Burns & Trauma最新文献

{"title":"Structure-optimized and microenvironment-inspired nanocomposite biomaterials in bone tissue engineering.","authors":"Zheng Lv, Ying Ji, Guoliang Wen, Xiayi Liang, Kun Zhang, Wei Zhang","doi":"10.1093/burnst/tkae036","DOIUrl":"10.1093/burnst/tkae036","url":null,"abstract":"<p><p>Critical-sized bone defects represent a significant clinical challenge due to their inability to undergo spontaneous regeneration, necessitating graft interventions for effective treatment. The development of tissue-engineered scaffolds and regenerative medicine has made bone tissue engineering a highly viable treatment for bone defects. The physical and biological properties of nanocomposite biomaterials, which have optimized structures and the ability to simulate the regenerative microenvironment of bone, are promising for application in the field of tissue engineering. These biomaterials offer distinct advantages over traditional materials by facilitating cellular adhesion and proliferation, maintaining excellent osteoconductivity and biocompatibility, enabling precise control of degradation rates, and enhancing mechanical properties. Importantly, they can simulate the natural structure of bone tissue, including the specific microenvironment, which is crucial for promoting the repair and regeneration of bone defects. This manuscript provides a comprehensive review of the recent research developments and applications of structure-optimized and microenvironment-inspired nanocomposite biomaterials in bone tissue engineering. This review focuses on the properties and advantages these materials offer for bone repair and tissue regeneration, summarizing the latest progress in the application of nanocomposite biomaterials for bone tissue engineering and highlighting the challenges and future perspectives in the field. Through this analysis, the paper aims to underscore the promising potential of nanocomposite biomaterials in bone tissue engineering, contributing to the informed design and strategic planning of next-generation biomaterials for regenerative medicine.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae036"},"PeriodicalIF":5.3,"publicationDate":"2024-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11162833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141295597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuregulin-1, a member of the epidermal growth factor family, mitigates STING-mediated pyroptosis and necroptosis in ischaemic flaps.","authors":"Xuwei Zhu, Gaoxiang Yu, Ya Lv, Ningning Yang, Yinuo Zhao, Feida Li, Jiayi Zhao, Zhuliu Chen, Yingying Lai, Liang Chen, Xiangyang Wang, Jian Xiao, Yuepiao Cai, Yongzeng Feng, Jian Ding, Weiyang Gao, Kailiang Zhou, Hui Xu","doi":"10.1093/burnst/tkae035","DOIUrl":"10.1093/burnst/tkae035","url":null,"abstract":"<p><strong>Background: </strong>Ensuring the survival of the distal end of a random flap during hypoperfusion (ischaemia) is difficult in clinical practice. Effective prevention of programmed cell death is a potential strategy for inhibiting ischaemic flap necrosis. The activation of stimulator of interferon genes (STING) pathway promotes inflammation and leads to cell death. The epidermal growth factor family member neuregulin-1 (NRG1) reduces cell death by activating the protein kinase B (AKT) signalling pathway. Moreover, AKT signalling negatively regulates STING activity. We aimed to verify the efficacy of NRG1 injection in protecting against flap necrosis. Additionally, we investigated whether NRG1 effectively enhances ischemic flap survival by inhibiting pyroptosis and necroptosis through STING suppression.</p><p><strong>Methods: </strong>A random-pattern skin flap model was generated on the backs of C57BL/6 mice. The skin flap survival area was determined. The blood supply and vascular network of the flap was assessed by laser Doppler blood flow analysis. Cluster of differentiation 34 immunohistochemistry (IHC) and haematoxylin and eosin (H&E) staining of the flap sections revealed microvessels. Transcriptome sequencing analysis revealed the mechanism by which NRG1 promotes the survival of ischaemic flaps. The levels of angiogenesis, oxidative stress, necroptosis, pyroptosis and indicators associated with signalling pathways in flaps were examined by IHC, immunofluorescence and Western blotting. Packaging adeno-associated virus (AAV) was used to activate STING in flaps.</p><p><strong>Results: </strong>NRG1 promoted the survival of ischaemic flaps. An increased subcutaneous vascular network and neovascularization were found in ischaemic flaps after the application of NRG1. Transcriptomic gene ontology enrichment analysis and protein level detection indicated that necroptosis, pyroptosis and STING activity were reduced in the NRG1 group. The phosphorylation of AKT and forkhead box O3a (FOXO3a) were increased after NRG1 treatment. The increased expression of STING in flaps induced by AAV reversed the therapeutic effect of NRG1. The ability of NRG1 to phosphorylate AKT-FOXO3a, inhibit STING and promote flap survival was abolished after the application of the AKT inhibitor MK2206.</p><p><strong>Conclusions: </strong>NRG1 inhibits pyroptosis and necroptosis by activating the AKT-FOXO3a signalling pathway to suppress STING activation and promote ischaemic flap survival.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae035"},"PeriodicalIF":5.3,"publicationDate":"2024-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11162832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141295596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory poly(L-lactic acid) nanofibrous membranes promote diabetic wound healing by inhibiting inflammation, oxidation and bacterial infection.","authors":"Yan Wu, Jin Zhang, Anqi Lin, Tinglin Zhang, Yong Liu, Chunlei Zhang, Yongkui Yin, Ran Guo, Jie Gao, Yulin Li, Yanhui Chu","doi":"10.1093/burnst/tkae009","DOIUrl":"10.1093/burnst/tkae009","url":null,"abstract":"<p><strong>Background: </strong>Given the significant impact on human health, it is imperative to develop novel treatment approaches for diabetic wounds, which are prevalent and serious complications of diabetes. The diabetic wound microenvironment has a high level of reactive oxygen species (ROS) and an imbalance between proinflammatory and anti-inflammatory cells/factors, which hamper the healing of chronic wounds. This study aimed to develop poly(L-lactic acid) (PLLA) nanofibrous membranes incorporating curcumin and silver nanoparticles (AgNPs), defined as PLLA/C/Ag, for diabetic wound healing.</p><p><strong>Methods: </strong>PLLA/C/Ag were fabricated via an air-jet spinning approach. The membranes underwent preparation and characterization through various techniques including Fourier-transform infrared spectroscopy, measurement of water contact angle, X-ray photoelectron spectroscopy, X-ray diffraction, scanning electron microscopy, assessment of <i>in vitro</i> release of curcumin and Ag⁺, testing of mechanical strength, flexibility, water absorption and biodegradability. In addition, the antioxidant, antibacterial and anti-inflammatory properties of the membranes were evaluated <i>in vitro</i>, and the ability of the membranes to heal wounds was tested <i>in vivo</i> using diabetic mice.</p><p><strong>Results: </strong>Loose hydrophilic nanofibrous membranes with uniform fibre sizes were prepared through air-jet spinning. The membranes enabled the efficient and sustained release of curcumin. More importantly, antibacterial AgNPs were successfully reduced <i>in situ</i> from AgNO₃. The incorporation of AgNPs endowed the membrane with superior antibacterial activity, and the bioactivities of curcumin and the AgNPs gave the membrane efficient ROS scavenging and immunomodulatory effects, which protected cells from oxidative damage and reduced inflammation. Further results from animal studies indicated that the PLLA/C/Ag membranes had the most efficient wound healing properties, which were achieved by stimulating angiogenesis and collagen deposition and inhibiting inflammation.</p><p><strong>Conclusions: </strong>In this research, we successfully fabricated PLLA/C/Ag membranes that possess properties of antioxidants, antibacterial agents and anti-inflammatory agents, which can aid in the process of wound healing. Modulating wound inflammation, these new PLLA/C/Ag membranes serve as a novel dressing to enhance the healing of diabetic wounds.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae009"},"PeriodicalIF":5.3,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11151119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141261178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular cold-inducible RNA-binding protein mediated neuroinflammation and neuronal apoptosis after traumatic brain injury.","authors":"Yu-Xiao Liu, Ming Zhao, Yang Yu, Jing-Peng Liu, Wen-Jia Liu, Ren-Qi Yao, Jing Wang, Rong-Li Yang, Yao Wu, Ning Dong, Yang Cao, Shou-Chun Li, Qin-Hong Zhang, Run-Min Yan, Yong-Ming Yao","doi":"10.1093/burnst/tkae004","DOIUrl":"10.1093/burnst/tkae004","url":null,"abstract":"<p><strong>Background: </strong>Extracellular cold-inducible RNA-binding protein (eCIRP) plays a vital role in the inflammatory response during cerebral ischaemia. However, the potential role and regulatory mechanism of eCIRP in traumatic brain injury (TBI) remain unclear. Here, we explored the effect of eCIRP on the development of TBI using a neural-specific CIRP knockout (KO) mouse model to determine the contribution of eCIRP to TBI-induced neuronal injury and to discover novel therapeutic targets for TBI.</p><p><strong>Methods: </strong>TBI animal models were generated in mice using the fluid percussion injury method. Microglia or neuron lines were subjected to different drug interventions. Histological and functional changes were observed by immunofluorescence and neurobehavioural testing. Apoptosis was examined by a TdT-mediated dUTP nick end labelling assay <i>in vivo</i> or by an annexin-V assay <i>in vitro</i>. Ultrastructural alterations in the cells were examined via electron microscopy. Tissue acetylation alterations were identified by non-labelled quantitative acetylation via proteomics. Protein or mRNA expression in cells and tissues was determined by western blot analysis or real-time quantitative polymerase chain reaction. The levels of inflammatory cytokines and mediators in the serum and supernatants were measured via enzyme-linked immunoassay.</p><p><strong>Results: </strong>There were closely positive correlations between eCIRP and inflammatory mediators, and between eCIRP and TBI markers in human and mouse serum. Neural-specific eCIRP KO decreased hemispheric volume loss and neuronal apoptosis and alleviated glial cell activation and neurological function damage after TBI. In contrast, eCIRP treatment resulted in endoplasmic reticulum disruption and ER stress (ERS)-related death of neurons and enhanced inflammatory mediators by glial cells. Mechanistically, we noted that eCIRP-induced neural apoptosis was associated with the activation of the protein kinase RNA-like ER kinase-activating transcription factor 4 (ATF4)-C/EBP homologous protein signalling pathway, and that eCIRP-induced microglial inflammation was associated with histone H3 acetylation and the α7 nicotinic acetylcholine receptor.</p><p><strong>Conclusions: </strong>These results suggest that TBI obviously enhances the secretion of eCIRP, thereby resulting in neural damage and inflammation in TBI. eCIRP may be a biomarker of TBI that can mediate the apoptosis of neuronal cells through the ERS apoptotic pathway and regulate the inflammatory response of microglia via histone modification.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae004"},"PeriodicalIF":6.3,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acidic fibroblast growth factor inhibits reactive oxygen species-induced epithelial-mesenchymal transdifferentiation in vascular endothelial cells via the miR-155-5p/SIRT1/Nrf2/HO-1 pathway to promote wound healing in diabetic mice.","authors":"Yue Zhang, Fenghui Hei, Yujie Xiao, Yang Liu, Juntao Han, Dahai Hu, Hongtao Wang","doi":"10.1093/burnst/tkae010","DOIUrl":"10.1093/burnst/tkae010","url":null,"abstract":"<p><strong>Background: </strong>Diabetic chronic wounds are among the most common and serious complications of diabetes and are associated with significant morbidity and mortality. Endothelial-to-mesenchymal transition (EndMT) is a specific pathological state in which endothelial cells are transformed into mesenchymal cells in response to various stimuli, such as high glucose levels and high oxidative stress. Acidic fibroblast growth factor (aFGF), which is a member of the fibroblast growth factor family, possesses strong antioxidant properties and can promote the differentiation of mesenchymal stem cells into angiogenic cells. Therefore, we investigated the role of aFGF in EndMT in diabetic wounds and analysed the underlying mechanisms.</p><p><strong>Methods: </strong>A diabetic mouse model was used to verify the effect of aFGF on wound healing, and the effect of aFGF on vascular endothelial cells in a high-glucose environment was examined <i>in vitro</i>. We examined the expression of miR-155-5p in a high-glucose environment and the miR-155 downstream target gene SIRT1 by luciferase reporter assays.</p><p><strong>Results: </strong>aFGF promoted wound closure and neovascularization in a mouse model of type 2 diabetes. <i>In vitro</i>, aFGF inhibited the production of total and mitochondrial reactive oxygen species (ROS) in vascular endothelial cells and alleviated epithelial-mesenchymal transdifferentiation in a high-glucose environment. Mechanistically, aFGF promoted the expression of SIRT1 and the downstream targets Nrf2 and HO-1 by negatively regulating miR-155-5p, thereby reducing ROS generation.</p><p><strong>Conclusions: </strong>In conclusion, our results suggest that aFGF inhibits ROS-induced epithelial-mesenchymal transdifferentiation in diabetic vascular endothelial cells via the miR-155-5p/SIRT1/Nrf2/HO-1 axis, thereby promoting wound healing.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae010"},"PeriodicalIF":5.3,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11129767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141157869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-125b-5p delivered by adipose-derived stem cell exosomes alleviates hypertrophic scarring by suppressing Smad2.","authors":"Chaolei Xu, Hao Zhang, Chen Yang, Ying Wang, Kejia Wang, Rui Wang, Wei Zhang, Chao Li, Chenyang Tian, Chao Han, Mengyang Li, Xu Liu, Yunwei Wang, Yan Li, Jian Zhang, Yu Li, Liang Luo, Yage Shang, Lixia Zhang, Yuxi Chen, Kuo Shen, Dahai Hu","doi":"10.1093/burnst/tkad064","DOIUrl":"10.1093/burnst/tkad064","url":null,"abstract":"<p><strong>Background: </strong>Hypertrophic scarring is the most serious and unmet challenge following burn and trauma injury and often leads to pain, itching and even loss of function. However, the demand for ideal scar prevention and treatment is difficult to satisfy. We aimed to discover the effects and mechanisms of adipose-derived stem cell (ADSC) exosomes in hypertrophic scarring.</p><p><strong>Methods: </strong>ADSC exosomes were isolated from the culture supernatant of ADSCs and identified by nanoparticle tracking analysis, transmission electron microscopy and western blotting. The effect of ADSC exosomes on wound healing and scar formation was detected by the wound model of BALB/c mice. We isolated myofibroblasts from hypertrophic scar tissue and detected the cell viability, proliferation and migration of myofibroblasts. In addition, collagen formation and fibrosis-related molecules were also detected. To further disclose the mechanism of ADSC exosomes on fibrosis in myofibroblasts, we detected the expression of Smad2 in hypertrophic scar tissue and normal skin and the regulatory mechanism of ADSC exosomes on Smad2. Injection of bleomycin was performed in male BALB/c mice to establish an <i>in vivo</i> fibrosis model while ADSC exosomes were administered to observe their protective effect. The tissue injury of mice was observed via hematoxylin and eosin and Masson staining and related testing.</p><p><strong>Results: </strong>In this study, we found that ADSC exosomes could not only speed up wound healing and improve healing quality but also prevent scar formation. ADSC exosomes inhibited expression of fibrosis-related molecules such as α-smooth muscle actin, collagen I (COL1) and COL3 and inhibited the transdifferentiation of myofibroblasts. In addition, we verified that Smad2 is highly expressed in both hypertrophic scar tissue and hypertrophic fibroblasts, while ADSC exosomes downregulated the expression of Smad2 in hypertrophic fibroblasts. Further regulatory mechanism analysis revealed that microRNA-125b-5p (miR-125b-5p) is highly expressed in ADSC exosomes and binds to the 3' untranslated region of Smad2, thus inhibiting its expression. <i>In vivo</i> experiments also revealed that ADSC exosomes could alleviate bleomycin-induced skin fibrosis and downregulate the expression of Smad2.</p><p><strong>Conclusions: </strong>We found that ADSC exosomes could alleviate hypertrophic scars via the suppression of Smad2 by the specific delivery of miR-125b-5p.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkad064"},"PeriodicalIF":5.3,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11102599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"1H-nuclear magnetic resonance analysis reveals dynamic changes in the metabolic profile of patients with severe burns","authors":"Sen Su, Yong Zhang, Dan Wu, Chao Wang, Jianhong Hu, Yan Wei, Xi Peng","doi":"10.1093/burnst/tkae007","DOIUrl":"https://doi.org/10.1093/burnst/tkae007","url":null,"abstract":"Background Severe burn injury causes a hypermetabolic response, resulting in muscle protein catabolism and multiple organ damage syndrome. However, this response has not yet been continuously characterized by metabolomics in patients. This study aims to quantify temporal changes in the metabolic processes of patients with severe burns. Methods We employed 1H-nuclear magnetic resonance (NMR) spectroscopy to scrutinize metabolic alterations during the initial 35 days following burn injury in a cohort of 17 adult patients with severe burns, with 10 healthy individuals included as controls. Plasma specimens were collected from patients on postburn days 1, 3, 7, 14, 21, 28 and 35. After performing multivariate statistical analysis, repeated-measures analysis of variance and time-series analysis, we quantified changes in metabolite concentrations. Results Among the 36 metabolites quantified across 119 samples from burn patients, branched-chain amino acids, glutamate, glycine, glucose, pyruvate, lactate, trimethylamine N-oxide and others exhibited obvious temporal variations in concentration. Notably, these metabolites could be categorized into three clusters based on their temporal characteristics. The initial response to injury was characterized by changes in lactate and amino acids, while later changes were driven by an increase in fatty acid catabolism and microbial metabolism, leading to the accumulation of ketone bodies and microbial metabolites. Conclusions Metabolomics techniques utilizing NMR have the potential to monitor the intricate processes of metabolism in patients with severe burns. This study confirmed that the third day after burn injury serves as the boundary between the ebb phase and the flow phase. Furthermore, identification of three distinct temporal patterns of metabolites revealed the intrinsic temporal relationships between these metabolites, providing clinical data for optimizing therapeutic strategies.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"125 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140953573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-mimetic vesicles derived from fibroblasts carrying matrine for wound healing.","authors":"Xinyue Zhang, Jiahua Huang, Jing Zhao, Lisha Li, Fengze Miao, Tingrui Zhang, Zhongjian Chen, Xing Zhou, Zongguang Tai, Quangang Zhu","doi":"10.1093/burnst/tkae015","DOIUrl":"10.1093/burnst/tkae015","url":null,"abstract":"<p><strong>Background: </strong>Chronic skin wounds are a leading cause of hospital admissions and reduced life expectancy among older people and individuals with diabetes. Delayed wound healing is often attributed to a series of cellular abnormalities. Matrine, a well-studied component found in <i>Sophora flavescens</i>, is recognized for its anti-inflammatory effects. However, its impact on wound healing still remains uncertain. This study aims to explore the potential of matrine in promoting wound healing.</p><p><strong>Methods: </strong>In this study, we utilized gradient extrusion to produce fibroblast-derived exosome-mimetic vesicles as carriers for matrine (MHEM). MHEM were characterized using transmission electron microscopy and dynamic light scattering analysis. The therapeutic effect of MHEM in wound healing was explored <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Results: </strong>Both matrine and MHEM enhanced the cellular activity as well as the migration of fibroblasts and keratinocytes. The potent anti-inflammatory effect of matrine diluted the inflammatory response in the vicinity of wounds. Furthermore, MHEM worked together to promote angiogenesis and the expression of transforming growth factor β and collagen I. MHEM contained growth factors of fibroblasts that regulated the functions of fibroblasts, keratinocytes and monocytes, which synergistically promoted wound healing with the anti-inflammatory effect of matrine.</p><p><strong>Conclusions: </strong>MHEM showed enhanced therapeutic efficacy in the inflammatory microenvironment, for new tissue formation and angiogenesis of wound healing.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae015"},"PeriodicalIF":5.3,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140944025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical application of digital technology in the use of anterolateral thigh lobulated perforator flaps to repair complex soft tissue defects of the limbs","authors":"Kai-xuan Dong, Ya Zhou, Yao-yu Cheng, Hao-tian Luo, Jia-zhang Duan, Xi Yang, Yong-qing Xu, Sheng Lu, Xiao-qing He","doi":"10.1093/burnst/tkae011","DOIUrl":"https://doi.org/10.1093/burnst/tkae011","url":null,"abstract":"Background It is challenging to repair wide or irregular defects with traditional skin flaps, and anterolateral thigh (ALT) lobulated perforator flaps are an ideal choice for such defects. However, there are many variations in perforators, so good preoperative planning is very important. This study attempted to explore the feasibility and clinical effect of digital technology in the use of ALT lobulated perforator flaps for repairing complex soft tissue defects in limbs. Methods Computed tomography angiography (CTA) was performed on 28 patients with complex soft tissue defects of the limbs, and the CTA data were imported into Mimics 20.0 software in DICOM format. According to the perforation condition of the lateral circumflex femoral artery and the size of the limb defect, one thigh that had two or more perforators from the same source vessel was selected for 3D reconstruction of the ALT lobulated perforator flap model. Mimics 20.0 software was used to visualize the vascular anatomy, virtual design and harvest of the flap before surgery. The intraoperative design and excision of the ALT lobulated perforator flap were guided by the preoperative digital design, and the actual anatomical observations and measurements were recorded. Results Digital reconstruction was successfully performed in all patients before surgery; this reconstruction dynamically displayed the anatomical structure of the flap vasculature and accurately guided the design and harvest of the flap during surgery. The parameters of the harvested flaps were consistent with the preoperative parameters. Postoperative complications occurred in 7 patients, but all flaps survived uneventfully. All of the donor sites were closed directly. All patients were followed up for 13–27 months (mean, 19.75 months). The color and texture of each flap were satisfactory and each donor site exhibited a linear scar. Conclusions Digital technology can effectively and precisely assist in the design and harvest of ALT lobulated perforator flaps, provide an effective approach for individualized evaluation and flap design and reduce the risk and difficulty of surgery.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"19 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140910617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of early exercise training following severe burn injury: a randomized controlled trial.","authors":"David R Schieffelers, Tianfeng Ru, Haonan Dai, Ziqing Ye, Eric van Breda, Ulrike Van Daele, Weiguo Xie, Jun Wu","doi":"10.1093/burnst/tkae005","DOIUrl":"10.1093/burnst/tkae005","url":null,"abstract":"<p><strong>Background: </strong>Despite being a stable component of burn rehabilitation at later stages of recovery, exercise training is not commonly provided during the acute phase of burns. A lack of evidence surrounding its efficacy and safety in severely burned adults has hampered its implementation in acute burn care. The aim of this study was to investigate the capacity of early exercise training to modulate parameters of postburn muscle wasting and quality of life.</p><p><strong>Methods: </strong>Adults <65 years of age with burns ≥40% total burn surface area (TBSA) were randomly allocated to either receive early exercise (n = 29) in addition to standard care or standard care alone (n = 29). Early exercise involved resistance and aerobic training, which commenced as early as possible and lasted for a duration of 6 to 12 weeks, in line with burn center length of stay. Ultrasound-derived quadriceps muscle layer thickness (QMLT) and rectus femoris cross-sectional area (RF-CSA), lower limb muscle force, Eurocol Quality of Life-5 Dimensions and Burn Specific Health Scale Brief (BSHS-B) were assessed 6 and 12 weeks after baseline. Mixed models were fitted to compare between-group changes over time.</p><p><strong>Results: </strong>A total of 58 adults [42 (95% confidence interval 40-45) years old; 40-94% TBSA range, 86% previously mechanically ventilated] participated in this study. Exercise commenced 7 days [IQR (interquartile range) 5-9] after burn center admission with an attendance rate of 93%. Allocation to the exercise group had a protective effect on the loss of muscle size from baseline to 6 weeks of follow-up (QMLT: β-coefficient: 0.05 cm, <i>p</i> = 0.010; RF-CSA: β-coefficient: 0.05 cm², <i>p</i> = 0.045), and resulted in an improved recovery from 6 to 12 weeks (QMLT: β-coefficient: 0.04 cm, <i>p</i> = 0.01; RF-CSA: β-coefficient: 0.06 cm², <i>p</i> < 0.001). Muscle force increased significantly more in the exercise group than in the control group (β-coefficient: 3.102 N, <i>p</i> < 0.001) between 6 and 12 weeks. Besides a marginally significant effect for the BSHS-B domains 'affect' and 'interpersonal relationships' between 6 and 12 weeks, no benefits were observed in the other assessed quality-of-life measures. No serious adverse events were reported in the exercise group.</p><p><strong>Conclusions: </strong>The results of this study support the use of early exercise training as a feasible and efficacious therapeutic strategy to manage burn-related changes in muscle size and strength in adults with acute severe burn injury.</p>","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"12 ","pages":"tkae005"},"PeriodicalIF":5.3,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11075770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}