Osteoarthritis is a chronic disabling disease that tends to occur in middle-aged and elderly population, the main pathological characteristics are the dynamic imbalance between the synthesis and degradation of articular chondrocytes, extracellular matrix and subchondral bone. The occurrence and development is related to many factors. This article reviews the structure, the function and the interaction between α2-macroglobulins and a disintegrin and metallo-proteinase with throm-bospondin motifs in the development of osteoarthritis.

The use of genetic approaches to probe relative genes that control sensitivity to volatile anesthetics in intact model has recently emerged as the powerful tools and strategies in dissecting mechanisms of anesthesia. Multiple model organisms such as yeast, nematodes, fruitflies and mammals are currently being exploited, and a number of sensitive genes have been screened, with some of them being cloned, located, and function identified. The emerging technologies are likely to provide further great advances for elucidating the specific anesthetic molecular sites.

G1.(3)Among 5 groups,the highest incidences of nausea,vomiting and pruritis were observed in group G1 for about 24% 32%,but with no statistical difference compared with other groups.Conclusion: With equal doses of bupivacaine and fentanyl mixed,the concentration/volume ratios may affect the analgesic effects of postoperative epidural analgesia in patients with hepatectomy.

500?mol/L) of propofol was needed; In biological system near the range of anaesthetic concentration, propofol effectively scavenged oxygen free radical produced by respiratory burst of PMN. Conclusion: Propofol scavenging hydroxyl radical generated in biological and nonbiological system,may be one of the main mechanisms of its antioxidation,the intralipid component of Diprivan may affect its antioxidation.

Objective To evaluate the role of extracellular signal-regulated kinase-cyclic AMP response element binding protein(ERK-CREB) signal pathway in glucocorticoid receptors-mediated chronic morphine tolerance in rats.Methods Male SD rats aged 2 months weighing 280-320 g were used in this study.A catheter was placed in subarachnoid space via foramen magnum according to Yaksh.Thirty-six rats in which intrathecal (IT) catheters were successfully implanted were randomly divided into 6 groups ( n =6 each):control group ( group C),chronic morphine tolerance group (group M),morphine + dexamethasone group (group MD),morphine + RU38486 group (group MR),dexamethasone group (group D),RU38486 group (group R).Normal saline 10 μl,morphine 10 μg,morphine 10 μg + dexamethasone 4 μg,morphine 10 μg + RU38486 2 μg,dexamethasone 4μg,RU38486 2 μg was administered IT twice a day(8:00 and 20:00)for 6 consecutive days in groups C,M,MD,MR,D,R respectively.Tail flick latency (TFL) was measured at 1 d before IT drug administration(baseline)and at 30 min after first IT drug administration during 1,3,5 d and at 1 d after last IT drug administration (T1～4).Maximum analgesic effect (MPE) was calculated.The animals were sacrificed after last TEL measurement.The L3～5 segment of the spinal cord was isolated for determination of the expression of phosphorylated ERK(pERK)and phosphorylated CREB(pCREB) by immunofluorescence staining.Results MPE was significantly T1 lower at T3,4 than at T1 in groups M and MD.Compared with group C,MPE was significantly increased,the expression of pERK and pCREB up-regulated in group M,but no significant change was found in the parameters mentioned above in groups R and D.Compared with group M,MPE was significantly increased,the expression of pERK and pCREB up-regulated in group MR,and MPE was significantly increased,the expression of pERK and pCREB down-regulated in group MD.Conclusion The mechanism by which glucocorticoid receptors-mediated chronic morphine tolerance may be associated with the inhibition of ERK-CREB pathway.

CT findings and complete clinical data of 185 cases with closed chest injuries were retrospectively analyzed.The diagnosis of 185 cases were pulmonary contusion ( n = 185 ),pulmonary laceration ( n = 35 ),Macklin effect ( n = 5 ) and lung herniation ( n = 1 ).CT findings of lung contusion appeared as thick and vagur lung marking (n =9),small points shadows (n = 12 ),blotchy shadows (n =48),small pieces shadows (n=10),ground-glass shadows (n=16),large pieces shadows (n =5),diffuse patchy clouding shadows (n = 17) or mixed lesions (n = 68).CT appearance of lung laceration included pulmonary hematomas (n = 12),cavitary lesions with air ( n = 19),cavitary lesions with air-fluid levels ( n = 53 ).Macklin effect appeared as bronchus-,pulmonary vessel-adjacent air collection and mediastinal air collection (n=5).Traumatic pulmonary hernia appeared as lung herniation through an intercostal space.Initial CT scan missed one case of pulmonary contusion and 2 cases of pulmonary laceration.

ObjectiveTo evaluate the role of the spinal cord proteasome in chronic morphine tolerance in rats.MethodsTwenty-four healthy male SD rats in which intrathecal catheters were successfully placed without complications were randomized into 4 groups ( n =6 each):normal saline group ( group NS),chronic morphine tolerance group (group M),chronic morphine tolerance + proteasome inhibitor MG-132 group (group M + MG) and MG-132 group (group MG).Normal saline 10 μl,morphine 10 μg,morphine 10 μg+ MG-132 2.5 μg and MG-132 2.5 μg were injected intrathecally twice a day for 7 consecutive days in groups NS,M,M + MG and MG respectively.Tail flick latency was measured on day 1 before intrathecal injection and on day 1,3,5 and 7 of intrathecal injection to calculate the percentage of maximum possible antinociceptive effect (MPAE).After the last intrathecal injection,5 rats were sacrificed,and L3-5 spinal cord was removed for determination of the expression of glutamate-aspartate transporter (GLAST) and excitatory amino acids carrier 1 (EAAC1)by Western blot.Results MPAE was gradually decreased during the intrathecal injection in groups M and M + MG( P ＜ 0.05).Compared with group NS,MPAE was gradually incresed during the intrathecal injection in groups M and M + MG,and the expression of GLAST and EAAC1 in the spinal cord was significantly down-regulated in group M (P ＜ 0.05).There was no significant difference in the parameters mentioned above between group MG and group NS ( P ＞0.05 ).Compared with group M,MPAE was significantly increased and the expression of GLAST and EAAC1 in the spinal cord was significantlyup-regulatedingroupM+MG(P＜0.05or0.01).ConclusionSpinal cord proteasome is involved in the development of chronic morphine tolerance in rats.

Osteoarthritis (OA) is a kind of chronic and frequently-occurring disease in the elderly.It is also called degenerative disease.Pain,stiffness,swelling,deformity and dysfunction of joints are the main clinical manifestations,which seriously affect the quality of life.Kaschin-Beck Disease (KBD) is a kind of endemic diseases;its main feature is cartilage degeneration and necrosis.Although KBD becomes a typical OA in late stage,it is different from OA.Osteoprotegerin (OPG) and insulin-like growth factor (IGF)-1 participate in the bone growth,repair,and alteration.In this paper,we summarized clinical manifestations and pathological changes of OA,and reviewed the current situation and development of OPG and IGF-1 in OA bone remodeling.

Objective:To investigate the influence of propofol on the binding function of GABA A receptor. Methods: By using radioligand receptor binding assay, effects of propofol on the specific binding of 3H GABA and saturation curves of GABA A receptor were observed in cortical membrane preparations from mouse cerebral cortex. Results: Specific binding experiments showed that propofol at the concentrations of 10 300 ?mol/L markedly enhanced the specific binding of 3H GABA( P 0.05). Conclusion: Clinical concentrations of propofol can enhance the binding function of GABA A receptor through increasing the affinity of the low affinity binding site of GABA.

Objective To investigate the role of spinal glucocorticoid receptors (GR) in phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signal pathway in rats with morphine tolerance.Methods Forty healthy male SD rats aged 8-10 weeks weighing 300-350 g in which intrathecal (IT) catheters were successfully implanted without complication were randomly divided into 4 groups (n =10 each):control group(group C) received IT injection of normal saline 10 μl twice a day for 7 consecutive days; morphine tolerance group(group M) received IT injection of morphine 10 μg twice a day for 7 consecutive days; dexamethasone (a GR agonist) group( group DEX)received IT injection of dexamethasone 4 μg 30 min before IT injection of morphine,twice a day for 7 consecutive days;RU38486(a GR blocker)group (group R) received IT injection of RU38486 2 μg 30 min before IT injection of morphine,twice a day for 7 consecutive days.Tail-flick test was measured once a day after first IT administration and 1 d after the end of IT administration,and the percentage of maximum possible antinociceptive effect (MPAE)was caculated.After the last measurem of tail-flick test,the spinal dorsal horns were removed for determination of PI3K,Caspase-3 expression and Akt activity.Results Morphine tolerance developed in groups M,DEX and R,but did not develop in group C.Compared with group C,Akt activity was decreased,PI3K expression was downregulated and Caspase-3 expression was up-regulated in group M (P ＜ 0.05).Compared with group M,MPAE and Akt activity were decreased,PI3K expression was down-regulated and Caspase-3 expression was up-regulated in group DEX,and MPAE and Akt activity were inecreased,PI3K expression was up-regulated and Caspase-3 expression was down-regulated in group R (P ＜ 0.05).Conclusion Spinal cord GR is involved in morphine tolerance by inhibiting PI3K/Akt signal pathway.