Efficacy and Safety of Intralesional Triamcinolone Versus Combination of Triamcinolone with 5-Fluorouracil in the Treatment of Keloids and Hypertrophic Scars: A Systematic Review and Meta-analysis.

BACKGROUND: Although keloids and hypertrophic scars are common benign hyperproliferative growths of dermal fibroblasts, the clinical problems including physical and psychological problems are significant and impairing, with few proven treatments. Intralesional triamcinolone acetonide (TAC) and combination of TAC with 5-fluorouracil (5-FU) are widely used to treat keloids and hypertrophic scars, but their efficacy and safety remain controversial. METHODS: We systematically searched MEDLINE, EMBASE, Cochrane Library, and CNKI for relevant trials. RESULTS: The mean scar height and the erythema score in the TAC + 5-FU group were lower than those in the TAC group after treatment (P < 0.05). The effectiveness based on observer assessment after treatment in the TAC + 5-FU group was superior than that in the TAC group (P < 0.05); further, the subgroup analysis showed the TAC + 5-FU group was also superior than the TAC group in the treatment of hypertrophic scars (P = 0.01), and there were no significant differences in the treatment of keloid (P = 0.12). The effectiveness based on patient self-assessment after treatment in the TAC + 5-FU group was also superior than the TAC group (P < 0.05). The overall complication rate in the TAC + 5-FU group was lower than the TAC group (P < 0.05). CONCLUSIONS: Combination of TAC with 5-FU is more effective and safer than TAC alone therapy in the treatment of keloids and hypertrophic scars. Data on keloids alone or hypertrophic scars alone are, however, limited. A better understanding of effective after intralesional combination of TAC with 5-FU in the treatment of keloids alone or hypertrophic scars alone is imperative. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

The Safety and Efficacy of Intralesional Verapamil Versus Intralesional Triamcinolone Acetonide for Keloids and Hypertrophic Scars: A Systematic Review and Meta-analysis.

BACKGROUND: Keloids and hypertrophic scars often result after skin trauma. Currently, intralesional triamcinolone acetonide (TAC) is the criterion standard in nonsurgical management of keloids and hypertrophic scars. Intralesional verapamil may be an effective alternative modality, but it has been insufficiently studied. Accordingly, the study authors conducted a systematic review and meta-analysis of randomized controlled trials to compare the efficacy and safety of the two drugs. METHODS: The study authors systematically searched the MEDLINE, EMBASE, Cochrane Library, and China National Knowledge Infrastructure databases for relevant trials published in any language through September 2018. RESULTS: According to the four studies included in this review, TAC improved scar pliability and vascularity more than verapamil after 3 weeks (P < .05). For scar height and scar pigmentation, no statistical difference was observed between the treatments (P > .05). The difference in effects on symptoms was not statistically significant (P = .89). For pain and telangiectasia, no statistical difference was observed (P > .05). Verapamil resulted in fewer cases of skin atrophy (P < .05). CONCLUSIONS: It appears that TAC is more effective than verapamil for improving scar pliability and vascularity in keloids and hypertrophic scars after 3 weeks of treatment. However, verapamil has fewer adverse drug reactions than TAC, which allows for a longer treatment period and the possibility that it might be effective for patients who cannot receive TAC.

Sinus Wounds Management.

With aging populations and the increased incidence of cerebrovascular disease, diabetes, and other diseases, more and more patients suffer from pressure injuries. Pressure injuries are often difficult to heal because of the presence of sinus tracts, which make it difficult to clean and change dressings. Sinus wounds are common in patients with pressure injuries, but also occur after abdominal wall incision and in patients who have experienced a physical trauma that created a wound. It is difficult for clinicians to observe, evaluate, and repair sinus wounds because of the small surface defect and large and deep basement of each wound. This article reviews existing assessment methods and treatments for sinus wounds and proposes a new evaluation method and treatment (three-dimensional reconstruction and endoscopic techniques) to further improve treatment and provide better quality of care for patients with this type of wound.

Interaction between long noncoding RNA and microRNA in lung inflammatory diseases.

BACKGROUND: Non-coding RNAs (ncRNAs) are a group of RNAs that cannot synthesize proteins, but are critical in gene expression regulation. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), the two major family members, are intimately involved in controlling immune response, cell proliferation, apoptosis, differentiation and polarization, and cytokine secretion. Their interactions significantly influence lung inflammatory diseases and could be potential therapeutic targets. OBJECTIVES: The review aims to elucidate the role of ncRNAs, especially the interactions between lncRNA and miRNA in lung diseases, including acute and chronic lung inflammatory diseases, as well as lung cancer. And provide novel insights into disease mechanisms and potential therapeutic methods. METHODS: We conducted a comprehensive review of the latest studies on lncRNA and miRNA in lung inflammatory diseases. Our research involved searching through electronic databases like PubMed, Web of Science, and Scopus. RESULTS: We explain the fundamental characteristics and functions of miRNA and lncRNA, their potential interaction mechanisms, and summarize the newly explorations on the role of lncRNA and miRNA interactions in lung inflammatory diseases. CONCLUSIONS: Numerous lncRNAs and miRNAs have been found to partipicate in all stages of lung inflammatory diseases. While ncRNA-based therapies have been validated and developed, there remain challenges in developing more stable and effective drugs for clinical use.

Long noncoding RNA XIST promotes cell proliferation and migration in diabetic foot ulcers through the miR-126-3p/EGFR axis.

BACKGROUND: The prevalence of diabetic foot ulcers (DFUs) has caused serious harm to human health. To date, a highly effective treatment is lacking. Long noncoding RNA X-inactive specific transcript (lncRNA XIST) has been the subject of mounting research studies, all of which have found that it serves as a protective factor against certain diseases; however, its function in DFUs is not entirely understood. This study was performed to determine the importance of the lncRNA XIST in the pathogenesis and biological function of DFUs. METHODS: Diabetic ulcer skin from rats was analysed using haematoxylin-eosin (HE), Masson's trichrome, and immunohistochemistry (IHC) staining. The differences in the expression of genes and proteins were examined with real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting. Next, the interaction was verified with a dual luciferase gene reporter assay. In addition, CCK-8, Transwell, and wound healing assays were used to assess the proliferation and migration of HaCaT cells. RESULTS: The lncRNA XIST and epidermal growth factor receptor (EGFR) were downregulated, while microRNA-126-3p (miR-126-3p) was increased in diabetic ulcer rat skin tissues and high glucose-induced HaCaT cells. In addition, we found that the lncRNA XIST binds to miR-126-3p and that EGFR is directly targeted by miR­126­3p. Silencing XIST contributed to upregulated miR-126-3p expression, thus lowering EGFR levels and inhibiting the proliferative and migratory abilities of high glucose-treated HaCaT cells; however, the miR-126-3p inhibitor and overexpression of EGFR reversed this effect. CONCLUSION: Decreased lncRNA XIST expression inhibits the proliferative and migratory abilities of high glucose-induced HaCaT cells by modulating the miR-126-3p/EGFR axis, causing delayed wound healing.

Microarray analysis of tRNA-derived small RNA (tsRNA) in LPS-challenged macrophages treated with metformin.

Metformin, a widely used anti-diabetic drug, has demonstrated its efficacy in addressing various inflammatory conditions. tRNA-derived small RNA (tsRNA), a novel type of small non-coding RNA, exhibits diverse regulatory functions and holds promise as both a diagnostic biomarker and a therapeutic target for various diseases. The purpose of this study is to investigate whether the abundance of tsRNAs changed in LPS versus LPS + metformin-treated cells, utilizing microarray technology. Firstly, we established an in vitro lipopolysaccharide (LPS)-induced inflammation model using RAW264.7 macrophages and assessed the protective effects of metformin against inflammatory damage. Subsequently, we extracted total RNA from both LPS-treated and metformin + LPS-treated cell samples for microarray analysis to identify differentially abundant tsRNAs (DA-tsRNAs). Furthermore, we conducted bioinformatics analysis to predict target genes for validated DA-tsRNAs and explore the biological functions and signaling pathways associated with DA-tsRNAs. Notably, metformin was found to inhibit the inflammatory response in RAW264.7 macrophages. The microarray results revealed a total of 247 DA-tsRNAs, with 58 upregulated and 189 downregulated tsRNAs in the Met + LPS group compared to the LPS group. The tsRNA-mRNA network was visualized, shedding light on potential interactions. The results of bioinformatics analysis suggested that these potential targets of specific tsRNAs were mainly related to inflammation and immunity. Our study provides compelling evidence that metformin exerts anti-inflammatory effects and modulates the abundance of tsRNAs in LPS-treated RAW264.7 macrophages. These findings establish a valuable foundation for using tsRNAs as potential biomarkers for metformin in the treatment of inflammatory conditions.

The Role and Mechanism of Metformin in Inflammatory Diseases.

Metformin is a classical drug used to treat type 2 diabetes. With the development of research on metformin, it has been found that metformin also has several advantages aside from its hypoglycemic effect, such as anti-inflammatory, anti-aging, anti-cancer, improving intestinal flora, and other effects. The prevention of inflammation is critical because chronic inflammation is associated with numerous diseases of considerable public health. Therefore, there has been growing interest in the role of metformin in treating various inflammatory conditions. However, the precise anti-inflammatory mechanisms of metformin were inconsistent in the reported studies. Thus, this review aims to summarize various currently known possible mechanisms of metformin involved in inflammatory diseases and provide references for the clinical application of metformin.

Upregulation of circ_0080968 in diabetic foot ulcer inhibits wound healing via repressing the migration and promoting proliferation of keratinocytes.

BACKGROUND: Diabetic foot ulcer (DFU) is a serious chronic complication of diabetes mellitus whose pathogenesis remains unclear. Circular RNA (circRNA) refers to a group of covalently closed non-coding RNAs that are reported to be dysregulated in patients with DFU. However, the mechanism whereby dysregulation in circRNAs contributes to DFU remains unclear. In this study, we investigated the role of dysregulated circRNAs in DFU. MATERIALS AND METHODS: A gene expression dataset was downloaded from the Gene Expression Omnibus portal and analyzed by the limma package of R. The levels of 24 upregulated circRNAs were detected in two independent cohorts by RT-qPCR. Interactions between miRNAs and circRNAs were predicted through bioinformatics and confirmed using a dual luciferase assay. The circularity and subcellular localization of circRNA-080968 was examined by northern blotting after digestion with RNase-R and in situ hybridization. Cell migration and proliferation were examined using Transwell and MTT assays. The apoptotic cells were detected by flow cytometry. RESULTS: The level of circRNA-080968 was upregulated in DFU tissues compared to that of non-DFU samples and normal human wounds. CircRNA-080968 was mainly localized in the cytoplasm and its overexpression inhibited the migration and promoted the proliferation of keratinocytes. MiR-326 and miR-766-3p were identified to interact with and be negatively correlated with circRNA-080968 levels. Increased glucose upregulated circRNA-080968, and its overexpression accelerated the degradation of both miR-326 and miR-766-3p. Reduced levels of miR-326 and miR-766-3p upregulated the expression of several genes controlling cell adhesion and proliferation which are related to the pathogenesis of DFU. CONCLUSIONS: The upregulation of circRNA-080968 in DFU induced the degradation of miR-326 and miR-766-3p, which further repressed the migration and increased the proliferation of keratinocytes.

Homogeneous silver nanoparticle loaded polydopamine/polyethyleneimine-coated bacterial cellulose nanofibers for wound dressing.

Utilizing mussel-inspired chemistry is an advanced strategy for surface modification, because dopamine (DA) can form a material-independent adhesive coating and further functionalization can be achieved, including the production of silver nanoparticles (AgNPs). Nevertheless, DA easily aggregates in the nanofiber network structure of bacterial cellulose (BC), which not only blocks the pores in the BC structure but also leads to the formation of large silver particles and the burst release of highly cytotoxic silver ions. Herein, a homogeneous AgNP-loaded polydopamine (PDA)/polyethyleneimine (PEI) coated BC was constructed via a Michael reaction between PDA and PEI. Under the action of PEI, the PDA/PEI coating was uniformly attached to the BC fiber surface with a thickness of approximately 4 nm, and homogeneous AgNPs were produced on the uniform PDA/PEI/BC (PPBC) fiber surface. The sustained release of silver ions was better from AgNPs@PPBC than from AgNPs@PDA/BC. The obtained AgNPs@PPBC exhibited excellent antibacterial activities and cytocompatibility. The results of the in vivo assay indicated that the AgNPs@PPBC dressing could inhibit S. aureus infection and inflammation, promote hair follicle growth, enhance collagen deposition, and accelerate wound healing within 12 days compared with BC. These results illustrate that the homogeneous AgNPs@PPBC dressing has great potential for treating infected wounds.

Designment of polydopamine/bacterial cellulose incorporating copper (II) sulfate as an antibacterial wound dressing.

Improving antibacterial performance is one of the prerequisites for the clinical application of bacterial cellulose (BC)-based dressings. In this study, a novel copper (Cu) ion loaded BC-based antibacterial wound dressing was prepared via codeposition of polydopamine (PDA) and copper ion. The scanning electron microscope (SEM) results showed that the copper ion/PDA coating was more uniform than the PDA coating, and the 3D nanopore structure of BC was retained in Cu2+@PBC. Cu ions were immobilized by forming a chelate with PDA. The thermal stability and mechanical properties of the Cu2+@PBC dressing decreased with the addition of copper ions. Cu2+@PBC-2 film with a certain amount of copper sulfate used (10 nM) exhibited favorable antibacterial properties against both S. aureus and E. coli without obvious cytotoxicity. The results of the in vivo study also demonstrated that the Cu2+@PBC-2 film can eliminate S. aureus infections and inflammatory response, promote collagen deposition, capillary angiogenesis, hair follicle growth and wound healing. These results suggest that the Cu2+@PBC-2 film has prospective application as a wound dressing.

Bi-layered nanofibrous membrane with osteogenic and antibacterial functions for periodontal tissue regeneration.

Guided tissue regeneration (GTR) membranes have great potential to promote periodontal tissue regeneration and reestablishment. However, the regeneration potential and microbial infection resistance of current GTR membranes still need to be improved. Here, a bi-layered nanofibrous membrane on the basis of poly (lactic-co-glycolic acid) (PLGA)/gelatin with osteogenic and antibacterial functions was fabricated for periodontal tissue regeneration. The antimicrobial layer (AL) of the bi-layered nanofibrous membrane was composed of nanofibrous PLGA/gelatin nanofibers loaded with nano-silver (nAg), while the osteoconductive layer (OL) of the nanofibrous membrane consisted of PLGA/gelatin nanofibers loaded with nano-hydroxyapatite (nHA). The bi-layered nanofibrous membrane was examined by scanning electron microscopy (SEM), energy dispersive spectrometer (EDS), transmission electron microscope (TEM), Fourier transform infrared spectroscopy (FTIR), X-ray photoelectron spectrometry (XPS) and X-ray diffractometry (XRD). The results showed that nHA and nAg particles were well evenly loaded or embedded in PLGA/gelatin nanofibers. The cell culture experiments suggested that the bi-layered nanofibrous membrane possessed good cytocompatibility and the OL of the bi-layered nanofibrous membrane possessed an enhanced osteogenic capacity for human osteoblast-like cells (MG63), which was verified by the good cell viability and the increased alkaline phosphatase (ALP) activity, respectively. The results of in vitro antimicrobial study displayed that the AL of the bi-layered nanofibrous membrane possessed an effective antibacterial capability. In conclusion, the prepared bi-layered nanofibrous membrane with osteogenic and antibacterial functions may have great potential for periodontal tissue regeneration and reestablishment.[Formula: see text].

The expression profile of lung long non-coding RNAs and mRNAs in a mouse model of smoke inhalation injury.

To study the potential expression of lung long non-coding RNAs (lncRNAs) and mRNAs during smoke inhalation injury (SII), using a SII mouse model that we created in our previous work. Microarray was used to investigate the lncRNAs and mRNAs profiles. A bioinformatics analysis was performed. Changes in the top 10 down-regulated and 10 up-regulated lncRNAs were validated using Quantitative Reverse Transcription-PCR (RT-qPCR). The acute lung injury (ALI) mouse model was successfully induced by smoke inhalation, as confirmed by the aberrantly modified cell numbers of red blood cells and neutrophils counts, increased levels of TNF-α, IL-1ß, Bax, caspase-7, caspase-3, and decreased Bcl-2 content in lung tissues. When compared to the control mice, 577 lncRNAs and 517 mRNAs were found to be aberrantly expressed in the SII mice. According to the Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, the altered mRNAs were enriched in acute-phase response, oxidoreductase activity, oxidation-reduction process, glutathione metabolism, the wnt signaling pathway, and ferroptosis. A lncRNA-related competitive endogenous RNA (ceRNA) network, including 383 lncRNAs, 318 MicroRNAs (miRNAs), and 421 mRNAs specific to SII, was established. The changes in NONMMUT026843.2, NONMMUT065071.2, ENSMUST00000235858.1, NONMMUT131395.1, NONMMUT122516.1, NONMMUT057916.2, and NONMMUT013388.2 in the lung matched the microarray results. Our findings help to provide a more comprehensive understanding of the pathogenesis of SII as well as new insights into potential therapeutic targets.

A painless and flexible bi-directional blood glucose-regulating system inspired by an inverter air conditioner.

Pursuing painless and flexible blood glucose regulation has been a century-long arduous mission. The current therapeutic systems can only regulate blood glucose unidirectionally (reduce), and the adjustment range is large, which is prone to the risk of hypoglycemia. Herein, inspired by the temperature fluctuation range controlled by the inverter air conditioner, we report a new bi-directional blood glucose-regulating drug delivery system (BDRS) consisting of glucose-loaded pressure-responsive nano-vesicles (Glu@PRNV), insulin-loaded black phosphorus nanosheets (Insulin@BPNs), hydrogel, and a painless blood sugar monitor patch. At first, BDRS could monitor blood glucose in real-time through visible color changes. Afterward, according to different requirements, BDRS could release glucose with the guidance of external pressure, or supplement insulin under near-infrared (NIR) irradiation, through which, the blood glucose level of diabetics could be accurately accommodated within a reasonable fluctuation range, thus minifying the likelihood of sudden hyperglycemia or hypoglycemia. Collectively, the supply-demand balance of blood glucose could be maintained via this real-time bi-directional drug delivery system, thereby improving the quality of life of diabetics. We have also verified the universality of this technique through a similar bi-directional sleep regulation.

Metformin Improves Burn Wound Healing by Modulating Microenvironmental Fibroblasts and Macrophages.

Metformin, a biguanide, exerts different functions through various signaling pathways. In order to investigate the function and mechanism of metformin in burn wounds, we established burn rat models, subcutaneously injected metformin to treat the wounds, and observed the morphologies and the expression of collagen I, collagen III, fibronectin, and pro-inflammatory markers. In vitro experiments were performed to investigate the effects of metformin on the proliferation, migration, and collagen I synthesis of the mouse embryonic fibroblast (NIH 3T3) cell line and on the proliferation, apoptosis, and immune response of the mouse mononuclear macrophage (RAW 264.7) cell line. Finally, we studied the regulatory effects of metformin on a co-culture of RAW 264.7/NIH 3T3 cells. We found that 100 mM of metformin reduced dermal thickness, collagen I deposition, and mRNA expression of IL1ß and CCL2 in rat burn wounds. In vitro experiments revealed that metformin inhibited the proliferation of NIH 3T3 and RAW 264.7 cells. Metformin attenuated NIH 3T3 cell migration via the AMPK/mTOR pathway and attenuated collagen I synthesis through the TGFß1/Smad3 pathway. Metformin inhibited the apoptosis of RAW 264.7 cells induced by 10 µg/mL LPS. Metformin downregulated the mRNA expression of IL1ß and CCL2 in RAW 264.7 cells under 1 µg/mL LPS induction by inhibiting NF-κB p65 phosphorylation. In a RAW 264.7/NIH 3T3 co-culture, metformin attenuated collagen I synthesis in NIH 3T3 cells by inhibiting RAW 264.7 paracrine secretion of TGF-ß1. This provides new evidence related to the development of metformin for potentially improving burn wound healing.

[Research progress on exosome-mediated immune regulation of acute lung injury].

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a respiratory disorder with high morbidity and mortality caused by various causes. Exosomes can mediate cell communication through paracrine pathways, transfer proteins, lipids, nucleic acids, etc., and interfere with the biological functions of recipient cells. Various cell-derived exosomes have been reported to play an immunomodulatory role in the ALI/ARDS inflammatory model. This article reviews the mechanism of exosomes involved in immune regulation of ALI/ARDS and possible therapeutic approaches.

rhKGF-2 Attenuates Smoke Inhalation Lung Injury of Rats via Activating PI3K/Akt/Nrf2 and Repressing FoxO1-NLRP3 Inflammasome.

Smoke inhalation injury is an acute pathological change caused by thermal stimulation or toxic substance absorption through respiratory epithelial cells. This study aims to probe the protective effect and mechanism of recombinant human keratinocyte growth factor 2 (rhKGF-2) against smoke inhalation-induced lung injury (SILI) in rats. The SILI was induced in rats using a smoke exposure model, which were then treated with rhKGF-2. The rat blood was collected for blood-gas analysis, and the levels of inflammatory factors and oxidative stress markers in the plasma were measured. The rat lung tissues were collected. The pathological changes and cell apoptosis were determined by hematoxylin-eosin (HE) staining and TdT-mediated dUTP nick end labeling (TUNEL) assay, and the PI3K/Akt/Nrf2/HO-1/NQO1, and FoxO1-NLRP3 inflammasome expression were verified by western blot (WB). Both of the human alveolar epithelial cell (HPAEpiC) and primary rat alveolar epithelial cell were exposed to lipopolysaccharide (LPS) for making in-vitro alveolar epithelial cell injury model. After treatment with rhKGF-2, GSK2126458 (PI3K inhibitor) and AS1842856 (FoxO1 inhibitor), the cell viability, apoptosis, inflammation, oxidative stress, reactive oxygen species (ROS), PI3K/Akt/Nrf2, HO-1/NQO1, and FoxO1-NLRP3 in HPAEpiC and primary rat alveolar epithelial cell were examined. The data suggested that rhKGF-2 reduced LPS-induced HPAEpiC cell and primary rat alveolar epithelial cell apoptosis and the expression of inflammatory factors and oxidative stress factors. Moreover, rhKGF-2 improved the blood gas and alleviated SILI-induced lung histopathological injury in vivo via repressing inflammation, NLRP3 inflammasome activation and oxidative stress. Mechanistically, rhKGF-2 activated PI3K/Akt pathway, enhanced Nrf2/HO-1/NQO1 expression, and attenuated FoxO1-NLRP3 inflammasome both in vitro and in vivo. However, pharmaceutical inhibition of PI3K/Akt pathway attenuated rhKGF-2-mediated protective effects against SILI, while suppressing FoxO1 promoted rhKGF-2-mediated protective effects. Taken together, this study demonstrated that rhKGF-2 mitigated SILI by regulating the PI3K/Akt/Nrf2 pathway and the FoxO1-NLRP3 axis, which provides new reference in treating SILI.

Negative-pressure wound therapy in skin grafts: A systematic review and meta-analysis of randomized controlled trials.

INTRODUCTION: Although skin grafts are widely used in reconstruction of large skin defect and complex wounds, many factors lead to suboptimal graft take. Negative-pressure wound therapy (NPWT) reportedly increases the graft take rates when added to skin grafting, but a summary analysis of the data of randomized controlled trials has yet to be performed. We conducted this systematic review and meta-analysis of randomized controlled trials to compare the effectiveness and safety of NPWT and non-NPWT for patients with skin grafts. METHODS: We searched PubMed, Embase, Cochrane Library, and CNKI for relevant trials based on predetermined eligibility criteria from database establishment to February 2020. Two reviewers screened citations and extracted data independently. The quality of the included studies was evaluated according to the Cochrane Handbook, whereas statistical heterogeneity was assessed using chi-square tests and I2 statistics. Review Manager 5.3 was used for statistical analysis. RESULTS: Ten randomized controlled trials with 488 patients who underwent NPWT or non-NPWT were included. Compared with non-NPWT, NPWT yielded an improved the percentage of graft take, a reduction in days from grafting to discharge, with lower relative risk of re-operation, and no increased relative risk of adverse event. Further, the subgroup analysis showed an improved the percentage of graft take in negative pressure of 80 mmHg, and no improved the percentage of graft take in negative pressure of 125 mmHg. CONCLUSION: NPWT is more effective than non-NPWT for the integration of skin grafts, and the negative pressure of 80 mmHg can be recommended. Data on adverse events and negative pressure are, however, limited. A better understanding of complications after NPWT and the ideal negative pressure for the integration of skin grafts is imperative.

Banana Peel-Derived Dendrite-Shaped Au Nanomaterials with Dual Inhibition Toward Tumor Growth and Migration.

PURPOSE: In order to prepare functional Au nanoparticles with low toxicity and high antitumor properties, we have used fruit waste (banana peel) to synthesize a new dendrite-shaped gold nanoparticle and used it for the treatment of tumors. METHODS: Dendrite-shaped gold nanoparticle (Au-dendrite) was synthesized through a facile hydrothermal process. The banana peel was used as both the reducing agent and the protective agent for reducing chloroauric acid to obtain Au-dendrite. The safety assessment of the Au-dendrite was conducted by H&E staining of the mouse's eyelid skin and CCK-8 assay. The antitumor effects were evaluated through in vitro tumor cytotoxicity experiments and in vivo treatment of animal tumors. RESULTS: In this work, a new type of gold nanomaterial (Au-dendrite) was synthesized by using a common agricultural waste (banana peel) through a facile hydrothermal process without any extra chemical reducing agent or protective agent. Subsequent experiments showed that, compared with some classical Au nanomaterials, the as-synthesized gold nanocomposites have superior biocompatibility and impressive characteristics of dual inhibition toward tumor growth and migration. CONCLUSION: We successfully synthesized a dendrite-shaped gold nanocomposite which was derived from a common agricultural waste (banana peel). A facile and environmentally friendly synthetic process was proposed accordingly without regular chemical additives. The as-prepared Au-dendrite nanocomposites not only had better biocompatibility than some classical gold nanoparticles but also exhibited unique advantages in tumor inhibition.

Stem cell derived exosomes-based therapy for acute lung injury and acute respiratory distress syndrome: A novel therapeutic strategy.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common critical disease which can be caused by multiple pathological factors in clinic. However, feasible and effective treatment strategies of ALI/ARDS are limited. At present, the beneficial effect of stem cells (SCs)-based therapeutic strategies for ALI/ARDS can be attributed to paracrine. Exosomes, as a paracrine product, are regarded as a critical regulatory mediator. Furthermore, substantial evidence has indicated that exosomes from SCs can transmit bioactive components including genetic material and protein to the recipient cells and provide a protective effect. The protective role is played through a series of process including inflammation modulation, the reconstruction of alveolar epithelium and endothelium, and pulmonary fibrosis prevention. Therefore, SCs derived exosomes have the potential to be used for therapeutic strategies for ALI/ARDS. In this review, we discuss the present understanding of SCs derived exosomes related to ALI/ARDS and provide insights for developing a cell-free strategy for treating ALI/ARDS.

BMSC-derived exosomes alleviate smoke inhalation lung injury through blockade of the HMGB1/NF-κB pathway.

AIMS: To investigate the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomes in smoke inhalation lung injury. MAIN METHODS: In this study, we initially isolated exosomes from BMSCs and identified them by western blot and transmission electron microscopy. BMSC-derived exosomes were then used to treat in vitro and in vivo models of smoke inhalation lung injury. Pathologic alterations in lung tissue, the levels of inflammatory factors and apoptosis-related factors, and the expression of HMGB1 and NF-κB were determined to evaluate the therapeutic effect of BMSC-derived exosomes. KEY FINDINGS: We found that BMSC-derived exosomes could alleviate the injury caused by smoke inhalation. Smoke inhalation increased the levels of inflammatory factors and apoptosis-related factors and the expression of HMGB1 and NF-κB, and these increases were reversed by BMSC-derived exosomes. HMGB1 overexpression abrogated the exosome-induced decreases in inflammatory factors, apoptosis-related factors and NF-κB. SIGNIFICANCE: Collectively, these results indicate that BMSC-derived exosomes can effectively alleviate smoke inhalation lung injury by inhibiting the HMGB1/NF-κB pathway, suggesting that exosome, a noncellular therapy, is a potential therapeutic strategy for inhalation lung injury.