Search PubMed⌕ Search

Biomedical subjects

Z Sheng

Publications and source records attributed to Z Sheng.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Gene expression of lipopolysaccharide receptor CD14 and tumor necrosis factor-alpha in rats after thermal injury].

OBJECTIVE: To investigate changes in lipopolysaccharide receptor CD14 and tumor necrosis factor-alpha (TNF-alpha) gene expression in vital organs, and their significance in the pathogenesis of systemic inflammation after burns. METHODS: Wistar rats were subjected to a 35 percent full-thickness scald injury, then sacrificed pre-burn, and postburn 12, 24, 48, 72 hours, respectively. Tissue samples from liver, kidney, lung and intestine were collected to measure CD14 and TNF-alpha mRNA expression. Peritoneal macrophages were harvested by peritoneal lavage to determine CD14 mRNA expression. RESULTS: CD14 mRNA expression increased markedly after thermal injury, peaking at both 12 and 48 hours. Likewise, CD14 mRNA levels were significantly up-regulated in peritoneal macrophages. Gene expression of TNF-alpha elevated markedly in liver, lungs, and kidneys after acute insults. Positive correlation was found between CD14 mRNA and TNF-alpha mRNA in liver, lung, and kidney tissues. CONCLUSIONS: Thermal injury per se can markedly up-regulate both CD14 and TNF-alpha gene expression in various organs. Excessive CD14 mRNA expression may enhance synthesis and release of TNF-alpha stimulated by endotoxin translocation, and the interaction between CD14 and TNF-alpha may play an important role in mediating multiple organ damage secondary to major burns.

Animals↗
PubMed1999

[Effect of escharectomy during burn shock stage on stress response].

OBJECTIVE: To investigate changes in hormones of plasma and the effect of escharectomy during burn shock stage on early stress response after burn. METHODS: Sixteen male minipigs were subjected to a 35% TBSA III degree burn injury. The burned minipigs were randomly divided into two groups: escharectomy during burn shock stage group (S group) and escharectomy group after burn shock stage (N group). The sequential changes in plasma levels of insulin, glucagon, cortisol, GH, IGF-I, albumin were analyzed. RESULTS: The serum concentration of insulin, glucagon, cortisol increased to some degree, whereas the serum concentration of GH, IGF-I decreased obviously after burn. As compared with the N group, no significant difference in the serum concentration of glucagon, cortisol, GH, IGF-I, was observed. CONCLUSIONS: Escharectomy during burn shock stage could not aggravate stress response after burn.

Animals↗
PubMed1999

[The effect of early escheractomy on expression of ICAM-1 and E-selectin mRNA of endothelial cells].

OBJECTIVES: To examine the effect of burned serum on change in endothelial cell ICAM-1 and E-selectin mRNA expression and whether these alterations can be corrected by the means of escharectomy during burn shock period. METHODS: One hundred and seventy-six Wistar rats with 30% III degree TBSA on back were studied. Endothelial cell ICAM-1 and E-selectin mRNA were tested with the method of RT-PCR. RESULTS: ICAM-1 and E-selectin expression showed an increase after stimulation by serum of 4 hours post burn, reaching peak levels 168 hours after injury. ICAM-1 and E-selectin expression levels could decrease to baseline within 168 hours in the rats which underwent escharectomy during shock stage, but kept higher than normal in rats without escharectomy or underwent 96 hours post burn. CONCLUSIONS: These findings suggest that eschar can induce endothelial cells to express adhesion molecule. Early escharectomy is important to prevent adhesion molecule expression and SIRS.

Animals↗
PubMed1999

[Preparation of collagen-based materials for wound dressing].

This article addressed the methods to develop collagen-based materials for wound dressing. Fresh frozen bovine tendon was treated with 0.05 M acetic acid at pH 3.2 for 48-72 h, then it was homogenized, filtered, and after the process of adding chondroitin sulphate(8%), it was dbubblized; thus 1.5%-2.5% collagen solution was finally prepared. The solution was lyophilized in prefrozen or un-prefrozen mold. The collagen sponge was crosslinked with 0.25% glutaraldehyde for 24 h. Three other wound dressings were developed by similar method, namely collagen membrane with polyurethane membrane onlay, polyurethane-coated collagen membrane and collagen membrane on gauze. It was demonstrated that the property of frozen bovine tendon was stable, and the prepared collagen sponge contained pores of 50-400 microns in diameter. Some factors influencing pore structure and size in the collagen sponge were discussed. The results of this preliminary study suggested that the collagen could be used as wound dressing.

Animals↗
PubMed1998

Randomised placebo-controlled trial of use of topical recombinant bovine basic fibroblast growth factor for second-degree burns.

BACKGROUND: Wound healing is a dynamic process that could be accelerated by growth factors. We investigated the effect of recombinant bovine basic fibroblast growth factor (rbFGF) on burn healing in a randomised placebo-controlled trial. METHODS: We recruited 600 patients with superficial or deep second-degree burns. Patients received 150 AU/cm2 daily topical rbFGF (n=300) or placebo (n=300) plus vehicle. We assessed healing by photography, punch-biopsy, and clinical examination. FINDINGS: All patients treated with rbFGF had faster granulation tissue formation and epidermal regeneration than those in the placebo group. Superficial and deep second-degree burns treated with rbFGF healed in a mean of 9.9 (SD 2.5) days and 17.0 (4.6) days, respectively, compared with 12.4 (2.7) and 21.2 (4.9) days (p=0.0008 and p=0.0003, respectively). No adverse effects were seen locally or systemically with rbFGF. INTERPRETATION: rbFGF effectively decreased healing time and improved healing quality. Clinical benefits would be shorter hospital stays and the patient's skin quickly becoming available for harvesting and grafting.

Administration, Cutaneous↗
PubMed1998

Regulation of matrix metalloproteinase-9 and inhibition of tumor invasion by the membrane-anchored glycoprotein RECK.

A human fibroblast cDNA expression library was screened for cDNA clones giving rise to flat colonies when transfected into v-Ki-ras-transformed NIH 3T3 cells. One such gene, RECK, encodes a membrane-anchored glycoprotein of about 110 kDa with multiple epidermal growth factor-like repeats and serine-protease inhibitor-like domains. While RECK mRNA is expressed in various human tissues and untransformed cells, it is undetectable in tumor-derived cell lines and oncogenically transformed cells. Restored expression of RECK in malignant cells resulted in suppression of invasive activity with concomitant decrease in the secretion of matrix metalloproteinase-9 (MMP-9), a key enzyme involved in tumor invasion and metastasis. Moreover, purified RECK protein was found to bind to, and inhibit the proteolytic activity of, MMP-9. Thus, RECK may link oncogenic signals to tumor invasion and metastasis.

3T3 Cells↗
PubMed1998

Ischemia and reperfusion impair the gene expression of endogenous basic fibroblast growth factor (bFGF) in rat skeletal muscles.

Our previous studies showed that the amount of endogenous basic fibroblast growth factor (bFGF) was reduced after ischemia and reperfusion insult. One of the mechanisms involved in the decrease of endogenous bFGF is the increased destruction of this growth factor associated with oxygen free radical activation and inflammation. We hypothesized that the wounding also impairs the secretion of bFGF and examined the bFGF gene expression in skeletal muscles after ischemia and reperfusion insult. In this study, a rat leg ischemia (4 h) and reperfusion (24 h) injury model was prepared and the in situ hybridization method and reverse transcriptase polymerase chain reaction technique (RT-PCR) were used to evaluate the bFGF gene expression and its localization in control (normal) and injured rat skeletal muscles. The results showed that the bFGF mRNA expression was localized in the cytoplasm in control skeletal muscle, especially at the periphery inside the cells. According to the intensity of the stain, four main classes of fibers could be identified: strongly, moderately, weakly, and negatively stained fibers. Based on the positive stain, about 82% of the total fibers examined were positive for bFGF mRNA stain. In ischemic or ischemic and reperfused rat skeletal muscles, the localization of bFGF mRNA expression was similar to that in normal skeletal muscles, but only 52% in ischemic muscles and 22% in ischemic and reperfused muscles had positive bFGF mRNA staining. RT-PCR confirmed a significant decrease in bFGF mRNA expression in ischemic and reperfused rat skeletal muscles. These results suggest that the acute ischemia and reperfusion not only induce the destruction of endogenous bFGF molecule, which is stored at the extracellular matrix of the fibers, but also downregulate the bFGF gene expression. The simultaneous dysregulation of endogenous bFGF gene expression and decreased synthesis of bFGF protein suggest a possible role of this growth factor in delayed wound healing.

Animals↗
PubMed1998

Opposing effects of Jun kinase and p38 mitogen-activated protein kinases on cardiomyocyte hypertrophy.

c-Jun N-terminal protein kinase (JNK) and p38, two distinct members of the mitogen-activated protein (MAP) kinase family, regulate gene expression in response to various extracellular stimuli, yet their physiological functions are not completely understood. In this report we show that JNK and p38 exerted opposing effects on the development of myocyte hypertrophy, which is an adaptive physiological process characterized by expression of embryonic genes and unique morphological changes. In rat neonatal ventricular myocytes, both JNK and p38 were stimulated by hypertrophic agonists like endothelin-1, phenylephrine, and leukemia inhibitory factor. Expression of MAP kinase kinase 6b (EE), a constitutive activator of p38, stimulated the expression of atrial natriuretic factor (ANF), which is a genetic marker of in vivo cardiac hypertrophy. Activation of p38 was required for ANF expression induced by the hypertrophic agonists. Furthermore, a specific p38 inhibitor, SB202190, significantly changed hypertrophic morphology induced by the agonists. Surprisingly, activation of JNK led to inhibition of ANF expression induced by MEK kinase 1 (MEKK1) and the hypertrophic agonists. MEKK1-induced ANF expression was also negatively regulated by expression of c-Jun. Our results demonstrate that p38 mediates, but JNK suppresses, the development of myocyte hypertrophy.

Animals↗
PubMed1998

The effects of fibroblast growth factors on ischemic kidney, liver and gut injuries.

OBJECTIVE: To explore the possibility of reducing reperfusion injuries of internal organ with acidic and basic fibroblast growth factors (aFGF and bFGF). METHODS: Two kinds of ischemia and reperfusion animal models were used in this study. In rat model of superior mesenteric artery (SMA) occlusion, microvascular clamp was placed on the root of SMA to cut off the blood flow for 45 minutes, and then the clamp was removed. In rat model of bilateral renal ischemia and reperfusion, both renal arteries were clipped to get complete cessation of blood flow for 60 minutes, then the blood flow was allowed to return. At the onset of reperfusion, the doses of 4.0 micrograms/rat of bFGF in SMA occluded rats or 2.6 micrograms/rat of aFGF in rats with acute renal injury were administered through the jugular vein. The liver and renal function examination, tissue bacterial study and histopathological evaluation were done to evaluate the treatment results. RESULTS: The functional impairment of ischemic liver, gut and kidney were reduced with venous administration of aFGF or bFGF at the onset of reperfusion. The results of pathological and tissue bacterial examination supported the assertion of significant protective effects of FGFs. CONCLUSIONS: The protective effects of FGFs may come from the non-mitogenic effects of FGFs at the early and the mitogenic effects at the late stage of tissue repair. These results indicate a potential for clinical use of FGFs as a therapeutic modality in ischemic visceral organ injuries in the future.

Animals↗
PubMed1998

Study on delay two-phase multiple organ dysfunction syndrome.

OBJECTIVE: To study the injury factors, pathogenic process and clinical features of delay two-phase multiple organ dysfunction syndrome (MODS) in severe burned patients and to replicate a standardized animal model that would accurately imitate the clinical features of MODS. METHODS: Forty-five human patients with burn size larger than 30% total body surface area (TBSA) were analyzed. All of them underwent severe burn shock in early stage and sepsis in late stage. Thirty-two goats were randomly divided into three groups: 1) hemorrhagic shock (group H, n = 6); 2) endotoxemia (group E, n = 6); and 3) hemorrhagic shock plus endotoxemia (group M, n = 20). Hemorrhagic shock was produced according to the method of Wigger (6.7 kPa for an hour, 1 kPa = 7.5 mmHg). Endotoxin (E. coli O111 B4) was given via the portal vein 24 hours after the resuscitation of hemorrhagic shock, in a dose of 30 ng/kg/min for 5 consecutive days. During the observation period of 10 days, all animals were hemodynamically monitored, given standard metabolic support and due cardiac and pulmonary support according to human intensive care. RESULTS: All the patients showed burn shock at 1-3 days and hyperdynamic circulation, hypermetabolism and systemic inflammatory responses over two weeks post-injury. Thirteen cases were found to develop MODS according to the prevailing diagnostic criteria, and 10 of them died with a mortality of 77%. Eighteen animals died in group M with a mortality of 90%, 12 of the 18 developed MODS, with overall incidence of 60%. Most animals in group M showed changes similar to that observed in human cases. The experimentation proved that in the pathogenic process of MODS, there was a two-hit phenomenon in the dvelopment of the syndrome. To prevent the development of MODS, it therefore was imperative to blunt the first hit or the second hit, so that an excessive inflammatory response was alleviated. This postulation has been verified in the treatment of extensive burns. Two patients with burn extent reaching 100% TBSA survived with only mild acute respiratory distress syndrome (ARDS) and renal dysfunction after comprehensive treatment of burn shock, including adequate fluid resuscitation, drugs to remove oxygen free radicals, rapid restoration of pHi, and early extensive excision of burn eschars. CONCLUSION: Both in human patients or animal experimentation, the typical delay two-phase MODS is shown to be produced by two successive insults in the forms of hypovolemic shock and sepsis. This postulation is helpful in formulating the prevention and treatment modality of MODS.

Adult↗
PubMed1998

[Clinical guidelines for timing of escharectomy and skin grafting during burn shock stage in extensively burned patients].

OBJECTIVE: To provide practical clinical guidelines to doctors who have no hemodynamic monitoring facilities in performing escharectomy during the shock period in extensively burned patients. METHODS: We analyzed our clinical experiences in 60 patients with extensive burn. RESULTS: Puting forward several clinical indexes for timing of escharectomy during burn shock stage: 1. Amount of fluids in the first 24 h postburn 2.6-3.0 ml.kg-1.1% TBSA-1; 2. Output of urine 80-100 ml/h; 3. Mentally fully conscious; 4. Thirst significantly alleviated and there is no nausea and vomiting; 5. Pulse 100/min; 6. Hb < or = 150 g/L; 7. Hct < or = 0.50. CONCLUSION: With the clinical indexes as guidelines, we assume that escharectomy could be performed during burn shock stage with reasonable safety.

Burns↗
PubMed1998

[Mechanisms of early gastro-intestinal ischemia after burn: hemodynamic and hemorrheologic features].

OBJECTIVE: To study the mechanisms of early gastro-intestinal ischemia developed in acute burn period and its relationships with hemodynamic and hemorrheologic changes. METHODS: Twelve pigs were randomly allocated into two groups: group C, a sham group that was subjected to all surgical procedures except burn; group B, 30% TBSA cutaneous thermal injury, and was resuscitated with Parkland formula one hour after burn. RESULTS: MAP remained stable after burn, but RAP, MPAP, PAWP and CI decreased significantly to the lowest level 4-8 hours after burn, and recovered after resuscitation 24 hours postburn. Intramucosal pH declined immediately (1 hour after burn) and remained abnormal throughout observation period. Portal venous blood flow demonstrated similar changes as pHi, and correlated well with intestinal pHi. Whole blood viscosity and plasma viscosity in portal venous blood elevated obviously after burn. CONCLUSIONS: 1. GI ischemia occurred early and recovered slowly during burn shock phase with conventional resuscitation regime. 2. GI ischemia correlated significantly with portal venous blood flow, but did not with systemic hemodynamic variables. 3. Hemorheologic changes in portal venous blood may exaggerate ischemia injuries.

Animals↗
PubMed1998

[Relationship between plasma D(-)-lactate levels and acute intestinal injury in rats following ischemia-reperfusion].

OBJECTIVE: To determine the kinetics of plasma D(-)-lactate levels in both portal and systemic circulations, and to examine whether elevated plasma D(-)-lactate would correlate to intestinal injury in rats subjected to acute intestinal ischemia-reperfusion. METHODS: Anesthetized rats underwent 75 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion. Plasma D(-)-lactate levels were measured by an enzymatic spectrophotometric assay. RESULTS: It showed that intestinal ischemia for 75 minutes resulted in a significant elevation in D(-)-lactate levels in portal vein blood compared to baseline values (P < 0.05). Plasma D(-)-lactate levels had a tendency to further increase after reperfusion up to 6 hours. Similar alterations in D(-)-lactate were also found in systemic circulation, there were no significant differences between the portal and systemic circulation at any time point. Moreover, the histopathological evaluation scores were significantly correlated to the portal D(-)-lactate levels in animals at various time points (r = 0.415, P < 0.01). In addition, a remarkable rise of endotoxin concentration within portal vein was already found at the end of 75-minute ischemia (P < 0.05), reaching a peak at 2 hours post-reperfusion. CONCLUSION: These data suggest that acute intestinal ischemia is associated with failure of mucosal barrier resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. The subsequent reperfusion might cause further increase in D(-)-lactate levels, which correlated to the histopathological alterations. Plasma D(-)-lactate may be a useful marker of intestinal injury following both ischemia and reperfusion insults.

Animals↗
PubMed1998

The role of gut as a cytokine-generating organ in remote organ dysfunction after intestinal ischemia and reperfusion.

OBJECTIVE: To test the hypothesis that in a rat model of acute intestinal ischemia/reperfusion injury, endotoxemia from the gastrointestinal tract would play a role in mediating tumor necrosis factor (TNF) response and remote organ dysfunction. METHODS: Wistar rats underwent 45 minutes of superior mesenteric artery occlusion followed by 6 hours of reperfusion. The rats were treated intravenously with either TNF monoclonal antibody (MoAb) or saline solution 90 minutes prior to the onset of ischemia. RESULTS: Significant elevation of plasma TNF level in both portal and systemic circulation was detected immediately after the onset of reperfusion. The level peaked at two hours after reperfusion (P < 0.01). Similarly, a remarkable TNF mRNA expression in the intestine in controls was detected at 0.5 hour post-reperfusion, and sustained a marked elevation throughout the observation period (P < 0.05-0.01). TNF elevation was found associated with gut-origin endotoxemia, and the maximal TNF response occurred approximately 0.5-2 hours after the initial appearance of endotoxin in the portal vein. Concomitantly, multiple organ dysfunction in response to local ischemic insult was also observed in untreated controls upon reperfusion, but it was significantly attenuated by pretreatment with MoAb against TNF. CONCLUSIONS: Intestinal injury can result in the gut becoming a cytokine-liberating organ. The escape of endotoxin and bacteria from the gut may be responsible for the TNF expression and release, which would be an important mechanism underlying pathophysiological alterations associated with intestinal ischemia/reperfusion injury.

Animals↗
PubMed1998

[Fatal complications in traffic accident injury].

OBJECTIVE: To discuss the relative factor, development tendency and prevention of the fatal complications in traffic accident injury. METHOD: We observed injury severity scale (AIS-ISS), clinical response time, and occurrence in traffic accident injury with fatal complications. Ridit mathematical statistics and Q test were used. RESULT: There were high ISS and long clinical response time in traffic accident injury with fatal complications. A significant relation was found between complications and the progress of time after trauma, thereby the clinical course could be divided into phases of cerebral hernia and shock (or acute), transition, infection and multiple organ dysfunction syndrome (MODS). There was higher head AIS in the cerebral hernia. ISS of shock patients was significantly higher than that of the others. Massive infections occurred in the patients with extremity trauma. There was a significant relation between the occurrence of MODS and infection. CONCLUSION: The occurrence of fatal complications is related to the location and severity of injury in traffic accident injury. A regularity is present in the occurrence of fatal complications with time progress.

Abbreviated Injury Scale↗
PubMed1998

[Effect of TNF-alpha monoclonal antibody on tissue lipopolysaccharide-binding protein mRNA expression in rats after thermal injury].

OBJECTIVE: To explore the effects of tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody (MAb) on tissue TNF-alpha and lipopolysaccharide-binding protein (LBP) mRNA expression, and multiple organ dysfunction in rats after thermal injury. METHOD: 24 male Wistar rats were subjected to a 35% total body surface area full-thickness thermal injury. RESULT: The tissue TNF-alpha and LBP mRNA expressions of liver, lung, intestine, and kidney were markedly increased (P < 0.05 approximately equal 0.01) after thermal injury. Treatment with TNF-alpha MAb could significantly lower TNF-alpha mRNA expression of lung, intestine and kidney, but had no effect on liver TNF-alpha mRNA expression (P > 0.05). Similarly, the tissue LBP mRNA expression also decreased significantly (36.0% - 72.9%), and returned to normal in lung, intestine and kidney. In addition, biochemical parameters including GPT, TBiL, BUN, CK-MB, and LDH were markedly elevated after thermal injury, and decreased significantly after treatment with TNF-alpha MAb. CONCLUSION: The increase of tissue TNF-alpha gene expression caused by thermal injury might be associated with a marked elevation of tissue LBP mRNA expression, which could contribute to the development of multiple organ dysfunction. The early use of TNF-alpha MAb seems to be effective in inhibiting significant LBP mRNA expression in various tissues and ameliorating multiple organ damage after major thermal injury.

Acute-Phase Proteins↗