Adult ; Aged ; Biomarkers ; metabolism ; Case-Control Studies ; Hepatitis B, Chronic ; drug therapy ; Humans ; Middle Aged ; Treatment Outcome ; Vitamin D-Binding Protein ; metabolism ; Young Adult

Objective To investigate the role of extracellular signal-regulated kinase(ERK)signal pathway in the spinal cord in the development of chronic morphine tolerance.Methods Thirty healthy male SD rats weighing 300-350 g in which intrathecal(IT)catheters were successfully implanted without complication were randomly divided into 3 groups(n = 10 each): group Ⅰ control(group C);group Ⅱ morphine tolerance(group M)and group Ⅲ morphine tolerance + PD98059(ERK upstream kinase MEK inhibitor)(group P).Morphine tolerance was induced with IT morphine 10 μg twice a day for 7 consecutive days.In group P PD98059 10 μg was injected IT at 30 min before each morphine administration.Tail flick latency(TFL)(the time between the onset of heat stimulus and voluntary tail withdrawal)was measured once a day at 30 min after first IT morphine administration and at 1 day after last IT morphine.Maximum analgesic effect(MPE)was calculated.MPE =(TFL after IT morphine - baseline TFL)/(12 - baseline TFL)× 100%.The animals were sacrificed after last TFL measurement.The L3-5 segment of the spinal cord was isolated for determination of the expression of μ-receptor and phosphorylated ERK 1/2(p-ERK1/2)by Western blot analysis and fluoroimmunoassay.Results Morphine tolerance was induced in group M and M + P.MPE was higher in group P than in group M.The expression of μ-receptor in spinal dorsal horn was significantly lower while the p-ERK1/2 expression was higher in group M than in group C.IT PD98059 significantly up-regulated μ-receptor expression and down-regulated p-ERK expression in group P as compared with group M.Conclusion ERK signal pathway is involved in the development of chronic morphine tolerance in rats.

Objective To investigate the changes in the expression of glutamate-aspartste transporter in spinal dorsal horn in rats with inflammatory pain and chronic morphine tolerance. Methods Thirty healthy male SD rats in which intrathecal (IT) catheters were successfully placed without complications were randomized into 3 groups ( n = 10 each): normal saline group ( group NS), arthritis group ( group A), and arthritis + morphine group (group AM). NS 50 μl was injected into the ankle joint of the left hindlimb in group NS, while complete Freund's adjuvant was injected in the other two groups instead. After 3 days, group NS and A received IT NS 10 μl twice a day for 7 consecutive days, group AM IT morphine 10 μg (10 μl) twice a day for 7 consecutive days. Mechanical pain threshold (MPT) was measured before IT administration and at day 2, 4, 6 and 8 after IT administration (T0-4). The animals were sacrificed after the last MPT measurement. The spinal cords were isolated for determination of GLAST expression in spinal dorsal horn. Results Compared with group NS, MPT was significantly decreased in the other groups and GLAST expression was down-regulated in group AM (P ＜ 0.05). Compared with group A, no significant change was found in MPT at T3,4 (P ＞ 0.05), while GLAST expression was down-regulated in group AM ( P ＜ 0.05). Conclusion The development of chronic morphine tolerance is related to the decrease in the function of GLAST in spinal dorsal horn in rats with inflammatory pain.

ObjectiveTo explore the effective way of first aid skill standard training in regional central hospital.Methods60 residents from different regional central hospitals were received aid skills training based on two ways:namely OSCE ( multi-station structured skills test ) which lay particular em phasis on skills and traditional face to face way; and were assessed by uniform standards.ResultsThe scores of residents who received OSCE training were significantly better than those which received traditional face to face training ( P＜0.05 ),including.ECG,cardiopulmonary resuscitation,endotracheal intubation and doctor examination.ConclusionFirst aid skills standard training used by OSCE approach in regional central hospital can improve their first aid skills and should be promoted.

Objective To investigate the role of glucocorticoid receptor (GR) in the induction of neuronal apoptosis in spinal dorsal horn in chronic morphine tolerant rats. Methods Twenty healthy male SD rats weighing 300-350 g in which intrathecal (IT) catheter was successfully implanted without complication were randomized into 4 groups ( n = 5 each): group Ⅰ control ( group C);group Ⅱ morphine ( group M );group Ⅲ morphine +RU38486 (GR antagonist) (group MR) and group Ⅳ morphine + dexamethasone (GR agonist) (group MD).Normal saline 10 μl, morphine 10 μg, morphine 10 μg + RU38486 2 μg and morphine 10μg + dexamethasone 4 μg were injected IT twice a day at 8:00 and 20:00 for6 consecutive days in group C, M, MR and MD respectively. Tail flick latency (TFL) to a thermal nociceptive stimulus was measured every day at 30 min after IT administration in the morning (8:00). Hyperalgesia was considered to be a sign of morphine tolerance. The animals were killed at 7 days after IT drug administration. The L3-5 segment of the spinal cord was isolated for determination of neuronal apoptosis in spinal dorsal horn by TUNEL staining. Apoptotic index was calculated ( the number of apoptotic neurons/the total number of neurons × 100% ). Results TFL was significantly prolonged at day 1 and 3 of IT morphine 10 μg twice a day and returned to baseline at day 5 and 7 indicating morphine tolerance. RU38486 inhibited while dexamethasone enhanced morphine tolerance. IT morphine significantly increased the number of apoptotic neurons in spinal dorsal horn. Morphine-induced neuronal apoptosis was decreased by IT RU38486 and increased by IT dexamethasone. Conclusion Glucocorticoid receptors may be involved in morphine tolerance by inducing neuronal apoptosis in spinal dorsal horn.

Objective To investigate the quality assurance(QA) and quality control(QC)of 16 slices helical CT angiography in the lower limb. Methods 42 cases clinically suspected as the arterial disease of lower limb undergoing MSCTA were analyzed retrospectively. All reconstructed images were reformed by means of MIP, VR, MPR and CTVE. Results 22 patients were diagnosed correctly by using MSCTA. Compared to DSA and/or surgical results. Sensitivity, specificity and accurate rate were all 100%. Conclusion It is important to strengthen the QA and QC of the 16 slices helical CT angiography in the lower limb.

Objective To observe the curative effect of simvastatin to treat carotid atheroma. Methods 106 patients with carotid atheroma were randomly divided into two groups. The treatment group( n=56) was given orally 20 micro-gram of simvastatin every night, while the matched control group( n = 50) was given 100 microgram of aspirin enteric-coated everyday for 4 months. Results After four months of follow-up, the carotid artery inner-intermediate thickness and the speckle's size,examined by the color Doppler, were obviously decreased ( P 0.05). Conclusion Simvastatin can obviously ameliorate the carotid atheroma. It can be served as one of the normal selections for treating the carotid atheroma.

Objective To evaluate the effect of compound K ( CK) on spinal Toll?like receptor 4 ( TLR4) expression during morphine?induced hyperalgesia in rats. Methods Thirty?six healthy male Spra?gue?Dawley rats in which intrathecal catheters were successfully implanted were randomly divided into 3 groups ( n=12 each) using a random number table: control group ( group C) , morphine?induced hyperal?gesia group ( group M) , and morphine + CK group ( group M+CK) . Starting from 5 days after successful implantation, normal saline 10 μl, morphine 10 μg, and morphine 10 μg + CK 10 μg were injected in?trathecally twice a day for 7 consecutive days. Tail?flick latency ( TFL) to a thermal nociceptive stimulus was measured at 1 day before administration ( T0 , baseline) and at 30 min after the initial administration on 1st, 3rd, 5th and 7th days (T1?4), and the percentage of maximum possible effect (MPE) was calculated. The rats were sacrificed after the last measurement of tail?flick latency, and the lumbar segment ( L3?5 ) of the spinal cord was removed for determination of the expression of TLR4 by Western blot. Results MPE was significantly lower at T3,4 than at T1 in M and M+CK groups ( P<0?05) . Compared with group C, MPE was significantly lower at T2?4 , and the expression of TLR4 was up?regulated in M and M+CK groups ( P<0?05). Compared with group M, MPE was significantly increased at T1?4, and the expression of TLR4 was down?regulated in group M+CK ( P<0?05 ) . Conclusion The mechanism by which CK alleviates mor?phine?induced hyperalgesia is associated with down?regulation of TLR4 expression in rats.

Adolescent ; Atherosclerosis ; drug therapy ; etiology ; prevention & control ; therapy ; Child ; Humans ; Hyperlipidemias ; complications ; prevention & control ; therapy ; Hypolipidemic Agents ; therapeutic use ; Life Style ; Obesity ; complications ; prevention & control ; Primary Prevention ; Risk Factors

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.