In clinical practice, skin defects resulted from various acute and chronic diseases occur frequently. Dermal substitute (DS), known as dermal regenerative template, is used more and more widely, but the slow process of vascularization limits its clinical application. At present, there are many strategies developed to enhance the process of vascularization, such as modifying the structure of dermal scaffolds, prevascularization by seeding stem cells and/or endothelial cells. Recently, negative-pressure wound therapy (NPWT) emerged and rapidly became popular in promoting wound healing due to its intrinsic advantages. Furthermore, some researchers introduced this technique to accelerate the vascularization process of DS. This paper represents a comprehensive overview on the efficiency of NPWT in different combination models, and the related mechanism.

Objective: To explore the influences of hydrogen-rich saline on acute kidney injury in severely burned rats and to analyze the related mechanism. Methods: Fifty-six Sprague Dawley rats were divided into sham injury group (n=8), burn group (n=24), and hydrogen-rich saline group (n=24) according to the random number table. Rats in sham injury group were treated by 20 ℃ water bath on the back for 15 s to simulate injury, and rats in burn group and hydrogen-rich saline group were inflicted with 30% total body surface area (TBSA) full-thickness scald (hereinafter referred to as burns) by 100 ℃ water bath on the back for 15 s. Immediately after injury, hydrogen-rich saline at the dose of 10 mL/kg were intraperitoneally injected to the rats in hydrogen-rich saline group at one time, while normal saline with the same dose were intraperitoneally injected to the rats in sham injury group and burn group. At post injury hour (PIH) 6, rats in the 3 groups were intraperitoneally injected with 4 mL·kg^-1·%TBSA^-1 lactated Ringer′s solution for resuscitation. Eight rats from sham injury group at PIH 72 and eight rats from burn group and hydrogen-rich saline group at PIH 6, 24, and 72 were sacrificed respectively after their blood samples from abdominal aorta were collected. Then their kidney tissue was harvested for histopathological observation and renal tubular injury scoring by hematoxylin and eosin staining, serum creatinine and blood urea nitrogen were detected by the clinical blood biochemical analyzer, expression distribution and mRNA expressions of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6 in renal tissue were evaluated by immunohistochemical staining and real time fluorescent quantitive reverse transcription polymerase chain reaction respectively, and protein expression of high mobility group protein 1 (HMGB1) was detected by Western blotting. Data were processed with Kruskal-Wallis H test, Dunn test, one-way analysis of variance, Bonferroni test. Results: (1) The renal tubular structure of rats in sham injury group at PIH 72 was complete with no inflammatory cell infiltration and no cellular degeneration or necrosis. Since PIH 6, the changes such as vacuolation and shape change of cells and aggregation of broken protein in renal tubules were observed in rats of burn group, and all these changes deteriorated with time. The renal injury of rats in hydrogen-rich saline group at different post injury time points were relieved compared with those of rats in burn group at the corresponding time points. The renal tubular injury scores of rats in burn group and hydrogen-rich saline group at PIH 6, 24, and 72 were significantly higher than the score in sham injury group at PIH 72 (P<0.05). The renal tubular injury scores of rats in hydrogen-rich saline group were significantly lower than those in burn group at PIH 6, 24, and 72 (P<0.05). (2) Except for those in hydrogen-rich saline group at PIH 6 and 72 (P>0.05), the levels of serum creatinine of rats in burn group at all the time points and hydrogen-rich saline group at the other time points were significantly higher than the level of serum creatinine of rats in sham injury group at PIH 72 (P<0.01). The levels of blood urea nitrogen of rats in burn group and hydrogen-rich saline group at PIH 6, 24, and 72 were significantly higher than the level of blood urea nitrogen of rats in sham injury group at PIH 72 (P<0.01). The levels of serum creatinine and blood urea nitrogen of rats in hydrogen-rich saline group at PIH 6, 24, and 72 were significantly lower than those in burn group at the corresponding time points (P<0.05). (3) There were certain degree of positive expressions of TNF-α, IL-1β, and IL-6 in renal tissue of rats in sham injury group at PIH 72, which were mainly observed in the cytoplasm of renal tubular epithelium cell. The expressions of above-mentioned inflammatory cytokines in renal tissue of rats in burn group at PIH 6, 24, and 72 were higher than those in sham injury group. The expressions of above-mentioned inflammatory cytokines in renal tissue of rats in hydrogen-rich saline group at all the time points were less than those in burn group at the corresponding time points. (4) Compared with those in sham injury group at PIH 72, the mRNA expression levels of TNF-α, IL-1β, and IL-6 of rats in burn group at PIH 6, 24, and 72 were significantly increased (P<0.01). The mRNA expression levels of TNF-α were significantly increased in hydrogen-rich saline group at PIH 6 and 24 (P<0.05 or P<0.01), and the mRNA expression level of IL-6 was significantly increased in hydrogen-rich saline group at PIH 6 (P<0.01). Compared with those at the corresponding time points in burn group, except for the mRNA expression level of TNF-α in hydrogen-rich saline group at PIH 6 showed no significant differences (P>0.05), and the mRNA expression levels of TNF-α, IL-1β, and IL-6 at the other time points in hydrogen-rich saline group were significantly decreased (P<0.05). (5) Compared with 0.39±0.03 in sham injury group at PIH 72, the protein expression of HMGB1 of rats in burn group at PIH 6, 24, and 72 (1.19±0.07, 1.00±0.06, 0.80±0.05) were significantly increased (P<0.05), while the protein expression of HMGB1 of rats in hydrogen-rich saline group at PIH 6, 24, and 72 (0.35±0.08, 0.47±0.06, 0.42±0.06) showed no significant differences (P>0.05). Compared with those in burn group, the protein expressions of HMGB1 of rats in hydrogen-rich saline group at PIH 6, 24, and 72 were significantly decreased (P<0.05). Conclusions Hydrogen-rich saline can alleviate the acute kidney injury in severely burned rats through regulating the release of inflammatory cytokines in renal tissue.

Objective:To explore the application of Miller's pyramid theory combined with Bahrain's team activities in the standardized residency training (SRT) of burn surgeons.Methods:Seventy-four residents who were on the SRT program in the Department of Burns & Wound Care in The Second Affiliated Hospital of Zhejiang University were enrolled in the study. The students were divided into control group and observation group according to the teaching methods. Thirty-seven students in the control group were provided with conventional teaching, and 37 students in the observation group were provided with training based on Miller' pyramid theory combined with Bahrain's team activities. The two groups were evaluated for teaching effectiveness and doctor-patient communication skills. SPSS22.0 was used for the chi-square test and t test. Results:The evaluation outcome of teaching effectiveness in the observation group was better than that in the control group ( t=3.01, 3.47, 3.49, 3.32, and 2.54; P=0.004, 0.001, 0.001, 0.001, and 0.013). After the training, the scores of Set Elicit Give Understand End scale in the two groups increased, with significantly higher scores achieved in the observation group than in the control group ( t=3.23, 2.99, 2.07, 3.62, 3.00, and 7.89; P=0.002, 0.004, 0.042, 0.001, 0.004, and <0.001). Conclusion:The application of Miller's pyramid theory and Bahrain's team activities in the SRT of burn surgeons can improve students' evaluation of teaching effectiveness and improve their doctor-patient communication skills.

Foreign body reactions induced by macrophages often cause delay or failure of wound healing in the application of tissue engineering scaffolds. This study explores the application of nanosilver (NAg) to reduce foreign body reactions during scaffold transplantation. An NAg hybrid collagen-chitosan scaffold (NAg-CCS) was prepared using the freeze-drying method. The NAg-CCS was implanted on the back of rats to evaluate the effects on foreign body reactions. Skin tissue samples were collected for histological and immunological evaluation at variable intervals. Miniature pigs were used to assess the effects of NAg on skin wound healing. The wounds were photographed, and tissue samples were collected for molecular biological analysis at different time points post-transplantation. NAg-CCS has a porous structure and the results showed that it could release NAg constantly for two weeks. The NAg-CCS group rarely developed a foreign body reaction, while the blank-CCS group showed granulomas or necrosis in the subcutaneous grafting experiment. Both matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were reduced significantly in the NAg-CCS group. The NAg-CCS group had higher interleukin (IL)-10 and lower IL-6 than the blank CCS group. In the wound healing study, M1 macrophage activation and inflammatory-related proteins (inducible nitric oxide synthase (iNOS), IL-6, and interferon-‍γ (IFN-‍γ)) were inhibited by NAg. In contrast, M2 macrophage activation and proinflammatory proteins (arginase-1, major histocompatibility complex-II (MHC-II), and found in inflammatory zone-1 (FIZZ-1)) were promoted, and this was responsible for suppressing the foreign body responses and accelerating wound healing. In conclusion, dermal scaffolds containing NAg suppressed the foreign body reaction by regulating macrophages and the expression of inflammatory cytokines, thereby promoting wound healing.
Animals ; Rats ; Swine ; Interleukin-6 ; Macrophage Activation ; Tissue Inhibitor of Metalloproteinase-1 ; Wound Healing ; Foreign-Body Reaction ; Foreign Bodies ; Chitosan