Role of inhibition of p38 mitogen-activated protein kinase in liver dysfunction after hemorrhagic shock and resuscitation.

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.

Pathogenic alteration in severe burn wounds.

The present study aims to define the trend of time related changes with local bacterial alteration of bacterial resistance in severe burns in our burn center during a 12-year period. Retrospective analysis of microbiological results on severely burned wounds between 1998 and 2009 was carried out. A study of 3615 microbial isolates was performed.

Unplanned decannulation of tracheotomy tube in massive burn patients: a retrospective case series study.

Background: Unplanned extubation is associated with adverse outcomes in intensive care unit. The massive burn patient differs from other critically ill patients in many ways. However, little is known about the unplanned decannulation (UD) in Burn Intensive Care Unit.

TLR4 mediates lung injury and inflammation in intestinal ischemia-reperfusion.

Background: Splanchnic ischemia is common in critically ill patients, and it can result in injury not only of the intestine but also in distant organs, particularly in the lung. Local inflammatory changes play a pivotal role in the development of acute lung injury after intestinal ischemia, but the underlying molecular mechanisms are not fully understood. We sought to examine the role of Toll-like receptor 4 (TLR4) in the mouse model of intestinal ischemia-reperfusion (I/R)-induced lung injury and inflammation.

mTOR partly mediates insulin resistance by phosphorylation of insulin receptor substrate-1 on serine(307) residues after burn.

Mammalian target of rapamycin (mTOR) is an important mediator for cross talk between nutritional signals and metabolic signals of insulin by downregulating insulin receptor substrate proteins. Therefore, mTOR inhibition could become a therapeutic strategy in insulin-resistant states, including insulin resistance induced by burn. We tested this hypothesis in the rat model of 30% TBSA full thickness burn, using the mTOR inhibitor rapamycin.

Effects of early excision and grafting on cytokines and insulin resistance in burned rats.

Unlabelled: Burn wound excision and grafting is a common clinical practice that decreases patient morbidity and mortality. It is not known, however, if the salutary effects of this procedure are related to effects on interleukin 6 (IL-6) and tumor necrosis factor (TNF-) α, and to reducing insulin resistance after burn. Sprague-Dawley rats were randomly divided into three groups: control, burn, burn ± excision groups.

Burn injuries caused by ship fire: a 12-year study in Shanghai.

Unlabelled: The 105 patients admitted to our Burn Institute from 1st January 1996 to 31st December 2007, with ship fire-related burns were studied retrospectively. The mean age was 30.2+/-12.

[Repair of deep burn and traumatic wounds in lower extremities with combined transplantation of multiple pedicled skin flaps].

Objective: To summarize the clinical experience in repair of deep burn and traumatic wounds with combined transplantation of different types of pedicled skin flaps in lower extremities.

Methods: Two hundred and thirty-six patients with 271 deep wounds in lower extremities after burn or trauma were repaired with muscular skin flaps, local fascial flaps and island flaps with vascular pedicle (more than 20 types) in our department from Jan. 1998 to Sept.

Angiotensin II induces type I collagen gene expression in human dermal fibroblasts through an AP-1/TGF-beta1-dependent pathway.

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-beta1.

The direct hospitalisation costs of paediatric scalds: 2-year results of a prospective case series.

Objective: To reveal the characteristic and distribution of length of hospital stay (LOS) and direct hospitalisation costs of paediatric scald.

Methods: A prospective case series observation was performed from January 2005 to December 2006 at the Burn Center, Changhai Hospital, Shanghai, China. The information, such as demographics, clinical diagnosis and treatments since admission, of the paediatric scald patients included in the series was recorded.

[Treatment of severe crush syndrome caused by earthquake: a report of 35 cases].

Objective: To discuss the diagnosis and treatment of the crush syndrome in the earthquake.

Methods: Thirty-five patients with crush syndrome caused by earthquake were involved the retrospective study. The role of nutritional support, active wound treatment and hemodialysis on the patients' recovery was observed.

Prevention and treatment of gastrointestinal dysfunction following severe burns: a summary of recent 30-year clinical experience.

Aim: To sum up the recent 30-year experience in the prevention and treatment of gastrointestinal dysfunction in severe burn patients, and propose practicable guidelines for the prevention and treatment of gastrointestinal (GI) dysfunction.

Methods: From 1980 to 2007, a total of 219 patients with large area and extraordinarily large area burns (LAB) were admitted, who were classified into three stages according the therapeutic protocols used at the time: Stage 1 from 1980 to 1989, stage 2 from 1990 to 1995, and stage 3 from 1996 to 2007. The occurrence and mortality of GI dysfunction in patients of the three stages were calculated and the main causes were analyzed.

Randomized, multicenter, double-blind, and placebo-controlled trial using topical recombinant human acidic fibroblast growth factor for deep partial-thickness burns and skin graft donor site.

Wound healing is a dynamic and complex biologic process that could be accelerated by growth factors. To investigate the efficacy of topical recombinant human acidic fibroblast growth factor (rh-aFGF) treatment in deep partial-thickness burn or skin graft donor sites, we designed a randomized, multicenter, double-blind, and placebo-controlled clinical trial. The healing rate, fully healed rate, and healing time were evaluated to assess the efficacy of rh-aFGF application.

[Amelioration of insulin resistance after scald by c-Jun N-terminal kinase inhibitor in rat].

Objective: To investigate the role and mechanism of c-Jun N-terminal kinase (JNk) inhibitor (SP600125) in amelioration of insulin resistance after scald.

Methods: Twenty-four Sprague-Dawley rats were randomized into sham (the process of scald was mimicked by water at room temperature) , scald, scald and SP600125 groups. The rats were inflicted with 30% TBSA full-thickness scald in the latter two groups.

[Role of c-Jun NH (2)-terminal kinase in insulin resistance after burn].

Objective: To investigate the role of c-Jun NH (2)-terminal kinase (JNk) in insulin resistance after burn and its mechanism.

Methods: Twenty-four Sprague-Dawley rats were randomized to control, burn and burn + anisomycin groups. The rats in control group received sham burn trauma, and burn and burn + anisomycin groups received 30% total body surface area (TBSA) full thickness burn injury.

Insulin resistance following thermal injury: an animal study.

Unlabelled: The aim of this study was to investigate the changes of glucose tolerance, insulin sensitivity, and euglycemic-hyperinsulinemic glucose clamps following a 30% TBSA full thickness third degree burn in rats. Sprague-Dawley rats weighing 160-170g received 30% TBSA full thickness third degree burn by immersing the back of trunk for 12s in a boiling water bath under anesthesia. Weight- and time-matched sham burn group (control) was treated in the same manner as the trauma group, except that they were immersed in a room-temperature water bath.

[Interaction between p38 mitogen-activated protein kinase signal transduction pathway and NF-kappaB/IkappaB system on the proinflammatory cytokines release after burn trauma].

Objective: To investigate the interaction between p38 mitogen-activated protein kinase signal transduction pathway and nuclear factor (NF)-kappaB/IkappaB system on the proinflammatory cytokines release after burn trauma.

Methods: Human monocyte line THP-1 were incubated with serum from eight healthy controls, burn sera, burn sera pretreatment with SB203580, and burn sera pretreatment with pyrrolidine dithiocarbamate (PDTC). After 24 hours incubation with serum, tumor necrosis factor (TNF)-alpha and interleukin-1beta (IL-1beta) levels in THP-1 culture supernatants were measured by ELISA.

[Activation of p38 MAPK signal transduction pathway by burn serum and the expression of VCAM-1 in HUVECs induced by NF-kappaB].

Objective: To investigate the influence of burn serum on the expression of vascular cell adhesion molecule-1 (VCAM-1) of human umbilical vein endothelial cells (HUVECs) andits signal transduction mechanism.

Methods: HUVECs cultured in vitro were employed for the experiment, and were divided into normal control (NC, with addition of normal serum), burn serum (BS, with addition of burn serum), SB203580 (with addition of 10 micromol/L SB203580 treatment 1 hour before burn serum treatment) and PDTC [with 10 mmol/L pyrrolidine dithiocarbamate (PDTC) 1 hour before burn serum treatment] groups. Protein and mRNA expression of VCAM-1 in HUVECs was measured by flow cytometry and reverse transcription polymerase chain reaction (RT-PCR) respectively at 0, 6, 12, 24 and 36 hours after burn serum treatment.

[Role of p38MAPK signal transduction pathway in Kupffer cells production of TNF-alpha and IL-1beta in severely burned rats].

Objective: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the Kupffer cells production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in severely burns rats.

Methods: Male health adult Sprague-Dawley rats were randomized into four groups: sham burn rats given vehicle, sham burn rats given the p38 MAP kinase inhibitor SB203580, rats given a 30% total body surface area (TBSA) full-thickness burn and fluid resuscitation plus vehicle, and burn rats given injury and fluid resuscitation plus SB203580. Rats from each group were killed at 24 h after burn or sham burn and Kupffer cells (KCs) were isolated.

p38 mitogen-activated protein kinase inhibition attenuates burn-induced liver injury in rats.

This study was made to evaluate the effect of SB203580, a specific p38 MAP kinase inhibitor, on burn-induced hepatic injury as well as the activation of nuclear factor (NF)-kappaB in severely burned rats. Sprague-Dawley rats were divided into three groups: (1) sham group, rats underwent sham burn; (2) burn group, rats given third-degree burns over 30% total body surface area (TBSA) and treated with vehicle plus lactated Ringer solution for resuscitation 4 ml/(kg% TBSA); and (3) burn plus SB203580 group, rats given burn injury and fluid resuscitation plus SB203580 (10 mg/kg i.v.

[Mechanism of p38 mitogen-activated protein kinase in postburn acute pulmonary injury in scalded rats].

Objective: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the production of the proinflammatory factors such as tumor necrosis factor (TNF-alpha) and interleukin 1beta (IL-1beta) in lungs and in the pulmonary endothelial cell injury in severely scalded rats.

Methods: Forty eight adult healthy SD rats were randomly divided into three groups with 16 rats in each group, i.e.

[Role of p38 mitogen-activated protein kinase signal transduction pathway in the acute lung injury of severely burned rats].

Objective: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the acute lung injury of severely burned rats.

Methods: Forty-eight adult healthy rats were randomly divided into three groups: sham group, burn control group, and burn + SB203580 group. A third-degree burns over 30% total body surface area rat model was used and pulmonary capillary permeability, lung water content, pulmonary histology and p38 MAPK activity were measured at 24 hours postburn.