Yongming Yao

307 Hospital of the Chinese People's Liberation Army, Peping, Beijing, China

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Publications (11)17 Total impact

  • Hongming Yang · Chao Hu · Yongming Yao · Jiake Chai · Ma Li · Feng Yongqiang · Chu Wanli ·
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    ABSTRACT: Aim of the study: To observe the effects of ulinastatin on T lymphocyte immune function and the expression of high mobility group box-1 protein (HMGB1) in rats with scald injury. Material and methods: A total of 96 Wistar rats were randomly divided into three groups (32 rats in each group): sham burn group (S), burn group (B), ulinastatin-treated group (BU). Sham-burned rats were immersed in distilled water at 37 C for 12 seconds and served as control, rats in the later two groups were inflicted with 30% TBSA full thickness burns at boiling water (94 C) for 12 seconds, followed by resuscitation with Ringer's solution (i.p.). The treatment group (BU) received ulinastatin and the control group was given the same amount of saline solution immediately following burn injury, wounds in rats were soaked in 1% povidone-iodine solution. Blood samples and spleens were collected at 1, 3, 5, 7 d after injury for further laboratory investigations. High mobility group box-1 protein expression was evaluated by western blotting, the presence of CD4+ CD25+ regulatory T cells were determined with flow cytometry, the plasma IL-4 and IFN-gamma levels were determined using ELISA. Results: Compared with the S group (0.22 +/- 0.05), during postburn days] to 7, the level of HMGB1 in splenic tissue was significantly elevated in the B group (p < 0.01), reached the maximum at 3 d after injury (0.66 +/- 0.10, p < 0.01). After treated with ulinastatin, HMGB1 level was markedly decreased, reached the lowest value at 5 d (0.32 +/- 0.07, p < 0.01). Compared with the sham burn group, percentage of CD4+ CD25+ Treg cells in B group gradually increased after injury and peaked at 3 d after injury (5.42% +/- 0.56%). After burn injury 1, 5, 7 d, percentage of CD4+ CD25+ Treg cells in BU group was significantly lower than the B group (p < 0.01), reached the lowest at 5 d (2.23% +/- 0.21%). The serum level of IFN-gamma in B group was significantly higher than the S group (p < 0.01), IL-4 was significantly higher than that of the S group (p < 0.01). After injury for 1 similar to 7 d, the content of IFN-gamma in BU group were significantly higher than the B group (p < 0.05 or p < 0.01), and IL-4 level was significantly lower than the burn group (p < 0.05 or p < 0.01). Conclusions: As an anti-inflammatory drug, ulinastatin effectively reduced the expression of HMGB1 in the spleen tissue of severely burned rats, which was associated with reduction in the level of regulatory T cells (Treg), and the functional polarization of splenic T cells levels and Th1/Th2 pattern changes. Taken together these data suggested that ulinastatin improved the immune function of rats with scald injury.
    Central-European Journal of Immunology 01/2013; 1(1):1-7. DOI:10.5114/ceji.2013.34351 · 0.28 Impact Factor
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    ABSTRACT: This study examined the effect of intensive insulin therapy on immune function and inflammatory factors at the early phase after severe trauma. At day 1, 3, 5, 7 after admission, subsets of CD4(+) helper T lymphocytes (Th1/Th2) and human leukocyte antigen (HLA)-DR expression on CD14(+) monocytes were flow cytometrically measured. Levels of cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10) and other immunity markers, such as IgA, IgG, IgM, C3, C4 and C reaction protein (CRP) were examined in two groups. The results showed that TNF-α, IL-6 and CRP levels in the intensive insulin therapy group were significantly lower than those in the conventional therapy group, whereas IL-10 levels were substantially increased after intensive insulin therapy. C3 level at day 3, 5, 7 and C4 levels at day 5, 7 were lower in the intensive therapy group than in the conventional therapy group. Th1/Th2 ratios decreased gradually over time in both groups, and were much lower at day 3, 5, 7 in intensive therapy group. There were significant differences among day 3 to day 7 after admission in HLA-DR expression in CD14(+) monocytes. It was concluded that the intensive insulin therapy could decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines in the elderly suffering from severe trauma, at the same time, with complement recovery being delayed. Moreover, intensive insulin therapy promoted immune suppression and, therefore, measures need be taken to address the issue.
    Journal of Huazhong University of Science and Technology 06/2012; 32(3):400-4. DOI:10.1007/s11596-012-0069-8 · 0.83 Impact Factor
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    ABSTRACT: The therapeutic effects of intensive insulin therapy in treatment of traumatic shock combined with multiple organ dysfunction syndrome (MODS) were investigated. A total of 114 patients with traumatic shock combined with MODS were randomly divided into two groups: control group (n=56) treated with conventional therapy, and intensive insulin therapy group (n=58) treated with conventional therapy plus continuous insulin pumping to control the blood glucose level at range of 4.4-6.1 mmol/L. White blood cells (WBC) counts, prothrombin time (PT), serum creatinine (SCr), alanine aminotransferase (ALT), serum albumin and PaO(2) were measured before and at the day 1, 3, 5, 7 and 14 after treatment. The incidence of gastrointestinal dysfunction, the incidence of MODS, hospital stay and the mortality were also observed and compared. After intensive insulin therapy, the WBC counts, SCr, ALT and PT were significantly reduced (P<0.05), but the level of serum albumin was significantly increased (P<0.05) at the day 3, 5, 7 and 14. In the meantime, the PaO2 was significantly elevated at the day 3, 5 and 7 (P<0.01) after intensive insulin therapy. The incidence of gastrointestinal dysfunction, the incidence of MODS, the length of hospital stay and the mortality were markedly decreased (P<0.01). The results suggest early treatment with intensive insulin therapy is effective for traumatic shock combined with MODS and can decrease the length of hospital stay and the mortality.
    Journal of Huazhong University of Science and Technology 04/2011; 31(2):194-8. DOI:10.1007/s11596-011-0251-4 · 0.83 Impact Factor
  • Liu Hui · Yongming Yao · Songbai Wang · Yan Yu · Ning Dong · Hongyun Li · Zhiyong Sheng ·
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    ABSTRACT: Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway plays an important role in sepsis, transducing a multitude of inflammatory signals. To date, knowledge of JAK/STAT pathway in sepsis is limited. This study was to investigate the potential role of JAK/STAT pathway in mediating multiple organ damage and mortality in septic rats. Our data showed that inhibition of JAK2/STAT3 attenuated cecal ligation and puncture-induced multiple organ damage and mortality in 48 hours in rats. A total of 98 male Wistar rats were randomly divided into 4 groups as follows: (1) normal control group (n = 10); (2) cecal ligation and puncture (CLP) group (n = 40), which was further divided into 2, 6, 24, 48-hour post-CLP groups; (3) AG490 (8.0 mg/kg, Calbiochem, La Jolla, CA) treatment group (n = 24), which was further divided into 2, 6, 24, 48-hour post-CLP groups; (4) rapamycin (0.4 mg/kg, Calbiochem, Calbiochem, La Jolla, CA) treatment group (n = 24), which was further divided into 2, 6, 24, 48-hour post-CLP groups; CLP was performed to induce experimental sepsis. AG490 (8 mg/kg) or rapamycin (0.4 mg/kg) was injected subcutaneously 0.5 hour before CLP in respective group. Animals were killed at destined time after CLP (not including the death rate observation group), and specimens of serum, liver, and lungs were harvested and stored in liquid nitrogen for subsequent analyses. In an additional experiment, 88 animals were randomly divided into three groups to compare the survival rate, including CLP group (n = 40), AG490 treatment group (8 mg/kg, n = 24), and rapamycin treatment group (0.4 mg/kg, n = 24). Mortality of rats in each group was recorded up to 48 hours after the procedure. After CLP challenge, myeloperoxidase (MPO), aspartate transaminase, and alanine aminotransferase levels, as well as activation of JAK2 and STAT3, were markedly increased. Administration of AG490 or rapamycin significantly decreased activation of JAK2 and STAT3, as well as high mobility group box-1 protein, MPO, alanine aminotransferase levels (p < 0.05 or p < 0.01). In addition, treatment with AG490 or rapamycin significantly improved the 48-hour survival rate from 37.5% (15 of 40) to 66.7% (16 of 24) and 70.8% (17 of 24), respectively (both p < 0.05). JAK2/STAT3 pathway might play a role in the development of multiple organ damage in septic rats, which suggested a potential strategy to control sepsis.
    The Journal of trauma 03/2009; 66(3):859-65. DOI:10.1097/TA.0b013e318164d05f · 2.96 Impact Factor
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    ABSTRACT: CASK (calcium/calmodulin-dependent serine protein kinase) is a kind of scaffolding protein that recruits or organizes other proteins at the plasma membrane to co-ordinate signal transduction pathways within the cytoplasm and nucleus. We have previously found that hCASK (human CASK) binds Id1 (inhibitor of DNA binding 1) through hCASK's GUK (guanylate kinase) domain and inhibits cell growth, probably via interactions with Id1. Overexpression of hCASK resulted in a reduced rate of cell growth, although inhibition of CASK via RNAi (RNA interference) promoted cell proliferation in ECV304 cells. This study revealed that hCASK regulates the protein and mRNA level of p21(wafi/cip1) (referred to throughout as p21), and activated the expression of p21 in a time-dependent manner. Two E-boxes in the proximal region at the TSS (transcription start site) play key roles in regulating hCASK-mediated p21 expression. We suggest that E2A (E12 and E47), a representative of the E proteins that binds the E-box elements, is a participant in the mediation of p21 expression by hCASK. The results of the present study suggest that hCASK regulation of cell growth might involve p21 expression, and that the bHLH (basic helix-loop-helix) transcription factor E2A probably participates in hCASK regulation of p21 expression. From these findings, we propose a novel proliferation signalling pathway mediated by hCASK.
    Biochemical Journal 02/2009; 419(2):457-66. DOI:10.1042/BJ20080515 · 4.40 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the occurrence and possible mechanisms of apoptosis in skeletal muscles after burn injury. After a 40% body surface area burn to rats, TA muscles were examined for apoptosis at varying times by TEM, TUNEL and cell death ELISA assay. Thermal injury was found to induce apoptosis in skeletal muscle on the first day and maximal apoptosis appeared 4 days post-injury. Apoptotic ligands in serum assessed by ELISA revealed rapidly increase of TNF-alpha and subsequent increase of sFasL to sFas ratio after burn injury. It implied TNF-alpha induced apoptosis in early stage and FasL induced apoptosis in later stage after burn injury. Apoptosis-related genes/proteins in skeletal muscles examined by real-time PCR array and Western blotting showed pro-apoptotic genes/proteins, including Tnfrsf1a, Tnfrsf1b and Tnfsf6 in TNF ligand and receptor family, Bax and Bid in Bcl-2 family, caspase-3 and caspase-6 in caspase family, Dapk1, FADD and Cidea in death and CIDE domain family, Apaf-1 in CARD family, and Gadd45a were up-regulated, while anti-apoptotic gene Bnip1 was down-regulated compared with that of time-matched controls. In addition, increment of caspase-3, caspase-8 and caspase-9 activity provided further evidence for their role in apoptosis in skeletal muscle. Significant increase in expression in pro-apoptotic genes/proteins and activity of caspases suggested that death receptor-mediated signaling pathways and other apoptotic related pathways participated in apoptosis in skeletal muscle after burn injury. However, it was found that some anti-apoptotic genes such as Bcl2l1, Mcl-1, Nol-3, Il-10 and Prok2 were also up-regulated, which might imply the co-existence of protective response of the body after burns. In conclusion, the data suggest that apoptosis and pro-apoptotic signaling are enhanced in muscles of burned rats. To further elucidate the underlying apoptotic mechanisms mediating the atrophic response is important in establishing potential therapeutic interventions that could prevent and/or reduce skeletal muscle wasting and preserve its physiological function.
    Apoptosis 12/2008; 14(1):52-65. DOI:10.1007/s10495-008-0277-7 · 3.69 Impact Factor
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    ABSTRACT: Early multiple organ dysfunction syndrome appears to be facilitated with bacterial translocation in severe burn injury, yet the mechanisms of bacterial translocation remain in dispute. The aim of this study was to characterize the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacterial translocation after burns and to analyze the effects of bifidobacterial supplement on gut barrier function. Wistar rats were randomly divided into burn group (Burn, n = 60), sham burn group (SB, n = 10) in experiment 1, and burn + saline group (BS, n = 30), burn + bifidobacteria group (BB, n = 30), and sham-burn + saline group (SS, n = 30) in experiment 2. Animals in BB group were fed bifidobacterial preparation (5 x 10(9) CFU/mL) after burns, 1.5 mL, twice daily. Animals in BS and SS were fed saline. Samples were taken on postburn days 1, 3, and 5. The incidence of bacterial translocation and counts of Bifidobacterium, fungi and Escherichia coli in gut mucosa, as well as the sIgA levels in mucus of the small intestine were determined. The positive sIgA expression in lamina propria and ileum mucosal injury were evaluated light microscopically by blinded examiners. The incidence of bacterial translocation was increased after burns, which was accompanied by significant decrease in number of bifidobacteria but significant increase in E. coli and fungi in gut mucosa, and elevation of levels of plasma endotoxin and IL-6 (p < 0.001). The incidence of bacterial translocation was markedly reduced after 3- and 5-day supplementation of bifidobacteria compared with control group (p < 0.05). The counts of mucosal bifidobacteria were increased by 4- to 40-fold, whereas E. coli and fungi were decreased by 2- to 30-fold and 10- to 150-fold, respectively, after bifidobacterial supplementation. The damage of mucosa tended to be less pronounced after 3-day bifidobacteria-supplemented formula compared with control group (grade 2 [0-6] versus grade 4 [3-6], p < 0.05). Moreover, the expression and release of sIgA was markedly augmented after 3-days of bifidobacteria-supplementation formula and it returned to normal range on postburn day 5. The decrease in counts and proportion of bifidobacteria to other flora in gut may play an important role in the development of bacterial translocation after thermal injury. Supplementation of exogenous bifidobacteria could improve gut barrier function, and attenuate bacterial/endotoxin translocation secondary to major burns.
    The Journal of trauma 09/2006; 61(3):650-7. DOI:10.1097/01.ta.0000196574.70614.27 · 2.96 Impact Factor
  • Zhigu Wu · Zhiyong Sheng · Tongzhu Sun · Miao Geng · Junyou Li · Yongming Yao · Zuxiu Huang ·
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    ABSTRACT: To describe the methods which were used to develop collagen-based materials for wound dressing. Fresh frozen bovine tendon was treated with 0.05 mol/L acetic acid at pH 3.2 for 48-72 hours, homogenized, filtered, mixed with 8% chondroitin sulphate, for creating a deaerated 1.5%-2.5% collagen solution. The solution was lyophilized in either a pre-frozen or non-pre-frozen mould. The collagen sponge was then cross-linked with 0.25% glutaraldehyde for 24 hours. Three other types of wound dressings were developed using a similar method: collagen membrane with a polyurethane membrane onlay, polyurethane-coated collagen membrane and collagen membrane on gauze. It was demonstrated that the use of frozen bovine tendon was stable, and that the prepared collagen sponge contained pores of 50-400 microm in diameter. Collagen could be used as wound dressing.
    Chinese medical journal 04/2003; 116(3):419-23. · 1.05 Impact Factor
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    ABSTRACT: To investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-origin bacteria/endotoxin translocation in scalded rats. Wistar rats inflicted with 30% III degree scalding on the back were employed as the model with the rats undergoing sham injury as the control. The intestinal bacteria/endotoxin translocation and the changes in cecal mucosal microflora were determined by routine methods. And the plasma IL-6 concentration was measured with ELISA. The incident of bacterial translocation into internal organs increased markedly in scalded rats (P = 0.001). The plasma LPS levels on 1, 3 and 5 postburn days (PBDs) in scalded rat group were much higher than those in sham injury group. The number of bifidobacteria decreased sharply 20 - 250 fold, the fungi increased 5 - 60 fold and E. coli increased 0.5 - 30 fold in the caecal mucosal microflora in the scalding group. The ratio of bifidobacteria to E. coli in the scalding group (4 - 800:1) was much lower than that in the sham injury group (25000:1). Furthermore, the plasma IL-6 level increased evidently in the scalding group. It was indicated by further analysis that compared with the rats without bacterial translocation, the bifidobacteria decreased 120 fold, the fungal number increased 50 fold and the E. coli number increased 30 fold in the scalded rats. The bifidobacterial number in the caecal mucosal microflora was negatively correlated with the plasma concentrations of IL-6 and LPS (P < 0.01) in the scalding rat group, and the plasma concentration of IL-6 was significantly and positively correlated with that of LPS. Severe scalding injury could lead to an the imbalance of intestinal microflora and the increased intestinal translocation of bacteria and LPS. The decrease of the ratio and number of bifidobacteria in the caecal mucosal microflora might be a contribute to the occurrence of postburn intestinal bacteria/endotoxin translocation.
    Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns 12/2002; 18(6):365-8.
  • Yongming Yao · Hongyun Li · Ning Dong · Yan Yu · Lianrong Lu · Zhiguo Shi · Zhiyong Sheng ·
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    ABSTRACT: To investigate the protective effect and its underlying mechanism of 2,4-diamino-6-hydroxy-pyrimidine (DAHP), an inhibitor of GTP-cyclohydrolase I (GTP-CHI), on postburn Staphylococcus aureus (S. aureus) sepsis in rats. Fifty-six Wistar rats were randomly divided into four groups, i.e. normal control, scalding control, postburn sepsis group and DAHP treatment group. Tissue samples from liver, kidneys, lungs and heart were aseptically taken, and in which the GTP-CHI and inducible nitric oxide synthase (iNOS) contents and the mRNA expression of tumor necrosis factor-alpha (TNFalpha) were determined. Furthermore, biopterin (BH(4)) and nitric oxide (NO) levels in these tissue were also measured. After the scalding injury followed by bacterial challenge, the GTP-CHI gene expression and biopterin levels were significantly increased in all tissue sampled, and so were iNOS mRNA expression and NO (P < 0.01), especially in liver and lungs. The expressions of GTP-CHI mRNA and iNOS mRNA and the production of BH(4) and NO in all tissue were evidently inhibited by the pretreatment with DAHP (P < 0.05 approximately 0.01). At the same time, the TNFalpha expression was also obviously decreased. In addition, The mortality at 6 hr in rats of DAHP treatment group was decreased. The prognosis of the scalding rats complicated by sepsis caused by G(+) bacteria could be improved by DAHP pretreatment, which might be related to the inhibition of the production of BH(4) and NO by DAHP.
    Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns 04/2002; 18(2):84-7.
  • Hongyun Li · Yongming Yao · Zhiguo Shi · Yan Yu · Ning Dong · Zhiyong Sheng ·
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    ABSTRACT: To investigate the potential role and changes in CD14 in postburn Staphylococcus aureus sepsis. Wistar rats were subjected to a 20% total body surface area (TBSA) full-thickness thermal injury and followed by Staphylococcus aureus challenge. Plasma and tissue samples from liver, kidneys, lungs and heart were collected to determine endotoxin (lipopolysaccharide, LPS) levels and CD14 mRNA expression. It was found that after thermal injury combined with Staphylococcus aureus sepsis, LPS levels in various tissues were markedly increased, peaking at 2 approximately 6 h (P < 0.05), then returned to baseline at 24 h. Plasma LPS level was also increased significantly at 2hrs after Staphylococcus aureus challenge compared with that in normal control animals (0.3056 EU/ml vs. 0.1250 EU/ml, P < 0.05). In addition, the intestinal diamine oxidase (DAO) activity decreased (P < 0.05). This indicated that the integrity of intestinal mucosa was damaged. Meanwhile, tissue CD14 mRNA expressions were up-regulated in all tissues (P < 0.05), especially in lungs. These data suggested that gut-originated LPS translocation and CD14 mRNA expression could be induced by thermal injury with Staphylococcus aureus sepsis. The up-regulation of CD14 gene expression might be associated with the local endotoxin activation secondary to postburn sepsis.
    Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns 04/2002; 18(2):88-91.