Objective To investigate the effect of cellular membrane phospholipids on CD14 protein expression of macrophage stimulated by LPS. Methods Changes of CD14 protein expression and CD14 mRNA of macrophages stimulated by LPS in vitro were determined by Western blotting and RT PCR. Effects of membrane phospholipids on CD14 protein expression were also detected. Results After stimulation by LPS, CD14 expression increased at 1 h, reached the peak value at 5 h and decreased to the normal level at 8 h but CD14 mRNA reached the peak value at 3 h and decreased at 5 h. The levels of phospholipids and membrane fluidity decreased at 5 h but CD14 protein expression increased after LPS stimulation. After pretreatment with liposomes, membrane phospholipid microenvironment improved and CD14 protein expression decreased. Conclusion LPS can up regulate CD14 protein expression, which might be regulated at least at the transcriptional level of the CD14 gene. Changes of membrane phospholipid microenvironment may be an important reason for the up regulation of CD14 induced by LPS.

Objective To investigate the changes of NGF mRNA expression and the effect of exogenous interleukin 1?(IL 1?) on it in rats after traumatic brain injury(TBI) and to explore the mechanism of NGF and IL 1? in TBI. Methods A brain trauma model of fluid percussion in rats was established. Changes of NGF mRNA expression and effect of exogenous IL 1? on it were observed by RT PCR, molecular hybridization and immunocytochemical techniques. Results NGF mRNA expression in the brain injury site and tissues adjacent to it began to increase at 12 h after trauma and increased markedly at 24 h and reached the peak value on the 3rd. Then it decreased gradually, but still higher than that of the control. NGF mRNA expression increased at 3 h after trauma in IL 1? treatment group and was significantly higher than that in simple trauma and control groups( P

OBJECTIVETo study the mechanism of macrophage injury after trauma-hemorrhagic shock.

METHODSWistar male rats underwent trauma (closed bone fracture) and hemorrhage (mean arterial blood pressure of 35 mm Hg+/-5 mm Hg for 60 minutes, following fluid resuscitation). Rats without trauma, hemorrhage or fluid resuscitation served as controls. Peritoneal macrophages were harvested at 6 hours and 1, 2, 3, 7 days after traumatic hemorrhagic shock to determine the effects of pertussis toxin (PTX, as a specific inhibitor to Gi(alpha) and cholera toxin (CTX, as a stimulant to Gs(alpha) on macrophage-Ia expression and TNF-alpha production and levels of Gi(alpha) and Gs(alpha).

RESULTSThe macrophages from the injured rats revealed a significant decrease of Ia positive number and TNF-alpha release in response to LPS. Wi th pretreatment with PTX 10-100 ng/ml Ia positive cells and LPS-induced TNFalpha production in both control and impaired macrophages populations were dos e dependently increased. Both macrophages populations were not responding to CTX treatment (10-100 ng/ml). Western blot analyses showed that the levels of Gi(alpha) protein expression increased as much as 116.5%-148.8% of the control level fro m 6 hours through 7 days after traumatic hemorrhage. The levels of Gs protein expression were reduced at 6 hours and decreased to the lowest degree; 36% o f the control at day 1, began to return at day 2 and returned to the normal level at day 7, following traumatic hemorrhagic shock.

CONCLUSIONSPTX-sensitive G-protein may participate in th e modulation of macrophage-Ia expression and TNF-alpha release following traumatic hemorrhagic shock. Analyses of the alteration of Gi(alpha) and Gs protein express ions further supports the concept that G-protein is involved in trauma-induced macrophage signal transduction pathways.

Analysis of Variance ; Animals ; GTP-Binding Proteins ; immunology ; metabolism ; Histocompatibility Antigens Class II ; immunology ; Immunoblotting ; Lipopolysaccharides ; pharmacology ; Macrophages, Peritoneal ; immunology ; metabolism ; Male ; Rats ; Rats, Wistar ; Shock, Hemorrhagic ; blood ; immunology ; Signal Transduction ; Tumor Necrosis Factor-alpha ; biosynthesis

OBJECTIVE: To observe effect of endothelin-1 (ET-1) on hepatic damage induced by endotoxin. METHODS: A total of 90 rats were randomly divided into control group (group C), endotoxin treated group (group LPS) and endotoxin plus ET-1 antibody treated group (group LEA). An observation was done on the changes of ET-1 concentration, and transcription and expression of ET-1 mRNA. Plasma glutamic pyruvic-transaminase enzyme (GPT), hepatic lactate dehydrogenase (LDH), adenosine triphosphate (ATP) and malondialdehyde (MDA) were also observed at 3, 6, 9, 12, 24 hours after saline, endotoxin (10 mg/kg) and ET-1 antibody (dalubine 1:2000, 2 ml/kg) administration. RESULTS: The results indicated that the concentration of plasma and hepatic ET-1 and expression of ET-1 mRNA in liver significantly increased following endotoxemia. The hepatic ET-1 levels were inversely correlated with the ATP concentration, and positively related to the MDA concentration. ET-1 antibody could partially protect the liver against damage induced by endotoxin. CONCLUSIONS: These results suggest that endotoxin may, on transcription and translation level, lead to an increase of ET-1 in synthesis. ET-1 may contribute to hepatic damage during endotoxemia.

Blood transfusion is still an imperative and effective therapeutic remedy for many diseases, especially for trauma and shock. But the donation of blood by healthy citizens is seriously inadequate, and, more recently, blood transfusion is a matter of great concern because of viral infections such as hepatitis and HIV. In addition, blood transfusion has some other limitations including difficulty of storage and transportation, and needing cross-matching because of blood group antigens. Thus, the development of an oxygen carrier, which could serve as a safe and effective alternative to human blood or red blood cell (RBC), has gained great interest worldwidely.

OBJECTIVE: To elucidate which one of &mgr;, delta and kappa opioid receptors is involved in the cardiovascular depression following traumatic hemorrhagic shock. METHODS: With traumatic hemorrhagic shock rat models, the changes of myocardial and brain &mgr;, delta and kappa opioid receptors and cardiovascular functions and their relationship with hemodynamic parameters were observed. The effects of delta and kappa opioid receptor antagonists on hemodynamic parameters of traumatic hemorrhagic shock rats were observed. RESULTS: Following traumatic hemorrhagic shock, the number of myocardial and brain delta and kappa opioid receptors significantly increased, their affinity did not alter, and the increased number of delta and kappa opioid receptors was significantly associated with the decreased hemodynamic parameters. However, &mgr; opioid receptor in heart and brain did not obviously change. delta opioid receptor antagonist ICI174,864 and kappa opioid receptor antagonist Nor-binaltorphimine (50 &mgr;g, Icv) could significantly reverse those decreased hemodynamic parameters. CONCLUSIONS: It suggests that opioid receptors, especially delta and kappa opioid receptors are closely related to the pathogenesis of traumatic hemorrhagic shock, and they play important roles in the depression of cardiovascular function following traumatic hemorrhagic shock.

Objective To systemically investigate 1) distribution of endogenous endotoxin (ET) in tissues and circulation; 2) its relationship with shock duration and organ damage; and 3) its possible mechanism after hemorrhagic shock.Methods To further elucidate the intrinsic relationship between endogenous endotoxin translocation and hemorrhagic shock, the present study systematically investigated the distribution of endogenous ET into the liver, lungs, kidneys and circulation, and the relationship between ET levels and the corresponding organ dysfunction with limulus amebocyte lysate (LAL) chromogenic assay following hemorrhagic shock in rats. Results It was found that ET levels in hepatic homogenate markedly increased (P=0.09) 1.5 hours following shock compared with that in the sham group. After resuscitation, ET levels in hepatic, pulmonary and renal tissues were all significantly elevated. The levels kept increasing with the prolonged experimental time, and reached as high as 3.88±0.95 EU (endotoxin unit)/g in the livers, 2.53±1.46 EU/g in the lungs and 2.51±0.89 EU/g in the kidneys 12 hours after shock. ET levels in plasma reached a peak of 1.13±0.42 EU/ml at 1 hour following resuscitation, then rapidly decreased to the sham levels 3 hours following resuscitation. There was a close relationship between endotoxin translocation and shock duration. Correlation analysis further indicated that the changes in glutamic-pyruvic transaminase (GPT), blood urea nitrogen (BUN) in plasma and angiotensin Ⅰ-converting exzyme (ACE) in pulmonary homogenate were significantly and positively correlated with the ET levels in the liver, kidneys and lungs after hemorrhagic shock. Conclusions Hemorrhagic shock can induce obvious endogenous ET translocation, which is closely related to the shock duration. Although only transient endotoxemia occurs after hemorrhagic shock, ET can massively accumulate in tissues (liver, lungs and kidneys), and may play an important role in the development of shock.

The cableway for the evacuation of the wounded is simple in structure,light in weight,and quite easy to be assembled and disass- embled.It is a perfect way not only for the evacuation of the wounded in the junglle and hilly zones but also for transport of light weaponry and means of livelihood?The cable way,particularly,can function distinctively wherever stretchers and modern conveyances are quite Iimited especially in the mountains,valleies or rivers.In addition,it is also a safe and rapid way to evacuate iarge puantities of the wounded group by group,Therefore it can enhance the efficiency ten times to thirty times.

Objective:To study the specific photochemical effects of a newly designed target photosensitizer. Methods Based on the technique of antisense nucleic acid and the principle of photochemical reaction effects,a specific sensitizer,TFO P has been designed and synthesized.When in coordination with long wave ultraviolet ray(UVA) ,this decorated complex (TFO P) was added into the blood cell suspension to inactivate the contaminating virus( duck hepatitis virus B,DHBV).The efficacy of specific binding to DHBV DNA and viral inactivation by TFO P was detected by gel shift blot assay and infection of primary culture of duck hepatocyte.Results The designed TFO P could specifically bind to different DHBV DNA line sample and present different linking level.With a TFO P concentration of 0.1 nmol/ml and UVA intensity of 1800 ?W/cm 2,the DHBV in blood cell suspension could be reduced by 1.90～5.40 logs.Conclcusion The photochemical effects of TFO P could significant inactivate DHBV in blood.

Thyrotropin releasing hormone (TRH) and naloxone were compared in their antagonism to the effects of analgesia,addicton-induction,movement restatraining,respiration depression,LD50:etc of morphine.It was found that TRH was entirely different from naloxone in that it was not antagonistic at all to the morphine effects mentioned above.So TRH would be a better choice than naloxone in the treatment of traumatic shock.