Dynamic activity of NF-kappaB in multiple trauma patients and protective effects of ulinastain / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the dynamic activity of NF-kappaB at the early stage of injury in multiple trauma patients and the protective effects of ulinastain.</p><p><b>METHODS</b>From January 2008 to May 2010, patients with multiple traumas admitted to our emergency department were enrolled in this study. Their age varied from 20-55 years. All enrolled patients were assigned randomly into control group (26 cases of multiple injury without ulinastain treatment), ulinastain group (25 cases of multiple injury with ulinastain treatment), and mild injury group (20 cases) for basic control. The inclusion criteria for mild injury group were AIS-2005 less than or equal to 3, single wound, previously healthy inhospital patients without the history of surgical intervention. In addition to routine treatment, patients in ulinastain group were intravenously injected 200 000 IU of ulinastain dissolved in 100 ml of normal saline within 12 hours after injury and subsequently injected at the interval of every 8 hours for 7 days. NF-kappaB activity in monocytes and the level of TNF-alpha,IL-1, IL-6 in serum on admission (day 0), day 1, 2, 3, 4, and 7 were measured. Data were compared and analyzed between different groups.</p><p><b>RESULTS</b>NF-kappaB activity in monocytes and TNF-alpha,IL-1 and IL-6 of these patients reached peak levels at 24 hour after trauma, with gradual decrease to normal at 72 hour after trauma. NF-kappaB activity and levels of TNF-alpha,IL-1 and IL-6 were lower in ulinastain group than control one, without any significant difference between the two groups. The mean duration for systemic inflammatory response syndrome and multiple organ dysfunction syndrome was 7 d+/-3.1 d and 10 d+/-3.5 d in ulinastain group and control group respectively, and showed a significant difference.</p><p><b>CONCLUSIONS</b>NF-kappaB activity in monocytes and the levels of inflammatory cytokines in multiply injured patients increased transiently at the early stage of trauma. Ulinastain may shorten the duration of systemic inflammatory response syndrome and multiple organ dysfunction syndrome, but does not show the ability to decrease the activity of NF-kappaB .</p>

The change of angiotensin II production and its receptor expression during wound healing: possible role of angiotensin II in wound healing / 中华整形外科杂志

<p><b>OBJECTIVE</b>This study was undertaken to observe the change in the local level of angiotensin II (Ang II) and the expression of its corresponding receptors AT1 and AT2 during wound healing, and explore the possible role of Ang II in wound healing .</p><p><b>METHODS</b>A model of full-thickness cutaneous wound was developed on the back of C57/BL6 mice. Specimens were taken from the wound of each mouse on the day 0, 1, 3, 5, 7, 9, 11, 13 and 15 after wounding. The change in the generation of Ang II in wounded tissue during the healing process was detected with ELISA. The proliferation and the apoptosis of cells were detected by bromodeoxyuridine (Brdu) and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling (TUNEL) method in wounded skin during the healing process, respectively. The cellular localization and the mRNA level change of Ang II receptors in wounded tissue during healing were detected with immunostaining and RT-PCR.</p><p><b>RESULTS</b>Ang II produced in wounded skin was increased in the first 7 days to reach the peak, and then gradually decreased during wound healing. BrdU labeling index was increased gradually in the first 7 days to reach the peak, and then gradually decreased during wound healing. The number of TUNEL-positive cells was increased slowly in the first 7 days after wounding. The increase in the number of TUNEL-positive cells was more markedly after epithelization of the wound. In normal mice, AT1 and AT2 receptor were found positively expressed in the whole epidermal layer, while positive expression was only found in the endothelial cells of the capillary vessels within the dermal layer, and positive expression was also found in appendages of the skin, i. e. hair follicle, sweat gland and sebaceous gland respectively. Positive staining signal of both AT1 and AT2 receptors were increased in the first 7 days to reach the peak, then gradually decreased. Expression of AT2R was increased again following the epithelization of wound. The result of RT-PCR showed that the expression of both AT1 and AT2 receptors was detectable, and AT1 receptor was increased in the first 7 days to the peak, and then gradually decreased during wound healing, while AT2 receptor expression reached its peak value on day 7, then gradually decreased, and increased again following the epithelization of wound.</p><p><b>CONCLUSIONS</b>These results indicate that Ang II participate in wound repair and related to remolding in the late stage of wound healing through the change in production of angiotensin II and expression of AT1 and AT2 receptors. AT1 receptor might be closely associated with cell proliferation, while AT2 receptor might play a role in cell apoptosis and remolding during wound healing.</p>

Comparison of severe trauma care effect before and after advanced trauma life support training / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To study the emergency care effect of in-hospital severe trauma patients with the injury severity score (ISS) larger than or equal to 16 after medical staff received advanced trauma life support (ATLS) training.</p><p><b>METHODS</b>ATLS training was implemented by lectures, scenarios, field practices, and examinations. The clinical effect of in-hospital severe trauma care was compared 2 years before and after ATLS training.</p><p><b>RESULTS</b>During 2 years (from January 1, 2004, to December 31, 2005) before ATLS training, 438 cases of severe trauma were admitted and treated emergently in our department. Among them, ISS score was 28.6+/-7.8 on average, and 87 cases died with the mortality of 19.9%. The duration in emergency department and from admission to operation were 69.5 min+/-11.5 min and 89.6 min+/-9.3 min respectively. Two years (from January 1, 2007, to December 31, 2008) after ATLS training, 382 cases of severe trauma were admitted and treated. The ISS was 25.3+/-6.1 on average and 62 cases died with the mortality of 15.1%. The duration in emergency department and from admission to operation were 47.8 min+/-10.7 min and 61.5 min+/-9.9 min respectively. The ISS score showed no significant difference between the two groups (P > 0.05), but the mortality, the duration in emergency department and from admission to operation were markedly decreased after ATLS training and showed significant difference between the two groups (P <0.05).</p><p><b>CONCLUSION</b>ATLS course training can improve the emergency care effect of in-hospital severe trauma patients, and should be put into practice as soon as possible in China.</p>

The effect of angiotensin II on phosphoinositide-3 kinase/Akt cascade in cultured fibroblasts derived from patients with hypertrophic scars / 中华整形外科杂志

<p><b>OBJECTIVE</b>To study the effect of angiotensin II on phosphoinositide-3 kinase/Akt cascade in cultured fibroblasts derived from patients with hypertrophic scars.</p><p><b>METHODS</b>The expression of AT1 and AT2 receptor was detected by immunofluorescence staining. Cultured human skin fibroblasts were treated with Ang II (10(-9) - 10(-7) mol/L), with or without an AT1 receptor blocker, valsartan or an AT2 receptor antagonist, PD123319. The phosphorylation of Akt was detected by western blotting, and PI3K activity was measured by Assay of PI3-K activity.</p><p><b>RESULTS</b>Immunofluorescence staining showed that cultured fibroblasts derived from hypertrophic scars expressed both AT1 and AT2 receptors. Ang II increased Akt phosphorylation and PI3K activity in cultured hypertrophic scar fibroblasts in a dose- and time-dependent manner. Additionally, Ang II-induced Akt phosphorylation was blocked by wortmannin, a PI3-K inhibitor. This Ang II-activated PI3-K/Akt cascade was significantly inhibited by valsartan, an AT1 receptor specific blocker (P<0.05), whereas enhanced by PD123319, an AT2 receptor antagonist (P<0.05).</p><p><b>CONCLUSION</b>These results indicate that Ang II receptors regulates PI3-K/Akt cascade of hypertrophic scars fibroblasts via AT1 and AT2.</p>

First aid strategy for severe traumatic patients in hospital / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To study the emergency management principles of severe trauma in hospital (injury severity score larger than or equal to 16).</p><p><b>METHODS</b>We used "ATP principle" to manage severe traumatic patients. The ATP principle is composed of: 1) attending surgeons offering initial management (A); 2) teamwork commencement immediately after patients admitted to hospital (T); 3) parallel principle, ie, emergency resuscitation, evaluation and laboratory test performed simultaneously (P). Clinical effects before and after applying ATP principle were retrospectively analyzed and compared.</p><p><b>RESULTS</b>During January 1, 2002 to December 31, 2003, 338 patients were treated without applying ATP principle, in which ISS was 25.9+/-6.4, 152 cases died with the mortality being 39.2%, and the time stayed in emergency department and the time to operation room after admission were (102.8+/-16.7) min, (140.3+/-20.6) min, respectively. During January 1, 2004 to December 31, 2005, 438 patients were treated based on ATP principle, in which ISS was 28.6+/-7.8, 87 cases died with the mortality being 19.9%, and the time in emergency department and the time to operation room after admission were (69.5+/-11.5) min, (89.6+/-9.3) min, respectively. ISS showed no significant difference between the two groups (P larger than 0.05) but the mortality, the time stayed in emergency department and the time to operation room after admission were greatly reduced and showed significant difference between the two groups (P less than 0.05).</p><p><b>CONCLUSIONS</b>Applying ATP principle to treat severe traumatic patients can shorten emergency treatment time in hospital and decrease mortality.</p>