Metabolomics is a novel emerging technology recently applied in management of severe diseases and trauma,and has been widely used in gene analysis of disease metabolic disorders,clinical biomarker screening and disease diagnosis.This review comprehensively summarizes the latest research progress of the metabolomics in severe trauma and burns recently like traumatic brain injury(TBI),traumatic hemorrhagic shock,severe burns and so on.The paper elaborates the metabolomic technology which can quickly reflect the real-time metabolic changes of severely injured patients at different stages after injury,and uncovers new clinical biomarkers and potential drug targets of the patients with severe injuries thus improves the diagnosis and treatment strategies.Finally,we look for-ward to the current metabolomics research projects and tackling challenges on the burn-blast combined injuries,and the simultaneous development of multi-omics technology as well as artificial intelligence algorithms,which promotes the development of precision medicine.

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.

Objective:To prepare advanced platelet-rich fibrin (A-PRF)/chitosan thermosensitive hydrogel (hereinafter referred to as composite hydrogel) and explore the effects of composite hydrogel on full-thickness skin defect wound healing in diabetic rats.Methods:This study was an experimental study. The composite hydrogel with porous mesh structure and thermosensitive characteristics was successfully prepared, containing A-PRF with mass concentrations of 10, 15, 20, 50, and 100 g/L. Diabetic model was successfully established in male Sprague-Dawley rats aged 6-8 weeks by intraperitoneal injection of streptozotocin, and 4 full-thickness skin defect wounds were established on the back of each rat (finally the model was successfully established in 36 rats). Three wounds of each rat were divided into blank group (no drug intervention), positive control group (dropping recombinant human granulocyte-macrophage stimulating factor gel), and chitosan hydrogel group (dropping chitosan hydrogel solution). Thirty rats were collected, and the remaining one wound of each rat (totally 30 wounds) was divided into 10, 15, 20, 50, and 100 g/L composite hydrogel groups, with 6 wounds in each group, which were dropped with composite hydrogel solution containing 10, 15, 20, 50, and 100 g/L A-PRF, respectively. Taking the remaining six rats, the remaining one wound from each rat was dropped with composite hydrogel solution containing 100 g/L A-PRF. On 14 d after injury, 6 rats with one wound dropped with composite hydrogel containing 100 g/L A-PRF were selected for hematoxylin-eosin (HE) staining to observe the inflammation, hemorrhage, or necrosis of the heart, liver, spleen, lung, and kidney. On 10 d after injury, 6 rats with one wound dropped with composite hydrogel containing 15 g/L A-PRF were selected to observe the blood perfusion of wounds in the four groups (with sample size of 6). On 7 and 14 d after injury, the wound healing rates in the eight groups were calculated. On 14 d after injury, the wound tissue in the eight groups was taken for HE and Masson staining to observe the formation of new epithelium and collagen formation, respectively; the positive expressions of CD31 and vascular endothelial growth factor A (VEGFA) were detected by immunohistochemistry, and the percentages of positive areas were calculated; the protein expressions of CD31 and VEGFA were detected by Western blotting; the mRNA expressions of CD31 and VEGFA were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction method (with all sample sizes of 4).Results:On 14 d after injury, no obvious inflammation, hemorrhage, or necrosis was observed in the heart, liver, spleen, lung, and kidney in the 6 rats. On 10 d after injury, the blood perfusion volume of wound in 15 g/L composite hydrogel group was significantly more than that in blank group, positive control group, and chitosan hydrogel group, respectively (with P values all <0.05). On 7 and 14 d after injury, the wound healing rates of blank group were (26.0±8.9)% and (75.0±1.8)%, which were significantly lower than those of positive control group, chitosan hydrogel group, and 10, 15, 20, 50, and 100 g/L composite hydrogel groups, respectively ((45.8±3.2)%, (49.8±3.7)%, (51.2±2.9)%, (68.5±2.4)%, (68.8±1.5)%, (72.7±2.1)%, (75.0±3.7)% and (79.1±1.9)%, (77.2±1.7)%, (82.3±1.3)%, (89.6±1.9)%, (89.8±1.3)%, (87.3±1.1)%, (87.9±1.3)%), P<0.05; the wound healing rates of positive control group, chitosan hydrogel group, and 10 g/L composite hydrogel group were significantly lower than those of 15, 20, 50, and 100 g/L composite hydrogel groups ( P<0.05). On 14 d after injury, the wound epithelialization degrees of 15, 20, 50, and 100 g/L composite hydrogel groups were higher than those of the other 4 groups, the new microvascular situation was better, and the collagen was more abundant and arranged more neatly. On 14 d after injury, the percentages of CD31 and VEGFA positive areas in wounds in positive control group and the percentage of VEGFA positive area in wounds in chitosan hydrogel group were significantly higher than those in blank group ( P<0.05), the percentage of VEGFA positive area in wounds in 10 g/L composite hydrogel group was significantly higher than that in blank group, chitosan hydrogel group, and positive control group (with P values all <0.05), and the percentages of CD31 and VEGFA positive areas in wounds in 15, 20, 50, and 100 g/L composite hydrogel groups were significantly higher than those in blank group, positive control group, chitosan hydrogel group, and 10 g/L composite hydrogel group ( P<0.05). On 14 d after injury, the protein and mRNA expressions of CD31 and VEGFA in wound tissue in chitosan hydrogel group, positive control group, and 10 g/L composite hydrogel group were significantly higher than those in blank group ( P<0.05); the protein expression of VEGFA in wound tissue in 10 g/L composite hydrogel group was significantly higher than that in positive control group ( P<0.05), and the mRNA expressions of CD31 and VEGFA in wound tissue in 10 g/L composite hydrogel group were significantly higher than those in positive control group and chitosan hydrogel group ( P<0.05); the protein and mRNA expressions of CD31 and VEGFA in wound tissue in 15, 20, 50, and 100 g/L composite hydrogel groups were significantly higher than those in blank group, positive control group, chitosan hydrogel group, and 10 g/L composite hydrogel group ( P<0.05); the mRNA expressions of CD31 and VEGFA in wound tissue in chitosan hydrogel group were significantly lower than those in positive control group ( P<0.05). Conclusions:The composite hydrogel has high biological safety, can improve wound blood perfusion, effectively promote the formation of blood vessels and collagen in wound tissue, thus promoting the wound healing of full-thickness skin defects in diabetic rats. 15 g/L is the optimal mass concentration of A-PRF in composite hydrogel.

BACKGROUND/OBJECTIVES: Previous studies have reported that protein supplementation contributes to the attenuation of inflammation. Serious trauma such as burn injury usually results in the excessive release of inflammatory factors and organs dysfunction. However, a few reports continued to focus on the function of protein ingestion in regulating burninduced inflammation and organ dysfunction.MATERIALS/METHODS: This study established the rat model of 30% total body surface area burn injury, and evaluated the function of blended protein (mixture of whey and soybean proteins). Blood routine examination, inflammatory factors, blood biochemistry, and immunohistochemical assays were employed to analyze the samples from different treatment groups. RESULTS: Our results indicated a decrease in the numbers of white blood cells, monocytes, and neutrophils in the burn injury group administered with the blended protein nutritional support (Burn+BP), as compared to the burn injury group administered normal saline supplementation (Burn+S). Expressions of the pro-inflammatory factors (tumor necrosis factor-α and interleukin-6 [IL-6]) and chemokines (macrophage chemoattractant protein-1, regulated upon activation normal T cell expressed and secreted factor, and C-C motif chemokine 11) were dramatically decreased, whereas anti-inflammatory factors (IL-4, IL-10, and IL-13) were significantly increased in the Burn+BP group. Kidney function related markers blood urea nitrogen and serum creatinine, and the liver function related markers alanine transaminase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase were remarkably reduced, whereas albumin levels were elevated in the Burn+BP group as compared to levels obtained in the Burn+S group. Furthermore, inflammatory cells infiltration of the kidney and liver was also attenuated after burn injury administered with blended protein supplementation. CONCLUSIONS In summary, nutritional support with blended proteins dramatically attenuates the burn-induced inflammatory reaction and protects organ functions. We believe this is a new insight into a potential therapeutic strategy for nutritional support of burn patients.

Objective:To explore the clinical effects of pre-expanded anterior perforator flap of transverse cervical artery in extensive facial and cervical scar reconstruction and contralateral pre-expanded thoracic random flap in relay in donor site repair.Methods:A retrospective cohort study was conducted. From May 2008 to December 2018, 10 patients with extensive facial and cervical scar after burns were treated in the Fourth Medical Center of PLA General Hospital, including 8 males and 2 females, aged 10-55 years. In the first stage of operation, two skin and soft tissue expanders of the same volume (with rated capacity of 250-600 mL) were respectively placed in the right side and left side of the chest according to the size of scar, and then the skin was expanded. The total amount of normal saline injected was 2 to 4 times of the rated capacity of the expander. In the second stage, the defect with area of 12 cm×8 cm-23 cm×15 cm caused by scar resection and release was repaired with unilateral pre-expanded anterior perforator flap of transverse cervical artery with area of 12 cm×9 cm-24 cm×16 cm. The contralateral pre-expanded thoracic random flap with the same area as that of the above-mentioned perforator flap was extended to repair the secondary defect with area of 8 cm×6 cm-17 cm×14 cm formed after transfer of the above-mentioned perforator flap. The exploration of perforating branch of transverse cervical artery, flap transfer and survival, injury repair, and complications were observed. The appearance and related function of donor and recipient sites and satisfaction of patients were followed up.Results:The perforating branches of transverse cervical artery appeared stably in the 10 patients. All the flaps were transferred to the recipient area without tension and survived. Both facial and cervical injuries were repaired successfully with no common complications. During the follow-up of 6 months-8 years, the color and texture of the pre-expanded anterior perforator flap of transverse cervical artery matched with the surrounding tissue, the functions of head raising and neck rotation of patients were significantly improved compared with those before operation, the color and texture of the flap transplanted in the first donor site matched with the original skin, linear scar left at the surgical incision, and 9 patients were satisfied with the restoration of the appearance and function of donor and recipient sites.Conclusions:The color and texture of the pre-expanded anterior perforator flap of transverse cervical artery match well with the face and neck, and the repairable area is large. After the perforator flap is removed, the secondary wound can be repaired with the pre-expanded thoracic random flap at the same time, and the injury of the chest donor site is alleviated. This relay repair method is a good choice for reconstructing extensive facial and cervical scar.

Objective:To investigate the expression and phosphorylation level change of adenosine monophosphate activated protein kinase (AMPK) in skeletal muscle of severely scald rats and its roles in skeletal muscle atrophy in severely scalded rats.Methods:The experimental research method was applied. Totally 100 6-week-old male Wistar rats were divided into sham injury group and scald group according to the random number table, with 50 rats in each group. After weighing the body weight, rats in scald group were inflicted with full-thickness scald of 30% total body surface area on the back, and rats in sham injury group were simulated with scald. At 6 h and on 1, 3, 5, and 7 d post injury, 10 rats in each group were taken to measure their body weights and weights of extensor digitorum longus and soleus muscle. At 6 h and on 1, 3, 5, and 7 d post injury, the tibialis anterior muscles were collected, the mRNA expressions of muscle atrophy F-box protein (MAFbx) and muscle-specific RING finger protein 1 (MuRF1) were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction; the content of adenosine monophosphate (AMP), adenosine diphosphate, and adenosine triphosphate (ATP) were detected by high performance liquid chromatography, and AMP/ATP ratio and energy charge were calculated; the protein expressions of AMPK-α and phosphorylated AMPK-α (p-AMPK-α) were detected by Western blotting, and the p-AMPK-α/AMPK-α ratio was calculated, with sample number of 4 in each time point of each group. Data were statistically analyzed with analysis of variance for factorial design and least significant difference test.Results:The body weights of rats in 2 groups before injury and at each time point post injury were close ( P>0.05). At 6 h post injury, the weight of extensor digitorum longus of rats in scald group was (0.107±0.007) g, which was significantly heavier than (0.086±0.0607) g of sham injury group ( P<0.01). On 3 d post injury, the weight of extensor digitorum longus of rats in scald group was (0.083±0.016) g, which was significantly lighter than (0.102±0.005) g of sham injury group ( P<0.01). The weight of soleus of rats in 2 groups were close at each time point post injury ( P>0.05). Compared with those of sham injury group, the mRNA expression of MAFbx in tibialis anterior muscle of rats in scald group was significantly up-regulated at 6 h post injury ( P<0.01), and the mRNA expressions of MuRF1 in tibial anterior muscle of rats in scald group were significantly up-regulated at 6 h and on 1 d post injury ( P<0.01). At 6 h and on 7 d post injury, compared with those of false injury group, the AMP/ATP ratios of the tibial anterior muscle of rats in scald group were significantly increased ( P<0.05 or P<0.01), and energy charges of the tibial anterior muscle of rats in scald group were significantly decreased ( P<0.01). At each time point post injury, the protein expressions of AMPK-α of the tibial anterior muscle of rats in 2 groups were close ( P>0.05). The p-AMPK-α/AMPK-α ratios of the tibial anterior muscle of rats in scald group at 6 h and on 7 d post injury were significantly higher than those in sham injury group ( P<0.05 or P<0.01). Conclusions:The decrease in energy charge and increase in AMP/ATP ratio of skeletal muscle of rats after severe scald activate AMPK. The activation of AMPK in the early stage of injury is consistent with the up-regulation of MAFbx and MuRF1 expressions and down-regulation of skeletal muscle weight. The above-mentioned changes may be one of the molecular mechanisms of skeletal muscle atrophy in rats with severe scald

Blast traumatic brain injury (bTBI) often causes irreversible damage to the brain which seriously endangers the lives of the wounded and can be accompanied by various complications, and has high disability and morbility in peacetime and wartime. The bTBI is divided into primary injury and secondary injury, resulting in a series of neuropsychiatric symptoms. The mechanism of bTBI contains cracking effect, implosion effect, inertia effect and cavitation effect. Multiple factors, such as shrapnel injury caused by explosion, collision of body being thrown with hard objects and smash of buildings, can lead to brain injury. There are challenges in the diagnosis and treatment of bTBI, because the injury is often closed, the onset is slow, the diagnosis is easy to missed, the pathogenesis is complex, and the clinical manifestations vary. The authors review the mechanism of bTBI and its preclinical treatment, hoping to provide a way for the preclinical treatment of bTBI.

The injury mechanism of high-voltage electric burn in limbs is complex and special. The soft tissue and vascular injuries caused by high-voltage electric burn are serious and concealed. It is difficult to judge the severity and extent of injury before surgery, which affects the diagnosis and treatment effects and remains a major problem in burn field. In recent decades, a series of clinical studies have been conducted by scholars at home and abroad, using various imaging methods for the judgment of soft tissue and vascular injuries, which have their own advantages and disadvantages. According to the principle of accuracy, precision, safety, and easy operation, magnetic resonance imaging and magnetic resonance angiography are required at the same time in general for the imaging judgment of soft tissue and vascular injuries in limbs with high-voltage electric burn. The B-mode ultrasonography shall be performed if a precise judgment of vascular injury is needed.

Objective: To explore the surgical methods for children with contracture deformity on hands after burn. Methods: From January 2014 to January 2018, 33 pediatric patients, a total of 42 hands with scar contracture deformities were reviewed. There were 24 males and 9 females, aged from 11 months to 6 years and 7 months. Among them, 20 hands were volar metacarpophalangeal joint contractures, 9 were volar interphalangeal joint contractures, 7 were dorsal metacarpophalangeal joint contractures (3 claw-shaped hands), 3 were hand back contractures, and 3 were palm contractures. Of the 42 hands, 36 hands were repaired with full-thickness skin grafts or split-thickness skin grafts, after the removal of contracted scar, and 6 hands were repaired with abdominal skin flaps, due to the tendon or bone exposure after the scar removal. Results: Skin grafts on 31 hands were all survived after 2 weeks. However, the survival area of 3 skin grafts was about 90%, and 2 skin grafts survived about 80%. All of them healed well after dressing changing. The 6 hands repaired with abdominal skin flap healed well too. After 1-2.5 years of follow-up, finger scar contracture occurred in 4 hands with skin grafting, and they were performed scar excision and sheet skin grafting. Three hands were treated with Z-plasty, due to web space contracture. The function of other hands were normal, without contracture or deformity. The skin color and texture were similar to the surrounding skin, with limited pigmented. Scars on the edge of skin grafts was not obvious. Patients and their families were satisfied. Conclusions The sheet skin graft is the main method for postburn scar contracture in children′s hands. The abdominal skin flap should be considered, if tendon or bone is exposed, especially for large wound or multiple sites.

Objective: To explore the effects of insulin therapy on skeletal muscle wasting (SMW) in severely scalded rats and its related mechanism. Methods: Totally 48 male Wistar rats aged 7-8 weeks were divided into simple scald (SS) group and insulin therapy (IT) group according to the random number table, with 24 rats in each group. After weighing the body mass and measuring the blood glycemic level of the tail end with a glucometer, the rats in the two groups were immersed in hot water at 94 ℃ for 12 seconds to make a full-thickness dorsal scald model involving 30% total body surface area. Rats in group IT were subcutaneously injected with 1 U/kg insulin glargine at 8: 00 a day from post injury day (PID) 1 to 7, whilst rats in group SS were given the same amount of normal saline. Rats in the two groups were given 10 mL/kg enteral nutritional emulsion by intragastric infusion at 8: 00 (after insulin administration), 13: 00, and 18: 00 a day respectively from PID 1 to 7. The blood glycemic levels of tail end of rats in the two groups were measured by glucometer before insulin administration on PID 1-4, 6, and 7 and on every morning of PID 8, 9, 11, 12, and 14. The body mass of rats in the two groups on PID 14 without any treatment was weighed. Eight rats from each group were collected respectively on PID 4, 7, and 14 to harvest tibialis anterior muscle (TAM) samples. The mass of TAM on PID 14 was weighed. The ultrastructural changes of TAM myocytes on PID 7 were observed with transmission electron microscope. The apoptotic rates of TAM myocytes on PID 4, 7, and 14 were assessed by the assay of terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphate-biotin nick end labeling, the expressions of cysteine-aspartic protease-3 (caspase-3) of TAM on PID 4, 7, and 14 were detected with immunohistochemistry, and protein expressions of endoplasmic reticulum (ER) stress (ERS) associated proteins glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein-homologous protein (CHOP), and activated caspase-12 of TAM on PID 4, 7, and 14 were detected with Western blotting. Data were processed with completely random design t test, analysis of variance for repeated measurement, analysis of variance for factorial design, t test, and Bonferroni correction. Results: The blood glycemic level and body mass of rats in the two groups before injury were similar (t=0.204, 0.405, P>0.05). There were no statistically significant differences in blood glycemic levels of rats between the two groups on PID 1, 6, 9, 11, 12, and 14 (t=0.229, 3.339, 1.610, 0.178, 0.181, 0.079, P>0.05). Compared with those of group SS, blood glycemic levels of rats in group IT were significantly lower on PID 2, 3, 4, 7, and 8 (t=7.245, 4.165, 4.609, 4.018, 3.995, P<0.05 or P<0.01). On PID 14, the body mass and TAM mass of rats in group IT were (271±19) g and (0.47±0.05) g respectively, both obviously higher than (254±12) g and (0.43±0.04) g of group SS (t=2.159, 2.375, P<0.05). On PID 7, nuclear pyknosis and deformation, chromosome misdistribution, and ER swelling in TAM myocytes of rats in group SS were observed; the apoptotic alterations and ER swelling of TAM myocytes were alleviated in rats of group IT as compared with those of group SS. The apoptotic rates of TAM myocytes of rats in group IT were obviously lower than those of group SS on PID 4, 7, and 14 (t=4.262, 9.153, 9.799, P<0.01). The expressions of caspase-3 in TAM of rats in group IT were obviously lower than those of group SS on PID 7 and 14 (t=10.429, 7.617, P<0.01). Compared with those of group SS, the protein expressions of GRP78 were obviously increased on PID 4 and 14 (t=4.172, 4.437, P<0.05), the protein expressions of activated caspase-12 were obviously decreased on PID 7 and 14 (t=11.049, 11.181, P<0.01), and the protein expressions of CHOP were obviously decreased on PID 4, 7, and 14 (t=13.837, 9.572, 6.930, P<0.01) in TAM of rats in group IT. Conclusions Insulin therapy may reduce skeletal muscle myocytes apoptosis and SMW by alleviating ERS in rats with severe scald.