The Janus kinase/signal transducer and activator of transcription (JAK/STAT) are a major signal transduction pathway in controlling and regulating a number of cytokine-mediated responses, including interferon-?, interleukin-1 (IL-1), IL-6, IL-10 and IL-4. The JAK/STAT pathway is particularly elegant because of its very rapid and simple cytoplasm-to-nucleus signaling. Recently, it has been found that JAK/STAT pathway might also be involved in the regulation of high mobility group box-1 protein (HMGB1), which plays an important role as a potential late mediator of sepsis. Inhibition of the activation of JAK/STAT pathway can down-regulate the gene expression of HMGB1 in vital organs, especially in the liver and lungs. In addition, treatment with JAK/STAT pathway inhibitors can effectively prevent the occurrence and development of multiple organ dysfunction syndrome following sepsis, and the probable underlying mechanism of which involves a reduction of direct or indirect harmful effect of HMGB1. Over the past few years, numerous investigations have contributed to our knowledge of the JAK/STAT pathway and its role in cytokine-mediated abnormality of immune function as well as inflammatory response during sepsis, and it might be helpful in further identifying a potential strategy of intervention for posttraumatic or postburn sepsis. This review summarizes the salient features of JAK/STAT pathway and focuses on the pathophysiological role of JAK/STAT in regulating proinflammatory cytokine activity and HMGB1 expression in vivo.

The present study was performed to investigate the significance and potential role of signal transducers and activators of transcription 3 (STAT3) activation in postburn Staphylococcus aureus sepsis. Seventy one male Wistar rats were randomly divided into five groups: normal controls, scald control group, postburn sepsis group, AG490 (JAK2 inhibitor) treatment group, and rapamycin (RPM, STAT3 inhibitor) treatment group. Tissue samples from the liver and lung were collected to determine activation of STAT3, and interferon ? (IFN ?) mRNA as well as protein expression. The results showed that activation of STAT3 was quickly up regulated at 0 5～1 hour following thermal injury combined with Staphylococcus aureus challenge in the liver and lung, and it gradually weakened after 2 hours. Treatment with AG490 or RPM could inhibit activation of STAT3 at 0 5 hour in the liver and lung. Meanwhile, IFN ? mRNA expression markedly declined at 2 hours after treatment with AG490 or RPM in the liver and RPM in the lung ( P

Objective To investigate the effects of inhibition of nuclear factor-kappa B (NF-?B) by pyrrolidine dithiocarbamate (PDTC) on tissue pro- and anti-inflammatory cytokine expression in rats with postburn Staphylococcus aureus sepsis and its potential regulating mechanism. Methods Thirty-four male Wistar rats were randomly divided into normal control group (n=6), scald control group (n=6), postburn sepsis group (n=12),and PDTC treatment group (n=10). Tissue samples from the liver, kidneys and lungs were collected to determine tumor necrosis factor-? (TNF-?) and interleukin-10 (IL-10) mRNA expression as well as their protein levels. Results Both TNF-? mRNA and protein expressions in the liver, kidneys and lungs of postburn septic animals were up-regulated rapidly at 0.5-2 hours (P

Objective To investigate the effect of rapamycin(RPM)on hepatic interleukin-10(IL-10)gene and acute liver injury in rats with postburn Staphylococcus aureus sepsis.Methods Fifty male Wistar rats were randomly divided into four groups:normal control group,scald control group,postburn sepsis group,and RPM treatment group.Tissue samples from liver and plasma were collected to determine IL-10 mRNA and protein expressions,and liver function parameters were also measured.Results Compared to postburn Staphylococcus aureus sepsis group,in RPM treatment group hepatic IL-10 mRNA expression and plasma IL-10 were significantly increased at 0.5 hour after RPM treatment(P

0.05).The level of interleukin-8 in the sputum showed a positive correlation with neutrophil proportion(r=0.544).Conclusion Neutrophil,IL-8 in the sputum are associated with respiratory tract inflammation in the healthy smokers,smoking is an important factor in the inflammation.

Objective To study the prognosis of hepatoblastoma (HB) in children.Methods Retrospective analysis on the clinical data and follow-up of children with HB admitted from September 2010 to February 2015 and sum up the clinical outcome and prognosis.Results Thirty-six children with HB (23 males and 13 females) were enrolled. The median age on diagnosiswas 20 months. Allthe36 patients received follow-up, the median follow-up time was 37 months (7~71 months).(1) Of the 36 patients, 8 died. The prognosis of patients with stageⅠorⅡwas signiflcantly better than those with stage Ⅲ or Ⅳ(P<0.05). The prognosis of patients with fetal type was signiflcantly better than those with other subtypes (P<0.05). (2) Serum AFP level of 35 newly diagnosed cases increased, AFP level of survivors returned to normal after treatment. Of the 8 died patients, 3 patients had AFP elevated when relapsed, 5 cases had a persistently high AFP level after adjuvant chemotherapy. The levels of LDH, CRP, and AST at diagnosis had signiflcant influence on the prognosis (P<0.05).Conclusions Serum AFP can be a monitoring indicator for recurrence and prognosis of hepatoblastoma. POG / CCG staging, pathology classiflcation are key points when assessing the prognosis of hepatoblastoma. The prognosis of patients with high levels of LDH, CRP, and AST might be worse.

Systemic inflammatory response syndrome (SIRS) and its lethal sequela multiple organ dysfunction syndrome (MODS) are common complications in critical illness, such as severe trauma, shock, infection and major operations. During the past three decades, the evolution in our understanding of SIRS and/or MODS could be divided into three stages. Particularly in recent years, advances in molecular and cellular biology have provided new insights in the pathogenesis of this complex condition. The earlier emphasis on the pro inflammatory mediators involved in propagation of inflammatory response, has gradually been replaced by a realization that SIRS/MODS are the result of an imbalance of pro and anti inflammatory mediators to create the final status of excessive inflammation or immunoparalysis'. Though prognosis remains poor, the knowledge that now exists about SIRS/MODS gives great hope for the future. Progress has been made in new treatment modalities and re evaluation of current available measures. Nevertheless, improved techniques to monitor immunological or other markers of inflammatory and host defense responses will be important in assessing the effects of future therapies on central mechanisms contributing to SIRS/MODS.

Dendritic cells(DCs),representing a heterogenous population of professional antigen-presenting cells,are the initiators and modulators of the immune responses.Studies indicate that regulatory T cells contribute to immune nullipotency and immune suppression via cell-cell contact or cytokine secretion.These two kinds of cells may be valuable tools for modulating immunity in the setting of autoimmunity,cancer,chronic viral infections and graft rejection,etc.Here we discuss the current knowledge on the functions of regulatory T cells and denditic cells-based immunoregulation and the applications.

High-mobility-group B1 (HMGB1), an abundant, highly conserved cellular protein, is widely known as a nuclear DNA-binding protein that stabilizes nucleosome formation, and facilitates gene transcription. Recent studies suggested that HMGB1 could be overexpressed and released from cellular nucleosome upon endotoxin and cytokine stimulation, or other stress challenge including burns, shock, as well as infection. Therefore, extracellular HMGB1 might be involved in the pathogenesis of sepsis and subsequent multiple organ dysfunction syndrome. Moreover, experimental data showed that extracellular HMGB1 might play vital roles in nerves development, tumor metastasis, atherosclerosis and restenosis after vascular damage.

Objective To evaluate intraperitoneal Composix Kugel prosthetic patch repair of vental hernia. MethodsThe clinical data of 10 cases were reviewed for the surgical procedures and perioperative management in the use of this technique. ResultsMean operation time was 62 min(ranging grom 43 to 80 min). There was no postoperative wound hematoma and infection except for 1 case with seroma. Follow up of 2 to 19 months found no hernia recurrence. Conclusion Intraperitoneal Composix Kugel patch repair of vental hernia has the advantages of short operative time, minimal invasiveness and rapid convalescence.