Animals ; Aorta ; metabolism ; Hyperlipidemias ; metabolism ; Mice ; Mice, Inbred C57BL ; Nitric Oxide Synthase ; metabolism ; Physical Conditioning, Animal ; Physical Endurance

Objective To compare the efficacy of rcmifentanil combined anesthesia and fentanyl or sufentanil combined anesthesia in patients undergoing cardiac surgery.Methods We searched the Coehrane library,PubMed,EMBASE,OVID and Chinese Biomedical Database for prospective randomized controlled trials involving the comparison of the efficacy of remifentanil combined anesthesia and fentanyl or sufentanil combined anesthesia in patients undergoing cardiac surgery.The quality of the studies was evaluated by the method recommended by Cochrane Collaboration.Evaluation indexes included the mechanical ventilation time after operation,duration of stay in hospital,and level of cardiac troponin,mortality,requirement for positive inotropic drugs and incidence of hyperalgesia and myocardial infarction during perioperative period.Meta-analysis was conducted using the RevMan 5.0 software.Results Sixteen prospective randomized controlled trials involving 1473 patients were included in our Meta-analysis.The patients were divided into 2 groups:fentanyl or sufentanil group ( n =644) and remifentanil group ( n =573).Compared with fentanyl or sufentanil group,the mechanical ventilation time after operation and duration of stay in hospital were significantly shortened,the level of cardiac troponin during the perioperative period was significantly decreased and the requirement for positive inotropic drugs during the perioperative period was significantly reduced ( P ＜ 0.05),and no significant change was found in the incidence of hyperalgesia or mortality of myocardial infarction during the perioperative period in remifentanil group ( P ＞ 0.05 ).Conclusion The efficacy of remifentanil combined anesthesia is better than that of fentanyl or sufentanil combined anesthesia in patients undergoing cardiac surgery.

Objective To observe the influence of ATP protection after brachial plexus injuries. Methods A total of 80 female Wistar rats,weighting 280～300 g,were randomly divided into ATP and con- trol groups.The right C_5～T_1 nerve roots were transected and then the intraperitoneal injection of 4m[ of ATP or normal saline was given immediately and once daily to the rats,respectively.The rats were sacrificed on postoperative days 14,28 and 42 respectively.The C_5-T_1 segments of the spinal cord were harvested.NT-3 activity was measured by enzymo-histochemistry method.Four weeks and 6 weeks postoperatively,ultrastruc- ture of the denervated skeletal muscles was observed.Results Compared to the control group,the expres- sions of NT-3 was increased in the treated groups with ATP injection (P

Objective To evaluate the role of activator protein-1 (AP-1) in the up-regulation of heme oxygenase-1 (HO-1) expression during lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 200-220 g,aged 2.5-3.0 months,were randomly divided into 4 groups (n=12 each): normal control group (group C),ALI group,curcumin + ALI group (group Cur+ ALI),and curcumin group (group Cur).In groups C and ALI,normal saline 0.5 ml and LPS 10 mg/kg (0.5 ml) were injected intravenously,respectively,30 min after 0.1％ dimethyl sulfoxide (the vehicle for curcumin) 0.5 ml was injected intraperitoneally.In groups Cur+ ALl and Cur,curcumin 20 mg/kg (0.5 ml) was injected intraperitoneally,and 30 min later LPS 10 mg/kg and normal saline 0.5 ml were injected,respectively.The rats were then sacrificed at 6 h after injection of LPS.The lungs were removed for microscopic examination.The pathological changes of the lung were scored.The malondialdehyde (MDA) content,superoxide dismutase (SOD)activity and expression of HO-1,AP-1 and HO-1 mRNA in lung tissues were determined.Results Compared with group C,the pathological score and MDA content were significantly increased,the SOD activity was significantly decreased,and the expression of HO-1,AP-1 and HO-1 mRNA was up-regulated in groups ALl and Cur +AL(l) (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group Cur (P ＞ 0.05).The pathological score and MDA content were significantly higher,and the SOD activity and expression of HO-1,AP-1 and HO-1 mRNA were significantly lower in group Cur + ALl than in group ALI(P ＜ 0.05).Conclusion Transcription factor AP-1 activation is involved in the up-regulation of HO-1 expression during LPS-induced ALI in rats.

Objective To evaluate the effect of electro-acupuncture (EA) at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits.Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups (n =10 each):group sham operation (group S); group zinc protoporphyrin-Ⅸ (ZnPP-Ⅸ) (group Z); group lipopolysaccharide (LPS) (group L); group LPS + EA (group EL) ; group LPS + sham EA (group SEL) and group LPS + EA + ZnPP-Ⅸ (group ELZ).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 400 mg/kg and tracheostomized.The animals kept spontaneous breathing.Right internal carotid artery was cannulated for BP monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg was injected iv in groups L,EL,SEL,ELZ.Endotoxin shock was confirmed by decrease in BP by 20 ％ of the baseline value and PaO2/FiO2 ≤ 300.ZnPP-Ⅸ (heme oxygenase (HO-1 ) inhibitor)10μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ.Bilateral 15 min EA stimulation of Zusanli and Feishu ( according to atlas of animal acu-points) was performed once a day for 5 days before LPS administration in groups EL and ELZ.The animals were sacrificed by blood-letting at 6 h after LPS administration.The lungs were removed for microscopic examination (0 =no injury,4 =most severe injury),detection of alveolar epithelial cell apoptosis (by TUNEL) and determination of HO-1 protein and mRNA expression.Results LPS significantly increased lung injury scores,alveolar epithelial cell apoptosis index (the number of apoptotic cells/total cells) and HO-1 protein and mRNA expression.EA significantly attenuated lung injury and alveolar epithelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L.The protective effects of EA was counteracted by ZnPP- Ⅸ in group ELZ.Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.

Objective To investigate the effects of CORM-2 via p38 mitogeu-activated protein kinase (p38MAPK) signaling pathway on the expression of the mitochondrial fission protein 1 (Fisl) in lipopolysaccharide (LPS)-induced mouse pulmonary macrophages.Methods The rat subculture alveolar macrophages were seeded on 96 well plates with 2 × 105/ml densities.After 24 hours of culture,it was divided into 4 groups by random number table method:normal control group (group C),group LPS (group L),CO releasing agent CORM-2 + LPS group (group LC),p38MAPK inhibitor SB203580 + CORM-2 + LPS group (group LCS).When the cells were incubated for 24 hours,the mitochondrial MDA content and SOD activity were determined by ELISA kit,the levels of HO-1、mitochondrial fission protein Fis1 and p38 were determined by Western blot,the expressions of HO-1 and mitochondrial fission protein Fis1 were detected by RT-PCR.Results Compared with the C group,the levels of MDA [(2.43 ±0.12) vs.(3.59 ±0.07)],HO-1 [(1.31±0.27) vs.(1.65±0.41)],Fis1 [(1.27±0.23) vs.(1.65±0.41)] andp38 [(1.01 ±0.24) vs.(1.36 ±0.17)] in group L were increased,and the activity of SOD [(81.7 ± 1.62) vs.(54.7 ± 1.62)] was decreased (P ＜ 0.05);Compared with the group L,the MDA content [(3.59 ± 0.07) vs.(3.08 ±0.52)] and the level of Fis1 [(2.01 ±0.35) vs.(1.48 ±0.39)] in group LC were down-regulated,and the levels of SOD [(54.7 ± 1.62) vs.(67.4 ± 1.32)]、and the expressions of HO-1 [(1.65±0.41)vs.(2.25±0.18)] andp38 [(1.36±0.17) vs.(1.78±0.23)] wereup-regulated (P ＜0.05).Compared with the group LC,the MDA content [(3.08 ±0.52) vs.(4.16 ±0.19)] and the expression of Fis1 [(1.48 ±0.39) vs.(1.96 ±0.31)] in group LCS were increased,and the level of SOD [(67.4±1.32)vs.(45.9±1.52)]、and the expressions of HO-1 [(2.25±0.18)vs.(1.78± 0.19)] and p38 [(1.78 ±0.23) vs.(1.12 ±0.29)] were decreased (P ＜0.05).Conclusions HO-1/CO system inhibits the expression of Fis1 in LPS-induced lung macrophages,which may be regulated by p38MAPK signaling pathway.

Objective To investigate the awaken effect of naloxon on dexmedetomidine anesthetized mice and its mechanism. Methods Thirty Kunming mice of clean grade were randomly divided into 3 groups which included NAL group (Naloxon group), ATI group(Atipamezole group)and NS group (Normal Saline group). All groups were given dexme?detomidine 1 mg·kg-1 intraperitoneally. Naloxon 2 mg·kg-1, atipamezole 2 mg·kg-1 and normal saline 10 mL·kg-1 were ran?domly given intraperitoneally to the NAL, ATI and NS group respectively 90 minutes after dexmedetomidine administration. At timepoints prior to dexmedetomidine administration and 5, 15, 30, 60, 90, 95, 105, 120, 180 minutes after it, the sedative and analgesic effects besides recovery time (based on restore of righting reflex loss) were assessed. Results Sedation and analgesia effects became apparent within 5 minutes, and peaked at approximately 60 minutes then spontaneously recovered at 180 minutes after injection of dexmedetomidine. The sedative and analgesic effects were reduced in both ATI and NAL groups. Compared with ATI group, the sedation scores were higher at 95, 105 and 120 minutes after dexmedetomidine admin?istration than those in NAL group (P<0.05) but the scores were not statistically significant at 180 minutes between these two groups. Compared with NS group, the sedation scores were lower at time points of 95, 105, 120 and 180 minutes than those in NAL group (P>0.05). The analgesic scores were not statistically significant at time points of 95, 105, 120 and 180 min?utes between NAL group and ATI group, but they were lower in NAL group compared with NS group at timepoints of 95, 105 and 120 minutes (P>0.05). The recovery time in ATI and NAL group were shorter than that in NS group (F=1 793.368, P<0.05), but it showed no statistical difference between ATI group and NAL group (P>0.05). Conclusion Naloxone had a certain awaken effect on dexmedetomidine anesthetized mice.

According to the World Health Organization (WHO), the basic sciences to support the human health are chemistry, physics and informatics. Chemistry is the base of pharmacy. Physics is the base of medical instruments and equipments (MIE). The diagnosis and therapy of diseases are relying on informatics. Therefore, as the fusion results of physics and medicine, medical physics is the creative source science of MIE. Among all diagnosis tools, medical imaging devices are the fastest-developed and the most-complicated MIE since Roentgen discovered X-ray which was quickly used in medical diagnosis in 1895. Among all treatment tools, the radiotherapeutical devices are the most-widely used and the most effective MIE for tumor treatments since Mrs. Courier found the nature radiation isotope Radium at the end of 19th century and began to use it in tumor therapy. Although the research and development (R&D) of so-complicated MIE need many subjects of science and engineering, the kernel science is medical physics. With the results of more than 50 years' development in developed countries, medical physics has defined its own field, which is the medical imaging physics and the radiotherapeutical physics. But, the definition has been expanded to be wider and wider. Therefore, we should pay more attention to the establishment of Medical Physics in China. In order to develop medical physics in china, the bases of R&D and clinical practice should be also built.
China ; Diagnostic Imaging ; Equipment and Supplies ; Health Physics ; Neoplasms ; diagnosis ; therapy ; Physics ; instrumentation

Objective To evaluate the role of mitochondrial fusion?fission in endotoxin?induced a?cute lung injury in rats. Methods Twenty healthy male Sprague?Dawley rats, weighing 160-180 g, were e?qually and randomly divided into either control group ( group C ) or endotoxin?induced acute lung injury group (group L) using a random number table. Lipopolysaccharide 5 mg∕kg was injected intravenously in group L, while the equal volume of normal saline 0?5 ml was given instead in group C. The animals were sacrificed at 6 h after administration of lipopolysaccharide or normal saline. The lungs were immediately re?moved for measurement of wet to dry lung weight ratio ( W∕D ratio) , superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content. The mitochondrial fusion proteins mitofusin 1 ( Mfn1) , Mfn2 and op?tic atrophy 1 ( OPA1) mRNA and protein expression was detected, and mitochondrial fission proteins dy?namin?related protein 1 (Drp1) and fission 1 (Fis1) mRNA and protein expression was also detected in lung tissues. Results Compared to group C, the W∕D ratio and MDA contents in lung tissues were signifi?cantly increased, SOD activity was decreased, Mfn1, Mfn2 and OPA1 mRNA and protein expression in lung tissues was down?regulated, and Drp1 and Fis1 mRNA and protein expression was up?regulated in group L. The pathological damage to lung tissues was obviously aggravated in group L when compared to group C. Conclusion The mechanism underlying endotoxin?induced acute lung injury is related to enhanced oxidative stress responses caused by decreased mitochondrial fusion and increased mitochondrial fission in rats.

Objective To investigate the effect of Panax notoginsenosides monomers ginsenoside Rg 1 in inhibiting hepatic fibro-sis .Methods The rat model of hepatic fibrosis was established by using 50% Ccl4 ,total 35 d .The different doses of Rg1was ad-ministered by hypodermical injection .At the end of the treatment ,the pathological changes of hepatic tissue were observed by light and transmission electron microscope .The stereological method was adopted to measure the volume density (Vvm) ,area density (Svm) ,specific surface(Qm) and surface number density (Nam) of liver cell mitochondria in various groups .Results The stereo-logical data of liver cell mitochondria showed that the statistical differences existed among various groups .Vvm in the Panax Notog-insenosides ,low dose Rg1 and isotonic saline groups were significantly increased compared with the normal control group with sta-tistical difference(P<0 .01);Vvm in the high dose Rg1 ,middle dose Rg1 and colchicine groups showed the increasing trend com-pared with the normal control group without statistical difference (P>0 .05);Vvm in the high ,middle and low dose Rg1 ,Panax No-toginsenosides and colchicine groups showed the decreasing trend compared with the isotonic saline group without statistical differ-ence(P>0 .05) .Svm in the low dose Rg1 ,Panax Notoginsenosides ,colchicine and isotonic saline groups were significantly increased compared with the normal group with statistical difference (P<0 .01);Svm in the high dose Rg1 ,middle dose Rg1 ,Panax Notogin-senosides and colchicine groups was significantly induced compared with the isotonic saline group with statistical difference (P<0 .01);Svm in the high dose Rg1 was reduced compared with the middle dose Rg1 group(P<0 .05) .Nam in the low dose Rg1 ,col-chicine and isotonic saline group was significantly increased compared with the normal group (P<0 .01);Nam in the high dose Rg1 , middle dose Rg1 and Panax Notoginsenosides groups were significantly reduced compared with the isotonic saline group with statis-tical difference(P<0 .01);Nam in the high dose Rg1 group was reduced compared with the middle dose Rg 1 group with statistical difference (P<0 .05) .Qm in all groups was reduced compared with normal group without statistical difference (P>0 .05) .Conclu-sion Rg1 has antifibrosis effects of Panax notoginsenosides ,even exceeds Panax notoginsenosides in some aspects ,and the above-mentioned effect is positively correlated with dose .Rg1 is an ideal drug for preventing and treating liver fibrosis .