Insulin resistance(IR) after severe burn may aggravate metabolic disturbance, delay wound healing and increase the probability of infection and MODS. The mechanism of IR may be the combined defects of insulin biological effects at pre-receptor, receptor and post-receptor levels. This article discusses the mechanism and intervention of postburn IR, aiming to improve treatment for extensive burn.

Cellular energy metabolism and intracellular pH of intact heart, kidney and liver of small animals were studied before and after burn with an effective technique of phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy. Advantages of this technique are that the measurement can be performed constantly without any complicated and destructive process, that it is possible to use this technique in clinical examination in the near future and that a lot of information can be obtained from only one spectrum.It was demonstrated that there were a short cellular energy source and a cellular acidosis in' heart, kidney and liver during burn shock. The high-energy phosphate compounds-lowered wavily but not straight, which could be divided into stress stage, compensation stage and decompensation stage. Intracellular pH decreased first in the heart, and then in the kidney and liver. In contrast to the results obtained by way of direct blood flow determination, the early and significant intracellular acidosis indicated the insufficiency of blood and oxygen supply in myocardium.

Although the research work on the permanent skin substitutes was started in our country later than in developed countries, the development has been promising in recent years. The results of this field of research would completely change the fact that deep burn wounds could only be repaired with autologous skin grafting. It is our expectation that with the advent of these permanent skin substitutes, the survival rate of severe trauma could be raised and the quality of wound repair could be improved. In a series of papers published in this issue, the development and the status quo of permanent skin substitutes will briefly be introduced.

This study was aimed to improve the therapeutic results of composite skin substitutes. Human vascular endothelial cell growth factor (hVEGF 165 ) gene was constructed to an eukaryotic expression vector pcDNA3. Transfection of recombinant vector pcDNA3 hVEGF 165 into human dermal fibroblast cells was performed. VEGF protein level in the supernatant of transfected fibroblasts culture was determined. Its biological activities were tested by observing the growth rate of the human umbilical vein endothelial cells/HUVEC after being stimulated with the said supernatant, and by performing the Miles assay in guinea pigs. The results showed that these transgenic cells were able to secrete VEGF to certain extent, with biological activities to enhance the growth of HUVEC in vitro and improve vascular permeability. It indicated that transgenic fibroblasts could resurface the dermal substitute of a composite skin.

Epidermal stem cells (ESCs) play a critical role in homeostasis and wound repair of skin tissue. Since ESCs are rare (fewer than 10% in total basal cells population) and lack specific markers,it is difficult to isolate and identify them from keratinocytes. Currently ,isolation of ESCs was achieved mainly by fast adhesion of ESCs to extracelluar matrix or flow cytometry. Several specific markers have been found in recent years for the identification of ESCs.

Objective To sum up the experiences in the prevention and treatment of systemic infection after burn injury. Methods 309 burn patients with systemic infection treated in our department from January 1990 to December 2003 were enrolled in this study. The patients were divided into two groups according to their hospitalized time: group 1(from 1990 to 1996) and group 2(from 1997 to 2003). The incidence and mortality of systemic infection were compared between the two groups, and the efficacy of different treatment strategies was analyzed. Results The morbidity of postburn systemic infection in the patients was 6.98%(309/4430). The incidence and mortality of systemic infection were 5.68% and 0.30% in the group 2, respectively, which were significantly lower than those in the group 1. Conclusion Rapid and adequate fluid resuscitation for burnshock, effective control of wound infection, early excision of crust and skin grafting for deep burnwounds, and reinforcement of organ support were key factors to decrease the incidence of systemic infection and increase the curative frequency. Once burn wound sepsis occurred, prompt removal of infectious necrotic tissues was a key means to ensure a good clinical outcome.

Pulse contour cardiac output (PiCCO) monitoring is a new type of invasive hemodynamic monitoring technology, which is more and more often applied in perioperative period and the patients suffering from multiple injuries, septic shock, and extensive burn. With PiCCO one is able to monitor patients' hemodynamic indexes safely, timely, accurately, and continuously to provide reference for judgment of patients' condition and proper quality and quantity of fluid administration. This technique has a good prospect in clinical application.
Cardiac Output ; physiology ; Fluid Therapy ; methods ; Hemodynamics ; Humans ; Monitoring, Physiologic ; instrumentation

Sepsis is one of the most common pathogenetic causes of acute lung injury (ALI), and at present there is still a lack of effective targeted techniques and methods for its prevention and treatment. Autophagy is a homeostatic mecha- nism common to all eukaryotic cells, including adaption to environment, defense against invasion of pathogens, and maintenance of cellular homeostasis. Autophagy is also involved in a variety of lung-related diseases. In septic lung injury, autophagy not only serves to dissipate dysfunctional organelles, but also inhibits the release of inflammatory cytokines. This review aims at eliciting the role of autophagy in sepsis-induced ALI and further exploring the potential targets of autophagy in inhibiting inflammation, in an effort to provide a new perspective for clinical treatment of sepsis-induced ALI.
Acute Lung Injury ; etiology ; metabolism ; Autophagy ; Cytokines ; metabolism ; Inflammation ; metabolism ; Lung ; metabolism ; Lung Injury ; Sepsis ; complications ; metabolism

Objectives:To study the alterations of NF-?B activation in PBMC, in order to clarify the signal transcription of NF-?B concerned in the mechanism of inflammatory reaction in severe burns. To evaluate the alterations of expression of NF-?B dependent proinflammatory cytokines mRNA. Thereby, to observe the regulating effects of NAC on NF-?B, and verify the medial effects of upstream signal molecules on cytokines expression. Methods:Sprague Dawley rats were randomly assigned to each group. A 30% TBSA full-thickness scald was performed by immersing in 100℃ water for 12 seconds. PBMC were isolated at different time point after scalding. From isolated PBMC, the total RNA was isolated and the nuclear protein purified by Trizol reagents. The NF-?B proteins were measured through EMSA. Message RNA expression of proinflammatory cytokines and Th2 cytokines were assayed by RT-PCR. Results:Lots of NF-?B proteins were sequester in nucleus in all burn groups. mRNA expression of proinflammatory cytokines were also enhanced and related to the activity of NF-?B protein in nucleus. NAC could decrease the activity of NF-?B protein in nucleus. NAC had also significantly inhibitory effects on the production of proinflammatory cytokines. However, all of Th2 cytokines measured in this study were enhanced too. Conclusions:NF-?B might be the second signal molecule from cytosol to nucleus and mediate the proinflammatory cytokines transcription in PBMC after burns. In signal transduction levels, enhancing scavengers of oxygen free radicals in PBMC may modulate the activity of NF-?B which mediate the expression of proinflammtory cytokines.

Objective To investigate the temporal activation of p38MAPK signaling transduction cascade,and the relationship between the activation and reactive oxygen species(ROS)in a well-defined experimental model of water-immersion restraint(WIR)stress-induced gastric mucosa ulceration.Methods Male Sprague-Dawley rats were randomly divided into control group,WIR group and tempol treated group.Animals were restrained and immersed in water bath to induce gastric mucosal lesions,with or without pretreatment with the free radical scavenger,tempol,and the WIR group animals were killed at different time points after WIR stress.Tempol treated animals underwent the same protocol followed 30min or 360min of stress,then the gastric mucosa was harvested,and the activity of gastric mucosal p38 was analyzed by Western blot.Malondialdehyde(MDA)activity and pro-inflammatory cytokine expression were detected.Results A rapid activation of p38MAPK in gastric mucosa occurred as early as 15 min after stress,and this activation was maximal after 90min of stress and still persisted until 360min after stress.Pretreatment with tempol prevented stress-induced p38MAPK activation at 30 min and 360min time points(0.77?0.24 and 0.58?0.12,respectively)compared with that in model groups(1.22?0.16 and 1.73?0.09,respectively,P