Plasma fibronectin (Fn) was determined in 180 healthy individuals. No significant difference was found between males and females; therefore the values were pooled. The mean value was 286.94?51.35 ?g/ml. In 16 burn patients, with burn extent ranging from 30% to 95%, plasma Fn was determined sequentially. It was found that there was a significant lowering in plasma Fn value in all cases on the postburn day 1 (112.56-173.04 ?g/ml) and postburn day 2 (44.03-218.4 ?g/ml). It returned to within normal range in 13 survivors on the postburn day 6. In 3 non-survivors, plasma Fn decreased progressively before death. In another 9 patients with minor burns (3%-25%TBSA), plasma Fn values were all within normal range on the postburn day 1.The causes of reduction of plasma Fn in patients with major burn injuries, as well as its relationship with the function of the monocyte-phagocyte system, were briefly discussed. The results of the present study suggests that the concentration of Fn in plasma might serve as an important prognostic index in the burn patients.

For the purpose of exploring the role of enterogenic infection in the pathogenesis of multiple system organ failure (MSOF), 40 dogs were subjected to partial occlusion of the superior mesenteric artery (SMA) for 1 hour. The results showed that ischemia and reperfusion of the intestine produced a breakdown of the intestinal mucosal barrier resulting in bacterial translocation. Subsequently, the liver, lung and cardiovascular system showed dysfunction of failure. Based on the experimental findings, it is suggested that the intestinal tract might be the target organ of reperfusion injury folowing hypovolemic shock, and it might pose as a "motor" of the development of MSOF.

The present article summarized briefly the experiences and lessons learned in the management of mass burn casualties,and also gave a brief account of the present status of the system of emergency care of mass casualties in our country.The authors proposed herewith an organizational system conforming to the status quo of our country.It was suggested that through learning from attending seminars and training in specialty centers,devotion to intensive research of relevant problems and constant interchange of experiences and ideas,the ability of professional staff to meet the needs of urgent and heavy duty could be raised in salvaging mass casualties both in peace time and war.

It is well known that in patients with severe burn, especially when complicated by sepsis, the breakdown of body proteins is acceleraled, producing a hypercalabolic response. Negative nitrogen balance and malnutrition will develop rapidly, predisposing to various complications. High calori intake and enhancement of anabolic process might fail to improve the patient′s nutritional condition. A skeletal muscles account for over 50% of body cell dry weight, their catabolism exerts profound effect on whole body metabolism. By using modern molecular biology techniques, one of the mechanisms underlying skeletal muscle proteolysis is shown to be activation of the ubiquitin proteasome pathway. The role of its possible modulating factors in inducing muscle protein breakdown after burn injury was explored in rat models of burn injury with or without sepsis. Muscle spesimens obtained from severely burned patient with sepsis was also collected for study.The results were as follows. (1)The total and myofibrillar proteolytic rate in extensor digitorum longus (EDL) muscle was increased markedly, especially the expressions of ubiquitin, and mRNA of subunit RC2(the largest subunit of 20s proteasome) were prominantly increased in EDL muscle. There was a significant positive correlation between the proteolytic rate and the expression of mRNA of ubiquitin, or mRNA of subunit RC2, after the stimulation of burn injury. On the other hand, there was no significant change in proteolytic rate and transcription of ubiquitin in soleus (SOL) muscle. (2)The myofibrillar proteolytic rate and the ubiquitin proteasome component were significantly enhanced in rats with sepsis compared with control group. There were significant positive correlations among plasma concentration of endotoxin, TNF ?, cortisol and respective values of myofibrillar proteolytic rate, and ubiquitin proteasome component. (3)There were significant positive correlations between the urinary output of 3 methylhistidine (3 MH)in 24h urine and respective values of plasma concentration of cortisol, TNF ?, and endotoxin in severely burned patients with sepsis. The expressions of ubiquitin mRNA 2 4 kilobase pair (?B), 1.2kb, C 2 subunit mRNA and the protein expressions of ubiquitin in quadriceps femoris muscle were significantly increased compared with the control group. (4)Muscle proteolytic rate was markedly enhanced when myotube was cultured with TNF ?. However, by using the ubiquitin proteasome inhibitor mG132, significant decrease in the muscle proteolyitc rate was observed. (5)Glucocorticoid could increase the skeletal muscle proteolytic rate, especially the myofibrillar proteolytic rate, through activating the ubiquitin proteasome system at gene level. However, this effect could be greatly bluned by glucocorticoid receptor antagonist RU38486. (6)NF ?B activity in skeletal muscle of burned rat with sepsis was markedly increased. However, by using inhibitor of NF ?B, the NF ?B activity was down regwlated in the muscle, and a decrease in the total and myofibrillar proteolytic rate was observed. (7)Decrease in transcriptional expression of ubiquitin and reduction in the skeletal muscle proteolytic rate were found when escharectomy was performed during early stage of burn injury. The results suggested that the treatment strategies for prevention of skeletal muscle proteolysis of postburn sepsis should firstly be aimed at eradication of devitalized tissues, i.e. prevention of sepsis by reonoval of the primary injury. Secondly, attention should be paid to modulating or controlling the process of ubiquitin proteasome pathway in response to burn injury, and this might provide an effective way to reduce skeletal muscle protein wasting by specifically inhibiting the specific enzymes or subunits involved in the enhancement of the activity of ubiquitin proteasome pathway after burn injury. However, more studies in the ubiquitin proteasome proteolytic pathway in severe burn injury are necessary to confirm this assertion.

Blood viscosity was determined in 50 normal individuals. No significant difference was found between males and females, therefore the values were pooled.In 10 burn patients (burn extent ranged from 30% to 90%). blood viscosity was determined in the first 3 postburn days. All of them received whole blood as a part of the resuscitational regime. The amount of whole blood given was approximately TBSA% burnedxbody weight (kg)?0.3ml. The blood viscosity returned to within normal range in all cases on the 3rd postburn day.Blood viscosity was determined in 20 uninjured dogs to obtain its normal values. A 25% napalm burn was inflicted upon the animals, and they were divided into 2 groups of 7 each. Group A received the same fluid replacement protocol as what was given in human patients, while Group B animals were replenished with balanced salt solution in the amount of 5ml/1%TBS A/kg in the first 24 hours, and dextran was given as a colloid in the second 24 hours. No significant difference in blood viscosity was observed between these two groups during the observation period.The above findings suggested that whole blood as one of the constituents of replacement fluids for burn shock would neither enhance blood (?)scosity nor impede its recovery to normalcy.

A method for measurement of neutrophil function and opsonic activity by chemiluminescence (CL) was reported in this paper.The factors influencing the emission of CL were discussed. The experimental results suggested that CL depends on the concentration of luminol, the dilution of serum opsonin, the number of neutrophils and the environmental temperature. The optimum conditions defined in present study were: the concentration of luminol was 1?105M, the number of neutrophils 2?106/mml, the reactive temperature 37℃. According to the relationship between CL emission and the bactericidal activity of phagocytizing neutrophils, the measurement of CL may be used as a rapid, simple and usefull tool to determine the funetion of humoral-phagocyte axis.

Since the emergence of the new syndrome, termed multiple system organ failure (MSOF), about two decades age, it has aroused an outburst of enthusiasm in clinical and experimental studies among many clinicians and investigators both abroad and at home. Nevertheless, it has also created much confusion in the concept as well as the diagnosis of the syndrome, mainly because the present term does not clearly differentiate this syndrome from some other irrelevant clinical conditions, such as senile dysfunction of multiple organs, agonal state etc. As it has been documented to occur almost as a rule after a septic state and also under the intricate interaction of many humoral and cellular mediators, we suggest that the diagnosis of MSOF should at least include two concurrent conditions, i. e. septic response and organ failure.Inasmuch as the present diagnosis of MSOF designates only the terminal state of a series of pat-hophysiological process, namely systemic inflammatory response---sepsis--septic syndrome--MSOF,it is not conducive to an early diagnosis, which is of utmost importance in the prevention and early treatment of this frequently fatal syndrome. In the light of current investigations, we propose that the name of the syndrome be changed to "sepsis and organ dysfunction" or "mediator injury of organs*. Our humble opinion welcomes further comments and discussion.

The scar formation and chronic ulcer development are the iain sequelae faced by surgeons in the treatmemt of wounds. Therefore,the prevention and treatment of these sequelae are the main tasks for clinicians.In this paper,the current research concerning both sequelae is reviewed.The authors emphasize that the use of some high technologiesl, such as stem cell technology, clone technology and tissue engineering may bring the hope in improving the treatment and prevention of these sequelae.

The Janus kinase/signal transducer and activator of transcription (JAK/STAT) are a major signal transduction pathway in controlling and regulating a number of cytokine-mediated responses, including interferon-?, interleukin-1 (IL-1), IL-6, IL-10 and IL-4. The JAK/STAT pathway is particularly elegant because of its very rapid and simple cytoplasm-to-nucleus signaling. Recently, it has been found that JAK/STAT pathway might also be involved in the regulation of high mobility group box-1 protein (HMGB1), which plays an important role as a potential late mediator of sepsis. Inhibition of the activation of JAK/STAT pathway can down-regulate the gene expression of HMGB1 in vital organs, especially in the liver and lungs. In addition, treatment with JAK/STAT pathway inhibitors can effectively prevent the occurrence and development of multiple organ dysfunction syndrome following sepsis, and the probable underlying mechanism of which involves a reduction of direct or indirect harmful effect of HMGB1. Over the past few years, numerous investigations have contributed to our knowledge of the JAK/STAT pathway and its role in cytokine-mediated abnormality of immune function as well as inflammatory response during sepsis, and it might be helpful in further identifying a potential strategy of intervention for posttraumatic or postburn sepsis. This review summarizes the salient features of JAK/STAT pathway and focuses on the pathophysiological role of JAK/STAT in regulating proinflammatory cytokine activity and HMGB1 expression in vivo.

Angiopoietin family is a recently discovered type of cellular factors that specifically bind to the TIE-2 receptors located exclusively in endothelial cell membrane. The protein structures of this family members are similar. They can be structurally divided into three domains: an N-terminal region lacking homology to any known structures, an alpha-helical rich coiled-coil segment, and a fibrinogen-like domain. The distribution and biological activity of these factors are different in organism. Angiopoietin-1 as a agonist, mostly locates in close proximity with vascular endothelial cells, keeps the stability of blood vessels, enhances the affinity of vascular endothelial cells with surrounding cells and matrix, decreases the leakage of vessel. Ang-2 is a naturally occurring antagonist of Ang-1, exists in the angiogenic remodeling region and is related to the decrement of the stability of vessel. Ang-3 is widely distributed in multiple mouse tissues, while Ang-4 is expressed only in lung. Although Ang-3 and Ang-4 are structurally diverged from each other, they appear to represent the mouse and human counterparts of the same gene locus. Biological functions of Ang-3 and Ang-4 have not been elucidated yet. Angiopoietin family has potentially clinical applications for incurring illnesses which lead to vessel wound and vascular abnormal development.