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Abstract: Angiotensin II is critically involved in skin wound healing, but the underlying mechanism remains unclear. This study investigated the effect of angiotensin II on type I collagen gene activation in human dermal fibroblasts and the possible mechanism involved. Angiotensin II stimulated the mRNA and protein expression of type I collagen and TGF-β1. Effects were abolished by the angiotensin AT1 receptor antagonist ZD7155 but not by the AT2 blocker PD123319. Blockade of TGF-β1 markedly inhibited angiotensin II-induced type I collagen gene expression. Activator protein-1 (AP-1) decoy ODNs transfection suppressed angiotensin II-induced TGF-β1 expression, and also, diminished type I collagen expression. These data indicated that angiotensin II induces collagen gene activation in human dermal fibroblasts through an AT1-mediated AP-1/TGF-β1 signaling pathway. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]

Abstract: Background: The liver is one of the organs most frequently affected by trauma and hemorrhagic shock; the exact role of p38 mitogen-activated protein kinase (MAPK) activation in response to hepatic hemorrhagic shock/resuscitation (HS/R) remains unclear. Materials and methods: C57Bl/6 mice were divided into four groups: sham-operated group, SB-only group, control group, and SB + HS/R group. Hepatocellular injury (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) and tumor necrosis factor (TNF-α) and interleukin (IL-1β) messenger ribonucleic acid (mRNA) expression in the liver were assessed 6 h after resuscitation, p38 MAPK activation in the liver was assessed at 30 min after resuscitation. Results: p38 MAPK activation was higher in the control group than other groups 30 min after resuscitation. p38 MAPK activation level in the SB + HS/R group did not change significantly compared with that of sham and SB-only groups, but was significantly lower than that in the control group. The TNF-α mRNA expression in the control group was significantly higher than that in the sham group. The TNF-α mRNA levels after HS/R in the SB + HS/R group were significantly lower than those in the control group and were roughly the same as those in the sham and SB-only groups. IL-1β mRNA expression showed similar changes in the four groups. Serum ALT and AST levels in the control group were significantly higher than those in the sham group. The increase in serum ALT and AST levels after HS/R in the SB + HS/R group was significantly less pronounced than that in the control group and markedly higher than that in the sham group. Conclusions: p38 MAPK was phosphorylated during the HS/R process. Inhibiting the activation of p38 MAPK may attenuate HS/R injury to the liver. [Copyright &y& Elsevier]