Retrospective study of primary reconstruction of facial traumatic events.

Facial traumatic events are commonly encountered in plastic and reconstructive surgery. Primary reconstruction is a reliable procedure with function and aesthetic considerations. We conduct a retrospective study of the experience of reconstructing facial traumatic defects in the first stage. One hundred and thirty-two cases (aged 18-65) with facial traumatic events were recruited in the study from 2008 to 2014. Facial traumatic events included injured soft tissue, maxillofacial fractures and facial nerve rupture, which were repaired primarily. After primary reconstruction, encouraging functional and aesthetic outcomes were attained. Ten cases were re-operated to reconstruct partial nasal defect. Four patients who had trouble with disabled occluding relations sought help from dentists. Inconspicuous scar and function restoration were presented. Facial wounds should be reconstructed in the first stage as far as possible. Then, satisfactory functional and aesthetic results can be achieved. However, combined injury should be carefully considered in those traumatic cases before we carry out the reconstructive surgery on the face.

Apoptosis and death receptor signaling in diaphragm of burnt rats.

BACKGROUND: Respiratory dysfunction is a frequent complication after severe burn injury. Respiratory muscle atrophy may induce respiratory dysfunction due to insufficient inspiratory motive power. Accumulated evidence suggests that apoptosis is very important in skeletal muscle atrophy in multiple pathologic conditions. Therefore, we hypothesize that myonuclear apoptosis contributes to diaphragm atrophy induced by burn injury, and death receptor signaling activation plays a role in this process. METHODS: Wistar rats in the burn-injured group were subjected to a full-thickness scald injury around 40% of total body surface area. Diaphragm samples were examined for myonuclear apoptosis by transmission electron microscope, terminal deoxynucleotidyl transferase-mediated nick end labeling assay, and immunohistochemistry for caspase-3. Serum level of apoptotic ligands were assessed by ELISA. Activation of death receptor signaling was examined by Western blotting. RESULTS: Burn injury resulted in significant reductions of diaphragm muscle mass and myofiber cross-section area. Apoptosis in diaphragm appeared from day 1 and peaked on day 4 after injury. The level of soluble TNF-related apoptosis-inducing ligand and the ratio of Fas ligand to soluble Fas in serum significantly increased after burn injury. In diaphragm of burnt animals, the expressions of proapoptotic proteins, such as cleaved caspase-8, cleaved caspase-3, and Bax-to-Bcl-2 ratio were upregulated, whereas expression of pAkt, an antiapoptotic protein, was downregulated. Immunohistochemistry revealed that the most of the caspase-3 was expressed in myofiber nuclei and their surrounding cytoplasm area in tissue sections. CONCLUSIONS: Severe burn injury induces myonuclear apoptosis in diaphragm, which could be a contributor to diaphragm muscle atrophy. Activation of death receptor signaling may be a mechanism of apoptosis in diaphragm.

Epidemiology of burns in pediatric patients of Beijing City.

BACKGROUND: This study aimed to assess the epidemiological characteristics of pediatric burns in Beijing City. METHODS: This was a retrospective study of pediatric patients (n = 400) admitted to four burn centers in Beijing City between June 2010 and May 2011. Burn severity was determined according to total body surface area (TBSA) percentage and degree. Patients were followed up for one year. Multivariate analyses were carried out to determine the factors (burn etiology, time and place of injury, living conditions, hospital type, first-aid treatment methods, and parent/guardian knowledge of burns, educational level, occupation) affecting burn properties (severity and pigmentation/scar). RESULTS: 191/400 (47.8 %) patients were aged 2-3 years, and scalding was the leading etiology (355/400, 88.8 %). Burn incidence peaked in May (14.8 %), at 10:00-12:00 and 17:00-20:00. Most burn events occurred indoors (272/400, 68.0 %), especially in the kitchen (180/400, 45.0 %). Roughly half of them involved head and neck; 188 (47.0 %) patients had mild burns, 140 (35.0 %) moderate, 44 (11.0 %) extensive, and 28 (7.0 %) critical burns; 184 (46.0 %) patients were treated only with cold-water rinsing or compress; 120 (30.0 %) received no first aid. Only 32 (8.0 %) patients visited a specialized institution. 164 patients underwent surgery. Hospitalization lasted for 14.8 ± 8.1 days. Independent risk factors for burn severity were occurrence month, living conditions, occupation of the mother, and first aid. 288 (72.0 %) patients developed pigmentation and scar within a year while no independent risk factors was observed. CONCLUSIONS: Pediatric burns often occurred indoors, especially in the kitchen, and a substantial proportion receives no first aid.

The extracellular matrix protein matrilin-2 induces post-burn inflammatory responses as an endogenous danger signal.

OBJECTIVE AND DESIGN: This prospective experimental study aims to investigate whether matrilin-2 is released from burn injury and induces post-burn inflammatory responses as an endogenous danger signal. SUBJECTS: Fifteen burn patients, 15 volunteers, 12 matrilin-2-deficient mice, 36 C57BL/6 mice and raw 264.7 cells. METHODS: Matrilin-2 levels were detected by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction. The inflammatory cytokines production in Matn2 deficient mice and wide type mice were detected by ELISA. Macrophages were activated by recombinant mouse MATN2 with or without adding anti-Toll-like receptor (TLR) 4 antibody. Student's t test and one-way analysis of variance were used for statistical analysis. RESULTS: The matrilin-2 levels in serum of burned patients were drastically elevated as compared to those of healthy controls. The matrilin-2 levels in burned mice were significantly increased than those of non-burned controls, whereas the matrilin-2 mRNA expression was not significantly changed after burn. In addition, Matn2 deficient mice showed remarkably less inflammatory cytokines production and less neutrophil infiltration in lung. Exogenous MATN2 induced potent expression of proinflammatory cytokines production in macrophages, which was inhibited by anti-TLR4 antibody. CONCLUSION: Matrilin-2 induces post-burn inflammatory responses as an endogenous danger signal, partly through a TLR4-mediated mechanism.

MicroRNA 26a prolongs skin allograft survival and promotes regulatory T cell expansion in mice.

MicroRNA 26a (Mir-26a) has been reported to play functions in cellular differentiation, cell growth, cell apoptosis, and metastasis. However, the role of Mir-26a in transplant rejection has never been investigated. Full-thickness skin grafts 1-2 cm in diameter were obtained from the tail-skin CBA/J donor mice and transplanted onto the back of wild-type C57Bl/6 recipient mice. Vectors encoding pre-Mir-26a (LV-26a) and an empty lentiviral vector (LV-Con) delivered approximately 2 × 10(7) transforming units of recombinant lentivirus were injected to mice once through the tail vein. Mir-26a overexpression results in prolonged skin allograft survival (MST = 9.5 days in LV-Con mice; MST = 22 days in LV-26a mice. P < 0.01) and promoted regulatory T cells (Tregs) expansion. The prolonged skin allograft survival induced by LV-26a was abrogated by depletion of Tregs with anti-CD25 antibodies. Mir-26a significantly promoted IL-10 expression and suppressed the expression of IL-6, IL-17, and IFN-γ. Furthermore, IL-6 overexpression led to complete suppression of the Mir-26a-induced upregulation of Foxp3. The prolonged allograft survival induced by LV-Mir-26a was also completely abrogated by IL-6 overexpression. In conclusion, Mir-26a prolongs skin allograft survival and promotes Tregs expansion in part through inhibition of IL-6 expression.

[Efficacies of fluid resuscitation volume after combined burn-blast injury shock].

OBJECTIVE: To explore the efficacies of resuscitation fluid volume after combined burn-blast injury versus a simple burn. METHODS: A total of 24 beagle dogs were randomly assigned into 3 groups of normal volume (N), decreased volume (D) and increased volume (I). Fluid volume for group N was calculated with the Parkland formula while groups D and I decreased or increased by 20% respectively. Urinary output (UOP), hemoglobin concentration (HB), cardiac output (CO), intrathoracic blood volume (ITBV), extravascular lung water index (ELWI), oxygen delivery (DO(2)) and oxygen consumption (VO(2)) were determined before and 4, 8, 24, 48 h after injury to evaluate the sufficiency of resuscitation in each group and examine the superiority. RESULTS: UOP were [(0.41 ± 0.13), (0.77 ± 0.17), (0.30 ± 0.13)] ml · kg(-1) · h(-1) at 4 h post-injury in groups N, I and D respectively. Group I was significantly higher than groups N and D (P < 0.001).It were [(0.59 ± 0.05), (0.88 ± 0.05), (0.53 ± 0.06)] ml · kg(-1) · h(-1) at 24 h post-injury in groups N, I and D respectively. Group I was significantly higher than groups N and D (P < 0.001). CO in group I was remarkably higher than those in groups N and D at 4 h and 8 h post-injury [(1.57 ± 0.19) vs (1.25 ± 0.17), (1.05 ± 0.17) L/min; (1.87 ± 0.20) vs (1.57 ± 0.24), (1.20 ± 0.19) L/min respectively] (P < 0.05); ITBV also significantly increased in group I than two other groups at 4 h and 8 h post-injury [(169 ± 16) vs (140 ± 12), (121 ± 12) ml; (161 ± 14) vs (135 ± 22), (112 ± 12) ml] (P < 0.05). VO2 in group I was significantly higher than that in group N at 24 h post-injury [(129 ± 10) vs (106 ± 12) ml · min(-1) · m(-2)] (P < 0.05). No differences were detected among 3 group in ELWI (P > 0.05). CONCLUSION: Larger fluid volume may compensate circulatory volume loss sooner, alleviate declining cardiac output better, maintain adequate organ perfusion, promote tissue oxygenation and improve anti-hypervolemia and anti-hypoxia.

[Effects of exogenous pulmonary surfactant on acute lung injury in rats with severe burn-blast combined injury].

OBJECTIVE: To observe the therapeutic effects of exogenous pulmonary surfactant (PS) on acute lung injury induced by severe burn-blast combined injury in a rat model. METHODS: A total of 180 adult male SD rats were randomly divided into 3 groups of sham, treatment and control (n=60 each). Severe burn-blast combined injury was induced by inflicting rats with a moderate blast injury and a full-thickness burn injury of 25% total body surface area. The treatment and control groups received exogenous PS (2 ml/kg) and saline (2 ml/kg) by trachea respectively. At the time points of 0, 6, 24, 48 and 72 h, 12 rats per timepoint in each group underwent PaO2, PaCO2 and pulmonary function tests respectively. And they were then sacrificed for other analyses. Lung tissues were harvested for histological studies. Their arterial blood samples were collected for blood gas analysis. All data were expressed as mean ± standard deviation and analyzed with SPSS 20.0 (SPSS Inc., Chicago, IL, USA). The differences were considered to be statistically significant at P < 0.05. RESULTS: After removing death drain during the experiment, 8 rats were put equally into five phase points of the last three groups, the results were analyzed statistically. PaO2: At each timepoint of 6, 24, 48, 72 h, the control group PaO2 were obviously lower than the sham group ((69.55 ± 5.11), (62.05 ± 6.54), (53.24 ± 7.65), (50.00 ± 7.45) vs (93.75 ± 3.41), (94.25 ± 2.19), (93.63 ± 2.33), (93.25 ± 1.83) mmHg (1 mmHg = 0.133 kPa), all P < 0.01); at 6 h treatment group was close to sham group ((92.63 ± 3.74) vs (93.75 ± 3.41) mmHg, P=0.594); at 6 h control group PaO2 decreased to 70 mmHg and then gradually declined. And at each timepoint the treatment group PaO2 was significantly higher than the control group ((92.63 ± 3.74), (87.50 ± 3.34), (78.75 ± 3.11), (71.38 ± 3.74) vs (69.55 ± 5.11), (62.05 ± 6.54), (53.24 ± 7.65), (50.00 ± 7.45) mmHg, all P < 0.01); PaCO2: treatment group PaCO2 was lower than that of control group at 6, 24, 48 h ((45.50 ± 6.79), (49.38 ± 7.52), (54.13 ± 4.82) vs (53.25 ± 2.76), (59.50 ± 6.61), (63.60 ± 7.33) mmHg, all P < 0.01), both treatment and control groups were significantly higher than those in the sham group ((59.63 ± 6.87), (68.88 ± 6.85) vs (36.38 ± 1.85) mmHg, all P < 0.01). No difference existed between the control and treatment groups (P = 0.051). Deep inspiratory capacity, central airway resistance, lung compliance and tissue elasticity, treatment group was significantly better than control group at 24 h (P < 0.05). And it was close to sham group (P > 0.05). The treatment group alveolar structural damage and pulmonary hemorrhage and edema were better than those in the control group. CONCLUSION: Exogenous pulmonary surfactant (PS) can improve oxygenation and alleviate pulmonary edema and pulmonary capillary membrane permeability of rats with severe burn blast combined injury.

Microencapsulated VEGF gene-modified umbilical cord mesenchymal stromal cells promote the vascularization of tissue-engineered dermis: an experimental study.

BACKGROUND AIMS: Tissue-engineered dermis (TED) is thought to be the best treatment for skin defect wounds; however, lack of vascular structures in these products can cause slow vascularization or even transplant failure. We assessed the therapeutic potential of microencapsulated human umbilical cord mesenchymal stromal cells (hUCMSCs) expressing vascular endothelial growth factor (VEGF) in vascularization of TED. METHODS: hUCMSCs were isolated by means of enzymatic digestion and identified by means of testing biological characteristics. hUCMSCs were induced to differentiate into dermal fibroblasts in conditioned induction media. Collagen-chitosan laser drilling acellular dermal matrix (ADM) composite scaffold was prepared by means of the freeze dehydration and dehydrothermal cross-linking method. hUCMSC-derived fibroblasts were implanted on composite scaffolds to construct TED. TED with microencapsulated VEGF gene-modified hUCMSCs was then transplanted into skin defect wounds in pigs. The angiogenesis of TED at 1 week and status of wound healing at 3 weeks were observed. RESULTS: The collagen-chitosan laser ADM composite has a uniform microporous structure. This composite has been used to grow hUCMSC-derived fibroblasts in vitro and to successfully construct stem cell-derived TED. Microencapsulated VEGF gene-modified hUCMSCs were prepared with the use of a sodium alginate-barium chloride one-step encapsulation technology. Seven days after the transplantation of the stem cell-derived TED and microencapsulated VEGF gene-modified hUCMSCs into the skin defect wounds on the backs of miniature pigs, the VEGF expression increased and the TED had a higher degree of vascularization. Re-epithelialization of the wound was completed after 3 weeks. CONCLUSIONS: Microencapsulated VEGF gene-modified hUCMSCs can effectively improve the vascularization of TED and consequently the quality of wound healing.

[Effect and mechanism of dantrolene on skeletal muscle of rats with severe scald injury].

OBJECTIVE: To explore the effect and mechanism of ryanodine receptor antagonist dantrolene on skeletal muscle of rats with severe scald injury. METHODS: A total of 56 Wistar rats were divided into control, scald and dantrolene treatment groups according to a random digital table. Rats in scald and dantrolene treatment groups were subject to 50% total body surface area (TBSA) full-thickness scald by a 12-second immersion of back and a 6-second immersion of abdomen in 94 °C water and then received an intraperitoneal injection of Ringer's solution. At the same time, the rats in scald group received 5% mannitol through caudal vein while those in dantrolene treatment group received dantrolene 2 mg/kg (dissolved in 5% mannitol). Rats in control group were sham-injured through an immersion of back and abdomen into 37 °C warm water. Tibialis anterior muscle samples were harvested at Days 1, 4 and 7 post-scalding. Changes of skeletal muscle ultrastructure were observed by transmission electron microscope, subcellular calcium ion (Ca(2+)) contents of skeletal muscle (including cytoplasm, mitochondria & sarcoplasm reticulum) were detected by electron probe X-ray microanalysis (EPMA) and the levels of calpain-1 and calpain-2 protein were determined by Western blot. And the activities of calpain were detected by enzyme-linked immunosorbent assay. RESULTS: In scald group, assorted arrangement appeared immediately at Day 1 post-injury and partial disappearance of Z lines at Day 7 post-injury. There were no significant ultrastructure changes in dantrolene treatment group at Day 1 and 4 post-injury. Curled filament and mild fracture occurred merely in dantrolene treatment group at Day 7 post-injury. The cytoplasmic contents of Ca(2+) were significantly higher in scald group than those in control group at Day 1 and 4 ((0.964 ± 0.060), (0.639 ± 0.067) vs (0.266 ± 0.029) µmol/L respectively, all P < 0.05) while the contents of Ca(2+) within sarcoplasm reticulum were obviously lower in scald group than those in control group at Day 1 and 4 ((0.368 ± 0.060), (0.814 ± 0.089) vs (1.337 ± 0.112) µmol/L respectively, all P < 0.05). However, those subcellular regions in dantrolene treatment group ((0.310 ± 0.069), (0.490 ± 0.039) and (1.241 ± 0.073), (1.161 ± 0.094) µmol/L) had no significant difference with control group (all P > 0.05). Calpain-1 and calpain-2 protein levels in scald group increased significantly at Day 1 and 4 post-injury versus control group (1.371 ± 0.034, 1.214 ± 0.030 vs 0.838 ± 0.017 & 1.464 ± 0.015, 1.390 ± 0.023 vs 0.806 ± 0.026 respectively, all P < 0.05), whereas calpain-1 and calpain-2 protein levels in dantrolene treatment (0.984 ± 0.031, 0.935 ± 0.023 and 0.836 ± 0.014, 0.741 ± 0.020) obviously were lower than those in scald group respectively (all P < 0.05). The activities of calpain in scald and dantrolene treatment groups at Day 1, 4 and 7 post-injury were (8.33 ± 0.21), (9.33 ± 0.21), (10.59 ± 0.18) and (7.76 ± 0.28), (7.86 ± 0.20), (7.91 ± 0.22) µmol/L respectively while the activity of calpain in control group was (7.62 ± 0.19) µmol/L. The activities of calpain in scald group were significantly higher than those in dantrolene treatment and control groups (all P < 0.05) whereas the activities of calpain in dantrolene treatment group had no obvious change versus control group (all P > 0.05). CONCLUSIONS: Dantrolene offers significant protection from skeletal muscle tissue damage and minimizes the ultrastructural change of tibialis anterior muscle induced by severe scald injury. The mechanism is probably through inhibiting an excessive release of Ca(2+) within sarcoplasm reticulum and down-regulated cytoplasmic expression and activity of calpain-1 and calpain-2.

[Effects of lipopolysaccharide pretreatment on endotoxin tolerance of human umbilical cord mesenchymal stem cells].

OBJECTIVE: To explore the effects of lipopolysaccharide (LPS) pretreatment on endotoxin tolerance of human umbilical cord mesenchymal stem cells (hUCMSCs) and its possible mechanism. METHODS: hUCMSCs (1×10(4) cells/well) were exposed to 0, 0.1, 1.0, 10.0, 20.0, 30.0, 40.0, 50.0 µg/ml LPS for 24 h respectively. And the cell viability of hUCMSCs was detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT). 1 µg/ml and 50.0 µg/ml LPS were used as pretreatment and apoptosis induction concentrations respectively. Pyrrolidine dithiocarbamate (PDTC) (20 µmol/L, pretreatment for 20 min) was used as a specific inhibitor of nuclear transcription factor NF-κB. hUCMSCs were randomly divided by Stata software into 7 groups: control (A), LPS induction (B), pretreatment + LPS induction (C), PDTC (D), PDTC+ pretreatment + LPS induction (E), pretreatment (F) and PDTC + pretreatment (G). The apoptosis of hUCMSCs was measured by Hoechst 33258 staining and flow cytometry (FCM). The expressions of NF-κB p65 and cellular FLICE-inhibitory protein (c-FLIP) were measured by Western blot. RESULTS: The cell viability of 0, 0.1, 1.0, 10.0, 20.0, 30.0, 40.0, 50.0 µg/ml LPS groups were 100%, (117.0 ± 8.8)%, (134.7 ± 6.9)%, (105.3 ± 8.3)%, (99.2 ± 8.3)%, (84.2 ± 9.3)%, (66.4 ± 6.6)% and (59.2 ± 8.0)% respectively. In comparison with 0 µg/ml LPS group, the cell viability of 1.0 µg/ml LPS group increased significantly (P = 0.004) while decreased in 40 and 50 µg/ml LPS groups (P = 0.005, 0.002). Hoechst 33258 staining indicated that chromatin of hUCMSCs was distributed evenly in group A; the apoptotic cell in group B dramatically increased; and the apoptotic cell in group C significantly decreased in comparison with that in group B. Apoptotic rates of groups A, B, C, D and E were (2.8 ± 0.8)%, (29.7 ± 3.4)%, (17.8 ± 3.0)%, (2.9 ± 0.4)% and (23.2 ± 2.6)% respectively. Compared with group A, apoptosis rate significantly increased in group B (P < 0.001). The apoptotic rate in group C significantly decreased than that in group B (P < 0.001) while group E was higher than group C (P = 0.015). The levels of NF-κB p65 and c-FLIP in group F (0.851 ± 0.031, 0.534 ± 0.053) was higher than that in group A (0.220 ± 0.021, 0.049 ± 0.009) (both P < 0.001), G (0.418 ± 0.007, 0.299 ± 0.061) (P < 0.001, P = 0.007). CONCLUSIONS: LPS pretreatment can resist LPS-induced hUCMSCs apoptosis and enhance the ability of endotoxin tolerance. And the mechanism may be related with activating the NF-κB signaling pathway and up-regulating the expression of c-FLIP.

Research progress and considerations on oral rehydration therapy for the prevention and treatment of severe burn shock: A narrative review.

Severe burns are a significant cause of life-threatening conditions in both peacetime and wartime. Shock is a critical complication during the early stages of burn injury, contributing substantially to mortality and long-term disability. Effective fluid resuscitation is crucial for preventing and treating shock, with prompt administration being vital. However, timely intravenous fluid resuscitation is often challenging, and errors in resuscitation significantly contribute to mortality. Therefore, exploring a more rapid and effective non-invasive method of fluid resuscitation is necessary. Oral rehydration therapy (ORT) has shown considerable potential in this regard. This paper reviews ORT's historical development and current research progress, discussing its application in early anti-shock treatment for burns. While ORT is generally safe, potential complications like diarrhoea, vomiting, and abdominal discomfort must be noted, particularly if the rehydration rate is too rapid or if gastrointestinal issues exist. Careful patient assessment and monitoring are essential during ORT administration. Based on a comprehensive review of relevant research, we present provisional guidelines for ORT in burn patients. These guidelines aim to inform clinical practice but should be applied cautiously due to limited clinical evidence. Implementation must be tailored to the patient's condition under healthcare supervision, with adjustments according to evolving circumstances: ① Initiation timing: Start as soon as possible, and the ideal start time is usually within 6 h after injury. ② Rate of application: Employing a fractional administration approach, wherein small quantities of approximately 150-250 millilitres are provided for each instance and the initial fluid rate of oral rehydration can be simplified to 100 mL/kg/24 h. ③ Composition combination: In addition to essential salts and glucose, the oral rehydration solution can incorporate various anti-inflammatory and cellular protection constituents.

Deleting fibroblast growth factor 2 in macrophages aggravates septic acute lung injury by increasing M1 polarization and inflammatory cytokine secretion.

Septic lung injury is strongly associated with polarization of M1 macrophages and excessive cytokine release. Fibroblast growth factor (FGF) signaling plays a role in both processes. However, the impact of FGF2 deficiency on macrophage polarization and septic acute lung injury remains unclear. To investigate this, we obtained macrophages from FGF2 knockout mice and examined their polarization and inflammatory cytokine expression. We also eliminated endogenous macrophages using clodronate liposomes and administered FGF2 knockout or WT macrophages intravenously in conjunction with cecal ligation and puncture (CLP) surgery to induce sepsis. In vitro analysis by flow cytometry and real-time PCR analysis demonstrated that FGF2 deficiency resulted in increased expression of M1 markers (iNOS and CD86) and inflammatory cytokines (CXCL1, IL1ß, and IL6), especially after LPS stimulation. Additionally, immunofluorescence demonstrated increased nuclear translocation of p65 NF-κB in FGF2 knockout macrophages and RNA-seq analysis showed enrichment of differentially expressed genes in the IL17 and TNFα inflammatory signaling pathways. Furthermore, in vivo experiments revealed that depletion of FGF2 in macrophages worsened sepsis-induced lung inflammation, lung vascular leak, and lung histological injury, accompanied by an increase in CD86-positive cells and apoptosis. Our study suggests that FGF2 deficiency in macrophages plays a critical role in the pathogenesis of septic ALI, possibly because of the enhanced M1 macrophage polarization and production of proinflammatory cytokines. These findings provide empirical evidence for potential therapeutic interventions targeting FGF2 signaling to modulate the polarization of M1 and M2 macrophages in the management of sepsis-induced acute lung injury.

Epidemiology and first aid measures in pediatric burn patients in northern China during 2016-2020: A single-center retrospective study.

Background and Aims: Burn and scald injuries are the fourth most common type of trauma. Pediatric burns account for a high proportion of the total number of burn patients and impose a high burden on public health. Understanding the epidemiology of pediatric burns can help improve science education and reduce the incidence of burn injuries. Methods: This study is a single-center retrospective study. One thousand five hundred and twenty-seven pediatric burn patients admitted to our burn center from January 2016 to December 2020 were included. Demographic and epidemiological data of included patients were extracted and analyzed. The correlations of categorical data were tested by the Chi-square tests, and differences of continuous data were tested by the Kruskal-Wallis tests. A p-value of less than 0.05 was considered to be statistically significant. Results: The results showed that children under 3 years of age were most susceptible to burn and scald injuries. Burn injuries were most likely to occur in the season of winter and at the place of home. 56.6% of included patients did receive first aid measures, while 1.8% received gold-standard first aid. Clinical variables related to the severity of injuries were statistically different between patients with and without cooling measures in first aid. Linear regression models showed that emergency treatment of burns in children and adolescents was associated with outcome indicators, including number of operations, total operation duration per total burn surface area (TBSA), cost per TBSA, and length of stay per TBSA. Conclusions: This study summarized the epidemiology and outcomes of pediatric burn patients admitted to a burn center in northern China. Adopting cooling measures in first aid can reduce the severity of injuries and reduce the burden on the medical system. Education on burn prevention and first aid measures to caregivers of children, especially preschool children, should be strengthened.

[New research direction of organ dysfunction caused by hemorrhagic shock: mechanisms of mitochondrial quality control].

Hemorrhagic shock (HS) is one of the leading causes of death among young adults worldwide. Multiple organ dysfunction in HS is caused by an imbalance between tissue oxygen supply and demand, which is closely related to the poor prognosis of patient. Mitochondrial dysfunction is one of the key mechanisms contributing to multiple organ dysfunction in HS, while mitochondrial quality control regulates mitochondrial function through a series of processes, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mitochondrial-derived vesicles, and mitochondrial protein homeostasis. Modulating mitochondrial quality control can improve organ dysfunction. This review aims to summarize the effects of mitochondrial dysfunction on organ function in HS and discuss the potential mechanisms of mitochondrial quality control, providing insights into the injury mechanisms underlying HS and guiding clinical management.

Black Phosphorus Nanosheets-Based Hydrogel for Efficient Bacterial Inhibition and Accelerating Wound Healing.

With the swift evolution of multidrug-resistant bacteria resulting from the intense and inappropriate use of antibiotics, there is a pressing need for innovative solutions. In this study, a thermosensitive hydrogel was developed for efficient bacterial inhibition and promotion of wound healing. The antibacterial chitosan (CS) thermosensitive hydrogel, cross-linked with two-dimensional photothermal nanomaterial black phosphorus (BP) nanosheets through electrostatic interactions, effectively encapsulates and sustains the release of angiogenic drug deferoxamine mesylate (DFO). This facilitates the acceleration of re-epithelialization and neovascularization by enhancing cell migration and proliferation. Following near-infrared (NIR) treatment, this hydrogel demonstrates rapid eradication of the most common multidrug-resistant bacteria encountered in clinical settings, achieved through physical disruption of bacterial membranes and photothermal therapies. Noteworthy is the significant upregulation of IL-19 expression via STAT3 signaling pathways by the BP/CS-DFO hydrogel in a full-thickness wound model. This results in the polarization of the anti-inflammatory M2 macrophage phenotype, altering the microenvironment to a pro-healing state and enhancing extracellular matrix deposition and blood vessel formation. In conclusion, the BP/CS-DFO hydrogel shows immense promise as a potential clinical candidate for wound healing and antimicrobial therapy. Its innovative design and multifunctional capabilities position it as a valuable asset in combating antibiotic resistance and enhancing efficiency in wound healing.

Downregulated microRNA-32 expression induced by high glucose inhibits cell cycle progression via PTEN upregulation and Akt inactivation in bone marrow-derived mesenchymal stem cells.

MicroRNAs regulate a host of physiological and pathological processes in mesenchymal stem cells (MSCs), although no published studies describe changes in microRNA expression or function in MSCs under in vitro hyperglycemic conditions. By using a microRNA microarray approach, we have identified that miRNA-32-5p expression is significantly reduced under hyperglycemic conditions in rat bone marrow-derived MSCs. Expression of miRNA-32-5p targets the 3'-untranslated region of the mRNA encoding phosphatase and tensin homologs deleted on chromosome 10 (PTEN), a negative regulator of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Exposure to high glucose levels reduced miR-32-5p expression, induced PTEN expression, and inhibited activation of the PI3K/Akt signaling pathway of MSCs. Conversely, overexpression of miR-32-5p inhibited the expression of PTEN, ameliorated the inhibitory effect of high glucose levels on the PI3K/Akt signaling pathway, and promoted cell cycle progression from G0/G1 to G2/M and S phases. Our study indicates that exposure of MSCs to hyperglycemic conditions reduces miR-32-5p expression and disturbs cell cycle progression through a PTEN-mediated inhibitory effect on the PI3K/Akt signaling pathway. In summary, MiR-32-5p is a potentially important therapeutic agent for preventing MSC dysfunction under hyperglycemic conditions.

Influence of hyaluronic acid on wound healing using composite porcine acellular dermal matrix grafts and autologous skin in rabbits.

This study aims to explore the influence of hyaluronic acid (HA) on wound healing during xenogeneic porcine acellular dermal matrix (PADM) composite skin grafting. The results will facilitate the development of methods for improving graft contracture and poor elasticity of composite transplantation. Exogenous HA was added to composite PADM grafts and to thin autologous skin grafts during rabbit full-thickness skin wound repair. The influence of HA on wound healing was evaluated according to its contracture rate and its expression of collagen types I and III. The possible mechanism was then explored based on HA metabolism and vascularisation in the skin graft. The results show that exogenous HA relieves graft contracture on rabbit wound surfaces, increases collagen I and III expression and decreases the ratio between collagen types. HA stimulates the generation of more CD44 receptors to strengthen its enzymolysis. The resulting metabolites promote the vascularisation of the wound surface, which are conducive for mitigating graft contracture, and further improve the composite grafting effect.

[Voltage dependent anion channel 2 involved mitochondrial apoptosis and its possible regulatory signal pathway in hearts of rats with severe scalds].

OBJECTIVE: To explore the role of voltage dependent anion channel 2 (VDAC2) involved mitochondrial apoptosis in heart injury of rats with severe scald injury and elucidate its possible regulatory signal pathway. METHODS: A total of 60 Wistar rats were divided into sham scald group (n = 30) and scald group (n = 30) according to a random digital table. Blood and heart tissue samples were harvested at Day 1, 7, 14 post scalding. Myocardial injury was assessed with cardiac troponin I (cTnI) by enzyme-linked immunosorbent assay (ELISA). Mitochondrial apoptosis activation was evaluated by the expressions of Bax/Bcl-2 ratio, cytoplasmic cytochrome C and VDAC2. And the levels of phosphatidylinositol 3-kinase, p-Glycogen Synthase Kinase-3ß and hexokinase 2 protein were determined by Western blot. RESULTS: The serum levels of cTnI were significantly higher in scald group than those in sham scald group at Day 1, 7, 14 ((1.41 ± 0.25) vs (0.53 ± 0.23) µg/L, (1.93 ± 0.53) vs (0.43 ± 0.23) µg/L, (1.62 ± 0.34) vs (0.41 ± 0.22) µg/L respectively, all P < 0.05). Compared with sham scald group, Bax/Bcl-2 ratio increased significantly in scald group at Day 1, 7 day post-scalding (3.360 ± 0.173 vs 0.623 ± 0.044, 2.736 ± 0.341 vs 0.698 ± 0.064, 1.290 ± 0.234 vs 0.718 ± 0.063 respectively, all P < 0.05), VDAC2 protein level in scald group decreased significantly at Day 1, 7, 14 (0.070 ± 0.009 vs 0.328 ± 0.026, 0.007 ± 0.002 vs 0.291 ± 0.025, 0.009 ± 0.004 vs 0.302 ± 0.037 respectively, all P < 0.05), the cytoplasmic levels of cytochrome increased significantly in scald group at Day 1, 7, 14 (0.418 ± 0.030 vs 0.022 ± 0.007, 1.685 ± 0.169 vs 0.030 ± 0.011, 0.300 ± 0.037 vs 0.098 ± 0.014 respectively, all P < 0.05), the expression of PI3K was significantly lower in scald group at Day 14 post-scalding (0.083 ± 0.015 vs 0.328 ± 0.011, P < 0.05), the expressions of p-GSK3ß all reduced significantly at Day 1, 7, 14 (0.098 ± 0.014 vs 0.446 ± 0.031, 0.064 ± 0.002 vs 0.476 ± 0.054, 0.074 ± 0.010 vs 0.442 ± 0.041, respectively, all P < 0.05) and the expressions of HK2 were lower at Day 7, 14 post-scalding (0.390 ± 0.027 vs 0.611 ± 0.070, 0.267 ± 0.018 vs 0.490 ± 0.042, respectively, all P < 0.05). CONCLUSIONS: VDAC2 involved mitochondrial apoptosis is activated in myocardium after severe scalds. And it may be regulated by the pathway of PI3K-GSK-HK2.

[Functions of exogenous application of connective tissue growth factor in stimulating human dermal papilla cells and human hair follicle outer root sheath cells for reconstructive tissue-engineering hair follicles].

OBJECTIVE: To explore the functions of connective tissue growth factor (CTGF) in the restoration of hair follicles with a mixture of human dermal papilla cells and human hair follicle outer root sheath cells in vitro in nude mice. METHODS: Human hair follicle outer root sheath cells (hfORS) and human hair dermal papilla cells (hDP) were cultured in vitro and mixed in a fixed ratio (hfORS: hDP = 5:1). Flow cytometry was used to detect the content of CD200(+) cells in human hair follicle outer root sheath cells.And 8 nude mice were divided randomly into 2 groups according to a random number table and back wounds produced. Group A was transplanted with cell mixture plus 20 µg/L CTGF. Group B was transplanted with cell mixture alone. After 8 weeks of transplantation, the development of hair follicle formation was observed histologically.PCR was used to detect the expression of human specific DNA and mice DNA in transplants. RESULTS: The portion of CD200(+) cells in cultured hfORS was 19.65%. At 8 weeks after implantation, hair follicle formation could be observed in Group A (268 ± 96) more than Group B (62 ± 20). The difference was statistically significant (P < 0.05). And PCR showed that there was human composition in transplant. CONCLUSION: CTGF can induce the formation of hair follicle by promoting the interference between hDP and hfORS.

[Clinical study of repairing donor site of thickness from cicatricial skin with auto-scalp grafting].

OBJECTIVE: To study the effects of using auto-scalp for repairing donor site of thickness from cicatricial skin with auto-scalp grafting. METHODS: A total of 13 cases with donor site of thickness from cicatricial skin from January 2011 to December 2011 were analyzed. Wounds of donor site from cicatricial skin were grafted with auto-scalp and scalp were fixation was applied with negative pressure. The survival rate of auto-scalp graft was observed at Day 7 post-operation. At Month 12, hyperplastic scars at these donor sites of cicatricial skin were assessed through Vancouver Scar Assessment Table, scar itch assessment and scar proliferation rate. Wounds in the other thirteen cases with donor site of thickness from cicatricial skin from January 2010 to December 2010 were covered with vaseline gauze as control. RESULTS: No significant difference existed in the gender and age of the two groups patients (P > 0.05). The auto-scalp graft all survived. And the average healing time of donor-site wound in cicatricial skin in grafting group (7 days) was significantly decreased than that of control group (a mean of 20 days) (P < 0.01). After followed up for twelve months, the scar formation assessment value (1.5 ± 0.5), scar itch assessment (1.2 ± 0.4) and scar proliferation rate (14.6% ± 7.6%) in grafting group were significantly less than those of control group (6.7 ± 1.1, 2.0 ± 0.7, 55.8% ± 12.2%, all P < 0.01). CONCLUSION: Auto-scalp grafting may greatly shorten the healing procedure and ameliorate the quality of donor-site of thickness from cicatricial skin.