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.

A model of traum a shook was established in rats by comminutedly fracturing of the right femur and bleeding of 15% of the body weight.In the 1st hour after injury,the content of malondialdehyde (MDA) of the heart and the lungs increased,the activity of sv.peroxide dismutase (SOD) in the lungs decreased,and the MDA content and SOD activity in hepatic mitochondria increased synchronously.In the 3rd hour after injury,the MDA content increased not only in the heart,the lungs and hepatic mitochondria but also in the liver and the kidneys,and the SOD activity increased in the heart,the kidneys and the intestinal tract but decreased in hepatic mitochondria.There were further marked elevation of MDA content and progressive inhibition on SOD activity in the 5 vital organs and hepatic mitochondria in the 5th hour after injury.When shock continued to progress,the plasma MDA content increased gradually,the SOD activity of the hemolytic blood decreased,and the activities of plasma acid phosphatase and ?-glucuronidase,the indicators of lysosome destruction,increased markedly.These findings suggest that the oxygen-derived free radicals are responsible for the damages to cells of the vital organs and subcellular organelles during traumatic shock.

The effects of oxygen-derived free radicals on the lipid peroxidation injury of the hepatic subcellular organelles were observed in rats after they were inflicted with endotoxic or hemorrhagic shock.It was found that in the early stage of shock,the content of malondialdehyde(MDA)of hepatic mitochondria and lysosome suspension were significantly increased(P

It was found that after 2 dosages of Pseudomonas aeruginosa suspension(7?109/kg and 2?1010/kg)were infused to rabbits respectively to induce septicemia,the elevation of the tumor necrosis factor(TNF)level in the circulating blood was higher in 2?1010/kg group than in 7?109/kg group.The dynamic changes of circulation TNF in P.aeruginosa septicemia were different from those in endotoxin shock.There was a continous increase of plasma glucagon,Iactic acid and ?-G(P

After intravenous infusion of recombinant human tumor necrosis factor(TNF)in the dosage of 60?g/kg or 130?g/kg to rabbits,it was found that their plasma malondialde-hyde(MDA)was significantly increased(P

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.

No. Ⅱ fluorocarbon blood substitute in divided doses was infused into the rats in a 12-day-period. Pathomorphological changes of the various organs of the animals were observed dynamically in the first year after the completion of the infusion. Fluorocarbon particles mainly accumulated in the organs with abundant reticulo-endothelial tissue particularly the liver and spleen. The changes of the weight of the liver and spleen and the existence of foam cells could be considered as the criteria to indicate the severity of the accumulation. It was found that at the end of the first year after the completion of No. Ⅱ fluorocarbon blood substhue infusion, the liver and spleen essentially resumed their normal weight but a small number of foam cells still existed, However, accumulated fluorocarbon particles exerted no harmful effects on the functions and structures of the organs observed.

The effects of endlbtoxin on lipid peroxidation injury of rat hepa-tocytes and the protective effects of exogenous superoxide dismutase (SOD) were studied in vitro.It was found that after the isolated rat hepatocytes and endotoxin (500 ng/ml) were incubated together for 6 hours,there was an obvious increase of malondialdlehyde (MDA) level and lactic dehydrogenase (LDH) and SOD activities,and the increase of LDH and SOD activities occurred earlier than that of MDA level.Polymorphonuclear neutrophils (PMN) after activated by endotoxin could destroy the hepatocytes and increase MDA level and LDH and SOD activities which could partially be inhibited with the pretreatment of exogenous SOD.These findings suggest that endotoxin can intensify the injurious effects of PMN on hepatocytes and it can also directly induce lipid peroxdatipn injury on hepatocyes but the mechanism was not clear.

Changes of hepatic mitochondrial respiratory function and the protective effects of several free radical scavenging enzymes or drugs on the mitochondrial functions were observed after superior mesenteric artery occlusion shock was inflicted to the rat.It was found that there was an obvious decrease of respiratory control rate (RCR) in the 1st hour after the occlusion was released and a further decrease in the 2nd hour,and P/O value decreased significantly at the same time,which indicates that mitochondrial dysfunction does occur.in the shock due to superior mesenteric artery occlusion.However,RCR ard P/O value did rot significantly decrease in the 1 st hour after occlusion releasing in the treated groups with allopurinol (ALLO),a combination of catalase (CAT) and superoxide dismutase (SOD),a combination of SOD and ALLO,and a combination of SOD,ALLO,and CAT as compared with those of the control,and were markedly higher as compared with those of the experimental group.In the 2nd hour after occlusion releasing,RCR of the ALLO treated group was significantly lower than that of the control and remained significantly higher than that of the experimental group.The average survival time of the animals was much longer in the treated groups than in the experimental group.Our findings demonstrate that free radical scavengers,SOD,CAT,and ALLO especially a combinaton of them can exert protective effects of different degrees on the mitochondrial respiratory function during a shock due to superior mesenteric artery occlusion.