlier, maximum likelihood, and weighted median methods. Based on the genome-wide significance level, genetically predicted uridine (P = 0.015, odds ratio [OR] = 1903.514, 95% confidence interval [CI] 4.280-846,616.433) and isovalerylcarnitine (P = 0.039, OR = 7.765, 95% CI 1.106-54.512) were positively correlated with hypertrophic scar risk, while N-acetylalanine (P = 0.013, OR = 7.98E-10, 95% CI 5.19E-17-0.012) and glycochenodeoxycholate (P = 0.021, OR = 0.021 95% CI 0.003-0.628) were negatively correlated. Gastranaerophilales and two unknown gut microbe species (P = 0.031, OR = 0.378, 95% CI 0.156-0.914) were associated with an decreased risk of hypertrophic scarring. Circulating metabolites and gut microbiome components may have either positive or negative causal effects on hypertrophic scar formation. The study provides new insights into strategies for diagnosing and limiting hypertrophic scarring.

Effect of pomegranate peel with/without autologous bone marrow on healing of acute cutaneous wounds in alloxan-induced diabetic rabbits.

Healing of bum wounds is commonly associated with many complications. Every year various new repair materials are developed and experimentally used for treating burn wounds. Humans with diabetes mellitus usually suffer from chronic wound healing. Vascular, neuropathic, immune function, and biochemical abnormalities each contribute to the altered tissue repair. One underlying factor that accompanies all diabetic ulcerations is poor vascular flow, a circumstance that impedes proper wound healing. Numerous studies have highlighted the importance of adequate vascular sufficiency and vessel proliferation in tissue repair and the lack thereof in diabetic wound healing. Other studies have looked at whether disarrayed capillary remodeling and maturation of vessels might play a role in impaired diabetic wound healing. This investigation has been planned to report the influence of treatment with a mixture of both the powder of pomegranate peel (PP) accompanied with an autologous bone marrow (BM) on the cure of burn injuries in experimentally induced diabetic rabbits. Alloxan monohydrate has been applied to create diabetes in 50 rabbits. Then in each rabbit, two deep second-degree burn wounds were experimentally created. The animals were then divided randomly into 5 treatment sections: non-treatment controls (C1), treated with an available commercial powder for wound (C2), treatment with powder of PP, treatment with alone BM, and the final group treated with PP powder with bone marrow (PPBM). The speed of wound closure and the histopathological changes during healing were measured. The levels of the biomarkers of rabbit platelet-derived growth factor AA (PDGF-AA) and rabbit protease-activated receptor 1 (PAR-1) were measured on days 0, 4, 8, and 12. Wound healing was markedly more rapid in all the treatment groups versus the control non-treated group. Interestingly, a rapid wound cure was significantly observed in the PPBM group versus the other treatment ones. The histological assessment clarified a significant elevation in the fibroblast and collagen scores in the PPBM group versus the other sections. In addition, there were significant increases in the serum levels of the biomarkers PDGF-AA and PAR-1 among groups. Dependent on the results of current research, it can be concluded that both PP powder with BM PPBM significantly accelerate the healing process of burn wounds in experimentally induced diabetic rabbits.

Utility of Fat Grafting in Chronic Wounds.

Introduction The history of wounds dates back to the evolution of mankind. Throughout the centuries, management modalities of wounds have undergone drastic changes. With the advent of technology, we have multiple options for wound care, but none of them can be called the gold standard of wound care. Autologous fat grafting (AFG) is one of the most routinely performed procedures in aesthetic surgery. Fat grafting has shown beneficial effects in the healing of wounds. The regenerative potential of autologous fat is contributed by the adipose-derived stem cells present within the stromal vascular fraction, which are capable of differentiating into multiple cell types. This study aims to analyze the usefulness of AFG in cutaneous wound healing. Materials and Methods This prospective, study was conducted in our institute between April 2021 and May 2023. Eighteen patients with nonhealing wounds were included in the study. For assessing wound healing all the patients were first managed with conventional dressing for 2 weeks before surgery. After routine preoperative workup, the procedure was performed under local anesthesia in most cases. Fat was harvested from the lower abdomen and after emulsification, was injected into the edge and floor of the ulcer. The dressing was changed on the third postoperative day and the outcome was assessed. Results Eighteen patients (M:F ratio 8:1), with a mean age of 35.61 ± 12. 64 years (range 10-65 years), were included in this study. The most common etiology was trauma (44%), others being postop infection (17%), veno-lymphatic ulcer (17%), burns (11%), insect bite (5%), and trophic ulcer (5%). Majority of the wounds (95%) healed without the need for any extra intervention. The mean period taken for complete wound healing was 5.05 weeks. Conclusion Complete wound healing was achieved in majority of the patients without any complications. We recommend the usage of AFG for nonhealing wounds, as the procedure is relatively simple and can be performed after basic training. Larger-scale randomized controlled trials should be conducted to prove their efficacy in the management of complicated wounds.

Quality improvement initiative to reduce Medical Adhesive Related Skin injury (MARSI) in very preterm babies admitted to neonatal intensive care unit

IntroductionSick preterm neonates are most vulnerable to developing skin injuries. Despite sound knowledge and application of evidence-based practices for preventing medical adhesive-related skin injury (MARSI), the incidence of MARSI was...