Burns ; pathology ; Humans ; Wound Healing

Calpains are intracellular nonlysosomal Ca(2+-) regulated cysteine proteases, widely located in the tissues of most mammals. Skeletal muscle tissue mainly expresses m-calpain, µ-caplain, n-calpain, and their endogenous inhibitor calpastatin. They are closely related to the cell apoptosis, cytoskeleton formation, cell cycles, etc. Calpains are also considered to be participating in the protein degradation process. Severe burns are typically followed by hypermetabolic responses that are characterized by hyperdynamic circulatory responses with increased proteolysis and cell apoptosis. Recently, overloading of Ca(2+) in skeletal muscle cells, which activates the calpains is observed after a serious burn. This paper aims to review the current research of the relationship between calpains and post-burn skeletal muscle wasting from the perspectives of structure, function, and physiological activities.
Animals ; Burns ; metabolism ; pathology ; Calpain ; metabolism ; Muscle, Skeletal ; metabolism ; pathology

Animals ; Biological Warfare ; Burns ; pathology ; Burns, Chemical ; pathology ; Chemical Warfare ; China ; Humans ; Military Medicine ; Radiation Injuries ; pathology ; Wounds, Gunshot ; pathology

Caustic esophageal burn is a common ailment in clinical practice. In some patients, scar stricture was formed in the late stage of injury, and it seriously undermined quality of life of the patients. We adopted various clinical interventions at an early stage in order to relieve and alleviate the formation and development of corrosive esophageal stricture as a result of chemical injury as well as to avoid invasive operations to make it more acceptable for the patients. This article summarized the progress in etiology, pathological changes, identification, early prevention, and surgical management of corrosive esophageal stricture.
Burns ; complications ; pathology ; Constriction, Pathologic ; etiology ; pathology ; Esophageal Stenosis ; etiology ; pathology ; Esophagus ; injuries ; pathology ; Humans

A series of studies demonstrated that myocardial damage and cardiac dysfunction occurs immediately following severe burn, even before significant reduction in blood volume due to increased capillary permeability. Such myocardial damage and cardiac dysfunction leads to cardiac deficiency, and it is a precipitating factor for burn shock and ischemic/hypoxic injury. In recent years, many experimental and clinical studies elucidated the pathogenesis and confirmed the clinical importance of prevention and treatment of"shock heart"in the early stage post severe burn.
Burns ; pathology ; therapy ; Heart ; physiopathology ; Humans ; Hypoxia ; pathology ; Myocardium ; pathology ; Shock ; pathology

Most of the major advances in burn treatment were made within the last five decades. However, hypermetabolic response after severe burn remains a problem in the treatment of patients with massive burn. As skeletal muscle accounts for over 50% of body cell dry weight, its catabolism exerts profound effect on body metabolism as a whole. Main mechanisms underlying skeletal muscle wasting induced by severe burn include activation of ubiquitin-proteasome pathway, bringing about breakdown of muscle protein, and myonuclear apoptosis. Therapeutic strategies for skeletal muscle wasting after burn mainly include maintenance of room temperature at (31.5 +/- 0.7) degrees C, early active and passive exercise of skeletal muscles, administration of beta adrenergic receptor blocker such as Propranolol, recombinant growth hormone, androgen, and insulin, which has lately been proven to possess the effect of suppressing myonuclear apoptosis after burn. Combination of multiple therapeutic strategies is beneficial in reducing complications of burn patients, particularly wide ranged skeletal muscle atrophy, to achieve a better clinical outcome.
Apoptosis ; Burns ; drug therapy ; metabolism ; pathology ; Humans ; Muscle, Skeletal ; metabolism

A great achievement has been made on burn pathology research in China since 1958. These advances include: pathological changes in burn wound, the healing process of burn wound and its mechanism modulated by growth factors especially bFGF, intermingled transplantation of allo-skin or xeno-skin with auto-skin for coverage of extensive third degree burns, characteristic postburn inflammatory reaction, pathological changes and evolution in various internal organs, multiple organ dysfunction syndrome (MODS), pathological changes in phosphorus burn, pathological changes in endotoxemia in burn, the role of vascular endothelial cell in pathogenesis of postburn visceral organ dysfunction as well as steam and smoke inhalation injury.
Burns ; pathology ; China ; Humans ; Skin Transplantation ; Wound Healing

Burns ; pathology ; therapy ; Humans ; Prognosis ; Treatment Outcome ; Wound Healing

OBJECTIVETo investigate the characteristics and differences of propofol pharmacokinetics in shock phase and hypermetabolic phase in severe burn in rabbits.

METHODSTwenty New Zealand rabbits were assigned to burn group (n = 10) and sham injury group (n = 10) according to the random number table. Rabbits in burn group were inflicted with 30%TBSA full-thickness scald (named burn below), resuscitated instantly, and were intravenously injected with 5.1 mg/kg propofol 6 hours after injury. 1.5 mL blood was collected from left external jugular vein at 1, 3, 5, 10, 15, 20, 30, 45, 60, 90 minute(s) after injection respectively. Above procedure was performed again 1 week later. Rabbits in sham injury group were treated similarly as rabbits in burn group but were sham scalded. Propofol concentration in plasma was determined with high performance liquid chromatography. Data of propofol concentration-time were analyzed with 3P97 practical pharmacokinetics calculating program, and then the most fit compartment model was selected to calculate pharmacokinetic parameters.

RESULTSThe blood concentration-time curve of propofol fitted in with the two-compartment model in burn group, and three-compartment model in sham injury group. During shock phase, comparing with central compartment distribution volume [Vc, (3.1 + or - 1.5) L/kg], area under curve [AUC, (25 + or - 7) mg x min x L(-1)], elimination phase half life [t1/2beta, (113 + or - 93) min], clearance [CLs, (110 + or - 50) mL x kg(-1) x min(-1)] of rabbits in sham injury group, Vc[(8.8 + or - 4.2) L x kg(-1)] and AUC [(44 + or - 10) mg x min x L(-1)] increased significantly (with t value respectively 3.191 and 3.668, and P values both below 0.01); t1/2beta [(339 + or - 258) min] prolonged (t = 2.932, P < 0.05); CLs [(40 + or - 30) mL x kg(-1) x min(-1)] decreased (t = -3.013, P < 0.05) in burn group. During hypermetabolic phase, CLs [(180 + or - 40) mL x kg(-1) x min(-1)] of rabbits in burn group was significantly higher than that in sham injury group [(90 + or - 30) mL x kg(-1) x min(-1), t = -3.013, P < 0.05]. Comparing with those of rabbits in burn group during shock phase, Vc [(4.1 + or - 1.3) L/g] and AUC [(24 + or - 5) mg x min x L(-1)] decreased significantly (with t value respectively 2.979 and 3.766, and P value both below 0.01); distribution phase half time [t1/2alpha, shock phase (16.1 + or - 13.1) min and hypermetabolic phase (8.3 + or - 2.5) min] and t1/2beta [(55 + or - 19) min] shortened obviously (with t value respectively 9.065 and 8.795, and P values both below 0.01); CLs increased significantly (t = 4.238, P < 0.01) during hypermetabolic phase.

CONCLUSIONSThere are great differences in propofol pharmacokinetics between shock phase and hypermetabolic phase in severely burned rabbits. The change is characterized by increase in Vc and AUC, extension of t1/2alpha and t1/2beta, decrease in CLs during shock phase and obvious increase of CLs during hypermetabolic phase.

The purpose of this study is to compare the effect of photocoagulation using between argon and diode infrared laser in experimental setting. A biomicro-scopic laser photocoagulation was performed with diode and argon laser to the same eye of the pigmented rabbit. The spot diameter of both lasers was fixed at 200 micrometer. To achive the same intensity of laser burns, we adjusted laser power settings under the indirect ophthalmoscopic examination. The average exposure time and power were 0.2 sec., 200mW in diode laser and 0.1 sec., 90mW in argon laser. Ophthalmoscopic findings were similar in both lasers. Histologically the effect of diode laser photocoagulation was deeper in layer. Argon laser photocoagulation was found to damage the inner retinal layer more severely than diode laser. This results suggest the use of diode laser has some advantage in preservation of the inner retinal layer and vitreretinal interface than argon laser in the treatment of retinal pathologies.
Argon* ; Burns ; Lasers, Semiconductor* ; Light Coagulation* ; Pathology ; Retinaldehyde