To investigate the levels of cytokines in subeschar edema fluid (SEF). Methods: A guinea pig model with III°30% total body surface area (TBSA) was designed. SEF was collected serially at the time of escharectomy ...To investigate the levels of cytokines in subeschar edema fluid (SEF). Methods: A guinea pig model with III°30% total body surface area (TBSA) was designed. SEF was collected serially at the time of escharectomy for up to 72 h after scald injury. The levels of tumor necrosis factor.(TNFα), interleukin-6 (IL-6) and interleukin-8 (IL-8) were determined by using the enzyme-linked immunosorbent assay (ELISA). Results: The levels of TNFα,IL-6 and IL-8 in plasma and SEF increased in the early phase of scald injury. Furthermore, the contents of TNFα， IL-6 and IL-8 in SEF were higher than those in plasma.Conclusion: The findings indicate that the subeschar edema fluid is a biologically active reservoir, and is an important participant in the postburn pathophysiologic process.展开更多
To investigate inhibitory effect of recombinant transforming growth factora-pseudomonas exotoxin fusion protein (TGFInhibitory effect of TGF_α-PE40; TP40) on neointimal proliferation following arterial injury.Methods...To investigate inhibitory effect of recombinant transforming growth factora-pseudomonas exotoxin fusion protein (TGFInhibitory effect of TGF_α-PE40; TP40) on neointimal proliferation following arterial injury.Methods: Forty-eight male rabbits fed with rich cholesterol diet were randomized into the treatment group(n= 24)and the control group (n=24). The rabbits in the treatment group were treated by local adiministration of TP40 (30 μg) 24 h after arterial injury, and the control group were treated by saline. LM and computer image analysis were used to study the rabbit arterial segments 2, 4 and & weeks after treatment. Results: Irregular thickening of the arterial intima. large amounts of smooth muscle cells within the neointima, and stenosis of the arterial cavity in the control group, and significant inhibition of intimal proliferation and no stenosis of the arterial cavity in the treatment group were observed microscopically. Computer image analysis showed that the neointimal area and the ratio of neointimal/medial area of the treatment group at 2, 4 and 8weeks after treatment were signifantly smaller than those of the control groups (P<0. 01 ). COnclusion: The results suggest that TP40 can significantly inhibit neointimal proliferation following carotid arterial injury.展开更多
文摘To investigate the levels of cytokines in subeschar edema fluid (SEF). Methods: A guinea pig model with III°30% total body surface area (TBSA) was designed. SEF was collected serially at the time of escharectomy for up to 72 h after scald injury. The levels of tumor necrosis factor.(TNFα), interleukin-6 (IL-6) and interleukin-8 (IL-8) were determined by using the enzyme-linked immunosorbent assay (ELISA). Results: The levels of TNFα,IL-6 and IL-8 in plasma and SEF increased in the early phase of scald injury. Furthermore, the contents of TNFα， IL-6 and IL-8 in SEF were higher than those in plasma.Conclusion: The findings indicate that the subeschar edema fluid is a biologically active reservoir, and is an important participant in the postburn pathophysiologic process.
文摘To investigate inhibitory effect of recombinant transforming growth factora-pseudomonas exotoxin fusion protein (TGFInhibitory effect of TGF_α-PE40; TP40) on neointimal proliferation following arterial injury.Methods: Forty-eight male rabbits fed with rich cholesterol diet were randomized into the treatment group(n= 24)and the control group (n=24). The rabbits in the treatment group were treated by local adiministration of TP40 (30 μg) 24 h after arterial injury, and the control group were treated by saline. LM and computer image analysis were used to study the rabbit arterial segments 2, 4 and & weeks after treatment. Results: Irregular thickening of the arterial intima. large amounts of smooth muscle cells within the neointima, and stenosis of the arterial cavity in the control group, and significant inhibition of intimal proliferation and no stenosis of the arterial cavity in the treatment group were observed microscopically. Computer image analysis showed that the neointimal area and the ratio of neointimal/medial area of the treatment group at 2, 4 and 8weeks after treatment were signifantly smaller than those of the control groups (P<0. 01 ). COnclusion: The results suggest that TP40 can significantly inhibit neointimal proliferation following carotid arterial injury.
