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The ability to effectively detect bacterial infection in human tissues is important for the timely treatment of the infection. However, traditional techniques fail to visualize bacterial species adhered to host cells

In response to coronavirus disease 2019 (COVID-19), the Shanghai Burn Clinical Quality Control Center organized experts to formulate and implement a set of rapid, simple, and effective prevention and control measures, and there have not been any cases of health care professionals or inpatients in burn units suspected or confirmed with COVID-19. This article elaborates on the specific measures in burn units in response to the epidemic, including the implementation of standardized procedures, remote consultations, strengthened follow-up, exchange of experience, and popular science, among others. We share experience from Shanghai to benefit related disciplines in other countries and regions.

Cutaneous thermal injury is commonly combat-related and is the most destructive form of trauma. Severe extensive burns and trauma increase patient’s sensitivity to infection, which may further develop into sepsis. Though modern resuscitation strategies continue to shrink the number of death resulted from ischemic shock, sepsis-related mortality has not declined in recent years. Actually, among the patients with burn injuries, infection has the highest mortality. Pathophysiology of burn- and trauma-associated pulmonary infection is complicated and multifold. Damage to defense mechanism is one important factor, which includes inhibition of cough reflex, increase of mucous secretion, compromised mucociliary clearance, and even injuries to tracheal epithelium. In severe cases, systemic inflammatory response syndrome (SIRS) is usually reported, which may contribute to multiple organ dysfunction syndrome (MODS) or even multiple organ failure. Meanwhile, SIRS is always complicated with immunosuppression. Nosocomial pneumonia is a commonly seen complication among burned and other patients with life-threatening conditions. Several routes have been identified, through which pathogens break defensive barriers and into burn patients’ body. Burn wound infection or sepsis is the primary route; opportunistic infection occurs when innate or adaptive host immune responses are compromised; gastrointestinal tract is sensitive to cutaneous thermal injury and may serve as another pool of pathogens, with subsequent bacterial translocation to the blood stream, burn wound, and even other systemic organs.

Building a powerful navy is the key to safeguarding China's maritime rights and interests and developing maritime strategy. Improving the level and capability of trauma care for naval battle is one of the important tasks for safeguarding naval combat capability and keeping up morale. This paper analyzes the characteristics of naval battle and both the key points and difficulties of medical support under the conditions of modern war, and draws lessons from the experiences of United States navy in the construction of medical support mode, force allocation and maritime health platform, and refers to its training mode and evaluation methods by relying on advanced medical equipment to carry out simulated trauma care efficiently. This paper considers and analyzes the mode of maritime health support, the allocation and utilization of mobile medical service force, the research work related to trauma for naval battle and the training of health professionals. The aim of this study was to provide some effective suggestions for improving capacity and efficiency of trauma care for naval battle. DOI: 10.11855/j.issn.0577-7402.2016.12.01

Acute lung injury (ALI) and respiratory distress syndrome are common, potentially lethal injuries that predominantly occur following chest trauma. Circular RNAs (circRNAs) are stable conserved non-coding RNAs that are widely expressed in different organs. To the best of our knowledge, no previous studies have shown whether circRNAs are involved in traumatic lung injury (TLI). The aim of the present study was to identify highly expressed circRNAs in plasma samples from patients with TLI and explore their potential functions in the pathogenesis of TLI. A high-throughput circRNA microarray was used to investigate the expression profile of circRNAs in plasma samples from five patients with TLI and paired control samples. Subsequently, a total of five abnormally expressed circRNAs were investigated using reverse transcription-quantitative PCR (RT-qPCR). A bioinformatics analysis was performed to predict a competitive endogenous RNA (ceRNA) network. In addition, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to identify the main biological processes and pathways. Finally, additional samples were tested to identify the expression profiles of the selected circRNAs. Among the 310 circRNAs that were highly expressed in the microarray analysis, 60 were upregulated and 250 were downregulated in patients with TLI. RT-qPCR results indicated that two downregulated circRNAs (circ_102927 and circ_100562) and one upregulated circRNA (circ_101523) matched the microarray results. The bioinformatics analysis constructed a targeting network based on the three validated circRNAs. GO and KEGG analyses identified the top ten enriched annotations. The expression of homo sapiens circular RNA 102927 (hsa_circRNA_102927) in the plasma of patients with TLI was 0.34-fold compared with the control group in expanded size validation. The results of the present study identified the differentially expressed circRNAs in the plasma of patients with TLI and provided evidence that highly expressed circRNAs involved in the ceRNA network may serve a role in the pathophysiology of TLI.

ObjectivesWe employed a comprehensive systematic review and meta-analysis to assess benefits and risks of a threshold of haemoglobin level below 7 g/dL versus liberal transfusion strategy among critically ill patients, and even patients with septic shock.DesignSystematic review and meta-analysis.Data sourcesWe performed systematical searches for relevant randomised controlled trials (RCTs) in the Cochrane Library, EMBASE and PubMed databases up to 1 September 2019.Eligibility criteriaRCTs among adult intensive care unit (ICU) patients comparing 7 g/dL as restrictive strategy with liberal transfusion were incorporated.Data extraction and synthesisThe clinical outcomes, including short-term mortality, length of hospital stay, length of ICU stay, myocardial infarction (MI) and ischaemic events, were screened and analysed after data collection. We applied odds ratios (ORs) to analyse dichotomous outcomes and standardised mean differences (SMDs) to analyse continuous outcomes with fixed or random effects models based on heterogeneity evaluation for each outcome.ResultsEight RCTs with 3415 patients were included. Compared with a more liberal threshold, a red blood cell (RBC) transfusion threshold 2=53%), length of hospital stay (SMD: −0.11, 95% CI: −0.30 to 0.07, p=0.24, I2=71%), length of ICU stay (SMD: −0.03, 95% CI: −0.14 to 0.08, p=0.54, I2=0%) or ischaemic events (OR: 0.80, 95% CI: 0.43 to 1.48, p=0.48, I2=51%). However, we found that the incidence of MI (OR: 0.54, 95% CI: 0.30 to 0.98, p=0.04, I2=0%) was lower in the group with the threshold ConclusionsAn RBC transfusion threshold

Burn injury continues to be a major cause of morbidity and mortality in modern combat. During the armed combats in Iraq and Afghanistan, the US army put their new five-class medical evacuation system into service with the aim to send back the wounded to duty as soon as possible. This new system indeed increased the efficiency of treatment and evacuation of casualties with extensive burn injury. Though the evacuation time was significantly shortened under the new system, the effective and efficient evacuation of burn patients remains to be rather important problems needing further study. This review summarizes the medical evacuation system of burn casualties and features of burn injuries in US Army in the said conflicts. It may provide some ideas for our burn casualty treatment in future armed conflicts, and it may serve as a reference for treatment of massive casualties caused by catastrophic events in peace time. DOI: 10.11855/j.issn.0577-7402.2015.01.16

Stress ulceration is a common complication in critically ill patients, but the mechanisms involved are poorly understood. In this study we investigated the temporal activation of the redox-sensitive transcription factor nuclear factor-kappaB and its roles in an experimental model of cold immobilization stress-induced gastric mucosal lesions.Prospective, controlled, and randomized animal study.University research laboratory.Male Sprague-Dawley rats.The rats were subjected to cold immobilization stress for a total of 6 hrs. The temporal profiles of nuclear factor-kappaB activation and expression of tumor necrosis factor-alpha, interleukin-1beta, cytokine-induced neutrophil chemoattractant-1 (CINC-1), intercellular adhesion molecule-1 (ICAM-1), and inducible nitric oxide synthase (iNOS) were determined in the gastric corpus mucosa of stressed rats. To study the roles of nuclear factor-kappaB activation, rats received an intravenous bolus of a specific nuclear factor-kappaB inhibitor Bay 11-7082 (20 mg/kg) 1 hr before stress. For antioxidant administration, rats were treated with intravenous injection of a free radical scavenger pyrrolidine dithiocarbamate (50, 100, and 200 mg/kg) 1 hr before stress.Exposure of rats to 6 hrs of stress led to a rapid and persistent activation of nuclear factor-kappaB, which was associated with transient degradation of inhibitory protein IkappaBalpha and slower but sustained degradation of IkappaBbeta. Nuclear factor-kappaB activation preceded the induction of tumor necrosis factor-alpha, interleukin-1beta, CINC-1, ICAM-1, and iNOS messenger RNAs, all of which were linearly increased with the duration of stress. Bay 11-7082 selectively blocked the stress-induced nuclear factor-kappaB activation and up-regulation of tumor necrosis factor-alpha, interleukin-1beta, CINC-1, ICAM-1, and iNOS messenger RNAs. Inhibition of expression of these proinflammatory genes prevented the increases in myeloperoxidase activity (an indicator of neutrophil infiltration) in gastric mucosa and the development of gastric damage. Pyrrolidine dithiocarbamate dose-dependently inhibited the stress-induced nuclear factor-kappaB pathway activation and consequential proinflammatory gene expression, neutrophil infiltration, and gastric damage, suggesting the involvement of reactive oxygen species in these processes.Sustained activation of nuclear factor-kappaB by reactive oxygen species is an important in vivo mechanism mediating stress-induced gastric inflammatory damage in rats.

Interleukin- (IL-) 37 is a novel anti-inflammatory cytokine that suppresses immune response and inflammation. This study was performed to determine whether IL-37 was elevated in patients with rheumatoid arthritis (RA) and investigate the correlation between IL-37 level and disease activity and the concentration of Th1/Th2/Th17-related cytokines. Clinical parameters of disease activity, including the 28-joint disease activity score (DAS28) and C-reactive protein (CRP), were collected in 34 RA patients and 34 age- and sex-matched healthy controls. Plasma IL-37 was measured by ELISA. Plasma levels of TNF-α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, G-CSF, GM-CSF, IFN-γ, MCP-1, and MIP-1βwere analyzed using the Bio-Plex suspension array system. It was found that IL-37 levels were elevated markedly in RA patients and almost undetectable in healthy controls. In addition, IL-37 levels in patients with active RA were significantly enhanced as compared with those in patients of remission. More importantly, IL-37 showed a significant correlation with disease activity (DAS28) and IL-4, IL-7, IL-10, IL-12, and IL-13 concentrations in RA patients. These findings suggest that IL-37 plays an important role in the pathogenesis of RA and may prove to be a potential biomarker of active RA.

Quality of life and functional recovery after burn injury is the final goal of burn care, especially as most of burn patients survive the injury due to advanced medical science. However, dysfunction, disfigurement, contractures, psychological problems and other discomforts due to burns and the consequent scars are common, and physical therapy and occupational therapy provide alternative treatments for these problems of burn patients. This guideline, organized by the Chinese Burn Association and Chinese Association of Burn Surgeons aims to emphasize the importance of team work in burn care and provide a brief introduction of the outlines of physical and occupational therapies during burn treatment, which is suitable for the current medical circumstances of China. It can be used as the start of the tools for burn rehabilitation.

This study was made to evaluate the effect of SB203580, a specific p38 MAP kinase inhibitor, on burn-induced hepatic injury as well as the activation of nuclear factor (NF)-kappaB in severely burned rats. Sprague-Dawley rats were divided into three groups: (1) sham group, rats underwent sham burn; (2) burn group, rats given third-degree burns over 30% total body surface area (TBSA) and treated with vehicle plus lactated Ringer solution for resuscitation 4 ml/(kg% TBSA); and (3) burn plus SB203580 group, rats given burn injury and fluid resuscitation plus SB203580 (10 mg/kg i.v., 15 min and 12 h after burn). Hepatocellular injury (measured by serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and hepatocellular function (determined by the indocyanine green dye retention rate (ICG R15)) were assessed at 24 h post-burn. Liver histologic changes were also analyzed. Burn trauma resulted in increased serum aminotransferases concentrations, decreased ICG R15, elevated serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta levels and hepatic TNF-alpha and IL-1beta mRNA expressions, and worsen histologic condition. The level of Nuclear Factor (kappa) inhibitor (IkappaBalpha) in liver was decreased and DNA-binding activity of Nuclear Factor-kappaB (NF-kappaB) was increased after thermal injury. p38 MAP kinase was more significantly activated in liver harvested from burn rats than from shams. SB203580 inhibited the activation of p38 MAP kinase, reduced the levels of TNF-alpha and IL-1beta, and prevented burn-mediated liver injury. Both the IkappaBalpha level and NF-kappaB activity in the liver following burns was not affected by administration with SB203580. These findings suggest that (1) p38 MAP kinase activation is one important aspect of the signaling event that may mediate the release of TNF-alpha and IL-1beta and contributes to burn-induced liver injury and (2) p38 MAP kinase does not influence the activation of NF-kappaB directly in the liver of severely burned rats.

OBJECTIVE: The purpose of this study was to determine the expression and regulation of vascular cell adhesion molecule (VCAM)-1 in human umbilical vein endothelial cells (HUVECs) induced by sera from severely burned patients. DESIGN: Controlled laboratory study. SETTINGS: Research laboratory in a university hospital. SUBJECTS: HUVECs. INTERVENTIONS: HUVECs were incubated with serum from eight healthy controls and eight patients with thermal injuries of >50% total body surface area. The experiment was repeated after pretreatment with pyrrolidine dithiocarbamate, an inhibitory effect on nuclear factor-kappaB activation, SB203580, a specific p38 mitogen-activated protein kinase inhibitor, and PD98059, a mitogen-activated protein/extracellular signal-regulated kinase inhibitor. MEASUREMENTS AND MAIN RESULTS: Protein and messenger RNA expression of VCAM-1 was measured by flow cytometry and reverse transcription-polymerase chain reaction respectively. Soluble VCAM-1 level in HUVECs culture supernatants was measured by enzyme-linked immunosorbent assay. Sera from severely burned patients showed a stimulatory effect on VCAM-1 messenger RNA levels and an increased VCAM-1 expression on the endothelial cell surfaces. The soluble form of VCAM-1 molecules was also elevated by the stimulation of burn sera. In vitro peripheral blood mononuclear leukocytes adherence to HUVECs incubated with burn sera was significantly increased compared with those incubated with control sera. Finally, these events were significantly inhibited by pretreatment with antioxidants pyrrolidine dithiocarbamate or SB203580, whereas PD98059 had no significant effect. CONCLUSIONS: These findings suggest that sera from severely burned patients induced up-regulation of VCAM-1 expressions in HUVECs, and this process might be largely dependent on oxidant-mediated nuclear factor-kappaB activation and p38 mitogen-activated protein kinase pathways.

This study was undertaken to evaluate the effect of SB203580, a specific p38 mitogen-activated protein (MAP) kinase inhibitor, on burn-induced lung injury as well as the release of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in rats to characterize the role of p38 MAP kinase in lung injury after burn trauma. Sprague-Dawley rats were divided into three groups: 1) sham group, or rats who underwent sham burn; 2) control group, or rats given third-degree burns over 30% total body surface area (TBSA) and lactated Ringer solution for resuscitation; and 3) SB203580 group, or rats given burn injury and lactated Ringers solution with SB203580 inside for resuscitation. Pulmonary injury was assessed at 24 h by pulmonary capillary permeability determined with fluorescein isothiocyanate-labeled albumin and lung histologic analysis. TNF-alpha and IL-1beta protein in bronchoalveolar lavage fluid and serum were measured by enzyme-linked immunosorbent assay and p38 MAP kinase was activity determined in lung by Western blot analysis. These studies showed that significant activation of p38 MAP kinase at 24 h postburn compared with control. Burn trauma resulted in increased pulmonary capillary leakage permeability, elevated levels of TNF-alpha and IL-1beta in bronchoalveolar lavage fluid and serum, and worsened histologic condition. SB203580 inhibited the activation of p38 MAP kinase, reduced the levels of TNF-alpha and IL-1beta, and prevented burn-mediated lung injury. These data suggest that p38 MAP kinase activation is one important aspect of the signaling event that may mediate the release of TNF-alpha and IL-1beta and contributes to burn-induced lung injury.

Background Accurate estimation of a burned area is crucial to decisions about fluid resuscitation, surgical options, nutritional support, and prognosis. Widely used clinical methods to estimate a burn area are two-dimensional. They do not consider age, sex, body mass, physical deformities, or other relevant factors. Computer-aided methods have improved the accuracy of estimating burned areas by including data analysis and reducing subjective differences. Three-dimensional (3D) scanning allows us to determine body dimensions rapidly and reproducibly. We describe an individualized, cost-efficient, portable 3D scanning system, BurnCalc, that can create an individual 3D model and then calculate body surface area (BSA) and the burn area accurately and quickly. Methods The BurnCalc system was validated by verifying the accuracy and stability of BSA calculation. We measured 10 regular objects in experiment 1, using Student’s t-test and the intraclass correlation coefficient (ICC) in the analysis. In experiment 2, artificial paper patches of known dimensions were attached to various parts of the body of 40 volunteers. Their sizes were then calculated using BurnCalc. The BurnCalc data were compared to actually measured values to verify accuracy and stability. Total BSAs of these 40 volunteers were also calculated by BurnCalc and compared to those derived from an accepted formula. In experiment 3, four experts using Chinese Rule-of-Nines or Rule-of-Palms methods calculated the percentages of the total BSA in 17 volunteers. Student’s t-test and ICC, respectively, were used to compare the results obtained with the BurnCalc technique. Results Statistically, in experiment 1, p = 0.834 and ICC = 0.999, demonstrating that there was no difference between the BurnCalc and real measurements. Also, the hypothesis of null difference among measures (experiment 2) was true because p > 0.05 and ICC = 0.999, indicating that calculations of the total BSA and the burn area were more accurate using the BurnCalc technology. The reliability of the BurnCalc program was 99.9%. In experiment 3, only the BurnCalc method exhibited values of p > 0.05 (p = 0.774) and ICC = 0.999. Conclusions BurnCalc technology produced stable, accurate readings, suggesting that BurnCalc could be regarded as a new standard clinical method.

Cutaneous burn trauma causes functional inhibition of the heart, but the mechanism is unclear. Using a high dissociation constant (K(D)) calcium indicator TF-BAPTA and 19F MR spectroscopy, the relationship between the changes of cytosolic free calcium and cardiac function after burn trauma was examined. Sprague-Dawley rats received scald (43% TBSA) or sham burns. Twenty-four hours later, the hearts were excised and perfused by the Langendorff method with a modified phosphate-free Krebs-Henseleit bicarbonate buffer. Left ventricular developed pressure (LVDP) was recorded through a catheter attached to an intraventricular balloon. At the same time, 31P and 19F nuclear magnetic resonance (NMR) spectroscopy was perforined before and after TF-BAPTA loading. LVDP of the heart from burned rats was 40% less than in sham burn rats (65+/-6 vs 110+/-12 mmHg, P0.01). Cytosolic free calcium increased about four-fold in those hearts from the burn group compared to the sham burn group (0.807+/-0.192 vs 3.891+/-0.929 microM). Loading TF-BAPTA in those hearts only caused about a 15-20% decrease in LVDP. PCr/Pi ratio also decreased significantly with this loading, but ATP signals were not affected. In conclusion, the inhibition of cardiac contractility caused by burn trauma correlated with the overload of cytosolic free calcium in the heart.

Cutaneous burn trauma causes cardiac contraction and relaxation defects, but the mechanism is unclear. Previous studies suggest that burn-related changes in myocyte handling of calcium may play an important role in postburn cardiac dysfunction. With the use of a high dissociation constant ( K d) calcium indicator 1,2-bis(2-amino-5,6-difluorophenoxy)-ethane- N,N,N′, N′-tetraacetic acid (TF-BAPTA) and 19F NMR spectroscopy, this study examined the correlation between the changes in cytosolic free calcium concentration ([Ca2+]i) and cardiac function after burn trauma. Sprague-Dawley rats were given scald burn (over 40% of the total body surface area) or sham burn. Twenty-four hours later, the hearts were excised and perfused by the Langendorff method with a modified phosphate-free Krebs-Henseleit bicarbonate buffer. Left ventricular (LV) developed pressure (LVDP), calculated from peak systolic LV pressure and LV end-diastolic pressure, was assessed through a catheter attached to an intraventricular balloon. At the same time, 31P and 19F NMR spectroscopy was performed before and after TF-BAPTA loading. LVDP measured in hearts from burned rats was 2+]i was increased fourfold in hearts from the burned group compared with that measured in the sham burn group (0.807 ± 0.192 vs. 3.891 ± 0.929 μM). Loading TF-BAPTA in hearts transiently decreased LVDP by 15%. Phosphocreatine-to-Pi ratio decreased, but ATP and intracellular pH remained unchanged by either TF-BAPTA loading or burn trauma. In conclusion, burn trauma impaired cardiac contractility, and this functional defect was paralleled by a significant rise in [Ca2+]i in the heart.