Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.

Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.

Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.

Objective To explore the value of computed tomography (CT)and magnetic resonance imaging (MRI)in the diagno-sis and delineation of the extent of malignant external otitis (MEO).Methods Clinical manifestations and imaging features of 10 pa-tients with definite diagnosis of MEO were collected and analyzed.Plain and contrast-enhanced CT of the ear were performed on all 10 patients,of which 6 patients also received MRI scans.Results Abnormal soft tissue opacity within the external auditory canal and involvement of surrounding structures were found in all 10 patients.Bone erosion of the external auditory canal was showed in 7 pa-tients.Other CT findings included bone erosion of skull base and intracranial involvement.Abnormal soft tissue of the external audi-tory canal,effusion in the mastoid cavity and medullary abnormalities were showed very well on MR images in 6 patients while the cortical bone erosion was not well showed.Conclusion Imaging features of the lesions in the external auditory canal,bone erosion of skull base and intracranial involvement play crucial roles in the diagnosis and delineation of the extent of the lesion in patients with MEO.

Objective To observe the effect of the modified Yulin Decoction on improving the living quality of patients with yang-deficiency of the spleen and kidney of premature ovarian failure. Methods One hundred and twenty-seven patients were divided into experimental group (80) and control group (47) by non-randomized noninferiority comparative study. The experimental group was treated with modified Yulin Decoction daily orally once a day. The control group was treated with oral estradiol valerate and progesterone cycle. Two groups received continuous medication for 21 d, and treatment interval was 5 d. Three cycles of treatment were set as one course, and treated for 2 courses. The SF-36 scale was used to calculate the total scores and scores of eight dimensions before and after treatment. Results Before treatment, there was no significant difference (P>0.05) in the scores of SF-36 dimensions (except somatic pain) and total score between the two groups. Compared with before treatment, the score and total score of SF-36 in the experimental group increased (P<0.05, P<0.01). The mental health score of the control group was higher than that of before treatment (P<0.05, P<0.01). After treatment, there was statistical significance in the two dimensions of vitality and mental health in the two groups (P<0.05). There were significant differences (P<0.01) in the total score and scores of SF-36 physiological function, physical pain, general health, vigor, social function, emotional function and mental health between the two groups. Conclusion Modified Yulin Decoction can improve the living quality of patients with yang-deficiency of the spleen and kidney of premature ovarian failure.

Objective Bone morphogenetic protein 4 ( BMP4) induces rat myocardial hypertrophy in H9c2 cells, but the spe-cific mechanism remains unclear .The study aimed to elucidate the role of autophagy in myocardial hypertrophy and its relationship with extracellular signal regulating kinase ( ERK1/2) signal transduction pathway . Methods H9c2 cardiomyocytes were randomly divided into 4 groups:control group, BMP4 group, BMP4+PD98059 (ERK1/2 signal pathway inhibitor) group and BMP4+3MA (autophagy inhibitor) group.With PD98059(50μmol/L) and 3MA(5mmol/L) blocking for 30min, BMP4 (50μg/L) were added.Expressions of tiny tube related proteins 1 light chain 3 (LC3) and p-ERK1/2 were detec-ted after culturing for 30min.48h later, measurements were made on cell surface area , average protein content and α-smooth muscle actin (α-SMA ) protein expression level .Cell morphology and size were measured respectively by inverted microscope and Image J software .Total protein content was detected by BCA , and western blot was used to measure the expressions of LC3, ERK1/2, p-ERK1/2 and α-SMA. Resul ts 30min later, the expressions of LC3 and p-ERK1/2 were significantly higher in BMP4 group than in control group [(1.54 ±0.05) vs (1.95 ±0.11),(0.94 ±0.04) vs (1.33 ± 0.06),P<0.01] and no significant difference was found in other two groups .Compared with BMP4 group, significant decrease was found in BMP4+PD98059 and BMP4+3MA [(1.95 ±0.11) vs (1.59 ±0.08), (1.36 ±0.02);(1.33 ±0.06) vs (0.87 ±0.05), (0.95 ±0.15), P<0.01], while no significant difference was found between BMP 4+PD98059 group and BMP4+3MA group.48h lat-er, the cell area, protein content and α-SMA protein expression level are significantly lower in control group than in BMP 4 group [(644.1 ±15.01)μm2 vs (745.6 ±14.43)μm2,(240.0 ±7.26)pg/cell vs (347.1 ±5.4)pg/cell,(1.22 ±0.06 vs 1.99 ±0.03),P<0.01], while the corresponding indexes were significantly higher in BMP 4+PD98059 and BMP4+3MA compared with BMP4 group [(745.6 ±14.43)μm2 vs (645.0 ±12.63)μm2, (647.7 ±13.89)μm2;(347.1 ±5.4)pg/cell vs (239.7 ±3.39)pg/cell , (241.1 ± 8.56)pg/cell;(1.99 ±0.03) vs (1.13 ±0.05);(1.12 ±0.02), P<0.01].No significant difference was found as to the indexes be-tween BMP4+PD98059 group and BMP4+3MA group(P>0.05). Conclusion Autophagy may participate in BMP4-induced rat myo-cardial hypertrophy in H9c2 cells through ERK1/2 signal transduction pathway .The clinical treatment of myocardial hypertrophy may benefit from the blocking of autophagy or ERK 1/2 signal transduction pathway .

Objective To investigate the effect of lipoxin A4(LXA4) on inflammatory response in a rat model of permanent focal cerebral ischemia (PFCI). Methods Seventy-two adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n = 24 each):group Ⅰ sham operation (group S); group Ⅱ PFCI and group Ⅲ LXA4. PFCI was induced by thread occlusion of right middle cerebral artery according to the method described by Longa in group Ⅱ and Ⅲ. In group Ⅲ LXA4 100 ng/5 μl was injected into right ventricle of the brain after PFCI was successfully induced, while in group Ⅰ and Ⅱ equal volume of normal saline was injected instead of LXA4. Six animals were killed at 6, 12 and 24 h of ischemia. Their brains were immediately removed for microscopic examination and determination of myeloperoxidase (MPO) activity, TNF-α, IL-10 and transforming growth factor-β1 (TGF-β1) contents in the ischemic cortex. The expression of glial fibrillary acidic protein (GFAP)was measured by immuno-histochemistry. Apoptosis in neurons was assessed using TUNEL. Results PFCI significantly increased MPO activity, TNF-α, IL-10 and TGF-β1 contents and GFAP expression in the ischemic cortex and neuronal apoptosis in group Ⅱ as compared with group S. LXA4 significanfly decreased MPO activity,TNF-α content, GFAP expression and neuronal apoptosis and increased IL-10, TGF-β1 contents at 12,24 h of ischemia. LXA4 significantly ameliorated PFCI-induced cerebral histopathologic damage. Conclusion LXA4 can protect the brain against PFCI injury by inhibiting inflammatory response.

Aim To investigate the protective effect of lipoxin A4(LXA4)on ischemic brain injury in a rat model of permanent focal cerebral ischemia.Methods Adult male Sprague-Dawley rats weighing 200～250 g were used and rats were randomly divided into four groups:sham group,ischemia alone group,LXA4 10 ng group and LXA4 100 ng group.Permanent focal cerebral ischemia was induced by improved thread occlusion of right middle cerebral artery.Approximately 10 mm of nylon surgical thread was inserted into the right internal carotid artery in the rats of sham group.After the middle cerebral artery occlusion,the same volume of LXA4(5 ?l)or isotonic Na chloride(5 ?l)was injected respectively into the right lateral ventricle of the rat in 10 minutes.After 24 h of ischemia,the neurological deficit and the infarct volume were assessed by the method of Longa's score and 2,3,5-triphenyltetrazolium chloride(TTC)staining;the levels of malondialdehyde(MDA)and actvities of myeloperoxidase(MPO)in the ischemia cortex were measured by spectrophotometer;the contents of tumor necrosis factor-?(TNF-?)and interleukin-1?(IL-1?)were assayed by ELISA method.The histopathological change was observed after HE staining.Results Treatment with LXA4 10 ng or 100 ng significantly improved functional recovery,reduced relative infarction volume,inhibited MPO activity,decreased MDA,TNF-? and IL-1? levels,and improved histopathological injury.Moreover,the effects of neurological recovery and decreasing TNF-? level in LXA4 100 ng group were better than those in 10 ng group.Conclusion Treatment with LXA4 protects against permanent focal cerebral ischemia injury in rats.

Objective To investigate the effect of lipoxin A4 ( LXA4 ) on the permeability of blood-brain barrier (BBB) after focal cerebral ischemia-repeffnsion (I/R) in rats. Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups ( n = 18 each): group Ⅰ sham operation (group S); group Ⅱ focal cerebral I/R ( group I/R) and group Ⅲ LXA4 ( group L). Focal cerebral I/R was produced by middle cerebral artery occlusion (MCAO) with a 4-0 nylon thread with rounded tip inserted into right internal jugular vein and threaded cranially in group Ⅱ and Ⅲ . In group Ⅲ LXA4 100 ng was injected into right lateral ventricle of the brain after MCA was successfully occluded. MCAO was maintained for 2 h. The neurological deficit was evaluated and scored (0 = no deficit, 5 = death) at 24 h of reperfusion. 2% Evans blue 4 ml/kg was injected via femoral vein at 1 h before the animals were sacrificed. The animals were killed and their brains were immediately removed for determination of brain water content, Evans blue content and expression of matrix metalloproteinase-9 (MMP-9)in the ischemic cortex. Results The neurologic deficit scores, the brain water and Evans blue content and MMP-9 protein expression in the cortex were significantly higher in I/R group than in S group. The cerebral I/R-induced changes were significantly attenuated in LXA4 group. Conclusion LXA4 can protect blood-brain barrier against cerebral I/R injury by inhibiting MMP-9 protein expression in the brain tissue.

Objective To explore the value of three-dimensional DSA (3D-DSA) in displaying the location of the origin of uterine artery.Methods A total of 90 female patients underwent uterine artery (UA) embolization were enrolled.The bilateral internal iliac artery catheterization were performed by 3D-DSA,then the images were reconstructed in every 5 degree interval to choose the optimum range of viewing angle.The origination and the degree of the origin artery and UA were calculated.The distance between the origin of UA and superior glutea artery which was identified as the locating point was measured.Results Bilateral and contralateral oblique position of ＞30°-60°were the optimal projection positions of UA.Totally 64.44％ (116/180) of UA originated from the anterior trunk of internal iliac artery,18.33％ (33/180) originated from the inferior gluteal trunk,9.44 ％ (17 / 180) originated from the internal pundenal artery,5.56 ％ (10 / 180) originated from internal iliac artery,and 2.22％ (4/180) originated from the superior gluteal artery;10.56％ (19/180) of the angle of the origin artery and UA were 0-30°,38.89％ (70/180) were ＞30°-60°,41.11％ (74/180) were ＞60°-90°,4.44％ (8/180) were＞90°-120°,2.78％ (5/180) were＞120°-150°,2.22％ (4/180) were＞150°-180°.Distance between the origin of UA and superior gluteal artery was 3.04-18.31 mm,average was (11.71±4.28)mm.Conclusion 3D-DSA can clearly display the origination,viewing angle and the distance away from superior gluteal artery.