Objective To investigate the correlation between middle cerebral artery (MCA) atherosclerotic plaques and single subcortical infarction (SSI) using high-resolution magnetic resonance imaging (HR-MRI).Methods The patients with SSI received HR-MRI examinations at the ipsilateral MCA horizontal segment stenosis from January 2012 to November 2014 were analyzed prospectively.They were divided into proximal SSI (pSSI) and distal SSI (dSSI).The longitudinal and transverse diameters and volume of different types of infarction pattern as well as the degree of luminal stenosis of MCA deep perforating parent artery,plaque distribution,plaque enhancement or not,white matter lesions,and general information of both groups were documented respectively.Results A total of 78 patients with SSI were enrolled,including 40 (51％) in the pSSI group and 38 (49％) in the dSSI group.The proportions of Fazekas scale grade 3 white matter lesions (63.5％vs.40.0％;x2 =4.183,P=0.041) and deep white matter lesions (50.0％ vs.15.0％;x2 =10.961,P =0.001) in the dSSI group were significantly higher than those in the pSSI group.The proportions of MCA plaque in the opening (35.0％ vs.13.2％;x2=3.930,P=0.047),plaque enhancement (87.5％ vs.30.0％;x2 =25.447,P ＜ 0.001) and posterosuperior wall plaques (42.5％ vs.21.4％;x2 =9.491,P ＜ 0.001) and the degree of luminal stenosis (60.38％ ± 10.20％ vs.45.00％ ±6.44％;t =3.625,P =0.031) in the pSSI group were all significantly higher than those in the dSSI group.In addition,the longitudinal and transverse diameters and volume of the infarcts in the pSSI group were significantly larger than those in the dSSI group (all P ＜ 0.001).Multivariate logistic regression analysis showed that MCA enhanced plaques on the lesionipsilateral sides (odds ratio[OR] 11.764,95％ confidence interval[CI] 2.081-66.511;P =0.005) and posterosuperior wall plaques (OR 6.131,95％ CI 1.012-23.339;P =0.037) were independently associated with pSSI,while deep white matter lesions (OR 0.280,95％ CI 0.203-0.648;P=0.012) was independently associated with dSSI.Conclusions The atherosclerotic plaques of MCA deep perforating parent artery are common in both the pSSI group and the dSSI group.pSSI is mainly associated with the location of atherosclerotic plaques of deep perforating parent artery and enhanced plaques,while dSSI is mainly associated with deep perforating artery vasculopathy.

Objective To evaluate the effect of hemorrhagic shock factor on the pharmacokinetics of rocuronium in pigs.Methods Sixteen pathogen-free Bama miniature pigs of both sexes,aged 3-5 months,weighing 22-25 kg,were divided into 2 groups (n=8 each) using a random number table:control group (group C) and hemorrhagic shock group (group HS).In group C,rocuronium 3.78 mg/kg was injected via the auricular vein.In group HS,the animals were subjected to volume-controlled hemorrhage,about 40％ of blood volume was withdrawn from the left femoral artery over 15 min (30 ml/kg),and rocuronium 3.78 mg/kg was injected via the auricular vein after the model was successfully established.At 0,2,4,7,10,15,20,30,60,120,180,240,300,360 and 420 min after rocuronium injection,blood samples were collected from the internal jugular vein for determination of the plasma concentration of rocuronium by high-performance liquid chromatography-tandem mass spectrometry.The pharmacokinetic parameters of rocuronium were calculated.Results Compared with group C,the plasma concentration of rocuronium was significantly increased at 20 and 60-420 min after rocuronium injection,the elimination half-life and mean residence time were prolonged,and the plasma effect-site equilibration rate constant was decreased in group HS (P＜0.05).There was no significant difference in the maximal concentration and area under the concentration-time curve between the two groups (P＞ 0.05).Conclusion The elimination of rocuronium is slower in a pig model of hemorrhagic shock.

ObjectiveTo explore the expression of p130Cas and paxillin in breast carcinoma and investigate the relationships of p130Cas and paxillin levels with clinical and pathological characteristics.MethodsReverse transcriptase polymerase chain reaction (RT-PCR) was applied to detect the expression of p130Cas and paxillin in tumor tissues from 30 cases of primary breast carcinoma,15 cases of normal breast tissues and 10 cases of breast fibroadenoma.ResultsThe levels of p130Cas and paxillin were 0.444 ± 0.088,0.493 ± 0.073,0.739 ± 0.092,0.755 ± 0.137 in normal breast tissues and breast fibroadenoma tissues.The levels of p130Cas and paxillin were 0.914 ±0.186,0.303 ±0.043 in breast carcinoma tissues.Breast carcinoma tissues showed higher levels of p130Cas and lower levels of paxillin than normal breast tissues and breast fibroadenoma tissues(P ＜ 0.01 ).The expression of p130Cas was related with age (r =0.599,P =0.000 ),menopausal status (t =5.602,P =0.000 ),estrogen receptor ( ER ),progesterone receptor ( PR ) status (t =5.768,P =0.000; t =4.151,P =0.000 ) and histological grades (r =-0.668,P =0.000 ),but not related with tumor size (F =0.717,P =0.497 ),lymph node status (F =1.230,P =0.308 ) and pathological stages(r =0.283,P =0.137).The expression of paxillin was related with rumor size (F=4.114,P =0.028 ),pathological stages( r =-0.520,P =0.003),and lymph node status(F=12.418,P=0.000 ),but not related with age(r =0.294,P=0.115),menopausal status(t =-0.403,P =0.690),ER,PR status(t =0.749,P =0.460;t =0.006,P =0.995) and histological grades (r =-0.173,P =0.362).Conclusions p130Cas and paxillin have relations with the malignant transformation,invasion and metastasis of breast carcinoma.Measurement of p130Cas and paxillin may provide useful prognostic information for patients with primary or metastatic breast carcinoma.

Objective To evaluate the effect of sevoflurane on myocardial injury induced by hemorrhagic shock and resuscitation (HS/R) in pigs.Methods Twenty-four Bama miniature pigs (12 males, 12 females) , weighing 20-25 kg, aged 3-5 months, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S) , HS/R group and sevoflurane group (group Sev).The left and right femoral arteries and right femoral vein were cannulated for blood pressure monitoring, blood-letting, blood sampling and fluid infusion.HS/R was induced by blood-letting maintaining for 1 h, followed by resuscitation with autologous blood reinfusion and infusion of lactated Ringer's solution 2 times the volume of the blood withdrawn.The pigs in group Sev were exposed to 2％ sevoflurane for 30 min before resuscitation.After cannulation, at 30 min after hemorrhagic shock, before resuscitation, and at 30 min, and 1.5, 2.5 and 3.5 h after resuscitation, blood samples were collected from the femoral artery for determination of creatine kinase-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration in serum using an automatic biochemical analyzer.Myocardial specimens were obtained at 3.5 h after resuscitation for detection of tumor necrosis factor-alpha (TNF-ot) and interleukin-6 (IL-6) contents (by ELISA) , and phosphor-signal transducer and activator of transcription 1 (p-STAT1) expression (by Western blot), and for examination of the pathological changes (with light microscope).Results Compared with S group , the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly increased, and the expression of p-STAT1 was up-regulated in HS/R and Sev groups (P＜0.05).Compared with HS/R group, the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly decreased, and the expression of p-STAT1 was downregulated (P＜0.05) , and the pathological changes of myocardia were alleviated in Sev group.Conclusion Sevoflurane can alleviate HS/R-induced damage to myocardia of pigs, and inhibited STAT1 activity and attenuated inflammatory responses in the myocardium are involved in the mechanism.

Objective To evaluate the changes in the expression of aquaporin-8 (AQP8) in intestinal mucosa in pigs with hemorrhagic shock.Methods Sixteen Bama miniature pigs,weighing 22-25 kg,were equally and randomly divided into sham operation group (group S) and hemorrhagic shock group (group HS).The animals were fasted for 8 h before operation.The animals were anesthetized with propofol 3 mg/kg injected via the auricular vein,and tracheostomized and mechanically ventilated.In group S,the femoral artery and internal jugular vein were only cannulated.In group HS,the femoral artery and internal jugular vein were cannulated for blood pressure and mean arterial pressure monitoring and blood sampling.Hemorrhagic shock was then induced by removing 40 percent of blood volume over 15 min.Before anesthesia (T0),and at 30 min and 1.0,1.5,2.0,3.0 and 4.0 h after the end of blood-letting (T1.6),blood samples were collected for determination of serum D-lactate and intestinal fatty acid binding protein (I-FABP) concentrations.After blood sampling at T6,the pigs were sacrificed,and intestinal specimens were obtained for microscopic examination and for determination of AQP8 cotent in intestinal mucosa (by ELISA).The water content of intestines was calculated by wet/dry weight ratio.Results Compared with group S,the serum D-lactate concentrations at T2-6,I-FABP concentrations at T1-6,and water content of intestines were significantly increased,and the cotent of AQP8 was up-regulated at T6 in group HS.No changes were found in the intestinal mucosa in group S.In group HS,severe damage to the intestinal mucosa was found,and bleeding,inflammatory cell infiltration,and epithelial cell necrosis were observed.Conclusion The mechanism of hemorrhagic shock-caused damage to intestines is related to up-regulated expression of AQP8 in intestinal mucosa in pigs.

Objective To explore the value of high-resolution MRI(HR-MRI) on clinical application in the differential diagnosis between Moyamoya disease(MMD) and atherosclerosis-related Moyamoya syndrome (A-MMS). Methods Seventeen cases of patients with MMD and 18 cases of patients with A-MMS in our hospital from January 2014 to September 2015 were prospectively enrolled in the study. Record the clinical data and the proximal middle cerebral artery (M1 portion) performance on HR-MRI, the max-vessel area, the min-vessel area, the max-lumen area, the min-lumen area, the wall max-thickness, the styles of M1 portion thickening (eccentric or concentric), whether the wall was enhanced or not, and analysis the recorded data statistically, t test and χ2 test were used for the statistical analysis. Results The wall max-thickness of MMD group was (0.94 ± 0.17) mm, which was smaller than that in A-MMS group (1.23 ± 0.42) mm, there was statistic significance (t=-2.977, P=0.006). The cases of M1 portion non-enhancement was 15, slight enhancement 2, strong enhancement 0 in MMD group, and non-enhancement 5, slight enhancement 5, strong enhancement 8 in the A-MMS group, the difference was significant statistically (χ2=9.794, P=0.001). The cases of M1 portion concentric thickening was 16, 9 cases in the A-MMS group, there was statistic difference between them (χ2=6.317, P=0.012). Wall concentric thickening diagnose the MMD with a sensitivity of 94.1% (16/17), specificity of 50.0% (9/18), accuracy of 71.4%(25/35). Wall strong enhancement appear in the A-MMS with a sensitivity of 44.4%(8/18), specificity of 100%(17/17), accuracy of 71.4%(25/35).With a cut-off the maximum wall thickness of 1.2 mm could be used to noninvasively differential diagnose the MMD and A-MMS with a sensitivity of 55.6%(10/18), specificity of 88.2%(15/17), accuracy of 71.4%(25/35). Conclusion HR-MRI is a good tool for the differential diagnosis between MMD and A-MMS.

Objective To investigate the effect of dexmedetomidine on acute kidney injury in endotoxemic rats.Methods Thirty adult male Sprague-Dawley rats,aged 4-6 months,weighing 180-220 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),lipopolysaccharide group (group L),and dexmedetomidine (group D).Lipopolysaccharide (LPS) 5 mg/kg was injected slowly into the femoral vein to establish the model of endotoxemic in rats anesthetized with chloral hydrate.In group D,after LPS injection,a loading dose of dexmedetomidine 7 μg/kg was injected intravenously,and 15 min later dexmedetomidine was infused for 6 h at 5 μg · kg-1 · h-1,while the equal volume of normal saline was given in L and C groups.At 6 h after the end of LPS administration,blood samples were collected from the femoral vein for determination of serum creatinine (Cr),blood urea nitrogen (BUN),tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) concentrations.At 24 h after the end of LPS administration,the animals were sacrificed and kidneys were removed for microscopic examination and for determination of the expression of tight junction proteins ZO-1 and occludin in renal tissues by Western blot.Results Compared with group C,the serum Cr,BUN,TNF-α and IL-6 concentrations were significantly increased,and the expression of ZO-1 and occluding was down-regulated in L and D groups.Compared with group L,the serum Cr,BUN,TNF-α and IL-6 concentrations were significantly decreased,the expression of ZO-1 and occluding was up-regulated,and the pathological changes of kidneys were mitigated in D group.Conclusion Dexmedetomidine can alleviate acute kidney injury in endotoxemic rats.

Objective To evaluate the effect of sevoflurane on activation of nuclear factor kappa B (NF-κB) during brain injury induced by hemorrhagic shock (HS) in pigs.Methods Thirty-two adult male Bama miniature pigs,aged 6 months,weighing 22-25 kg,were divided into 4 groups (n=8 each) using a random number table:sham operation group (group Sham),HS group,sevoflurane preconditioning group (group Sev-Pre) and sevoflurane postconditioning group (group Sev-Post).The animals were anesthetized,and tracheostomized and mechanically ventilated.In group Sham,the bilateral femoral arteries and internal jugular veins were only cannulated.HS was induced by removing 40％ of blood volume within 15 min (30 ml/kg) via the right femoral artery and maintaining at this level for 1 h before resuscitation in HS,Sev-Pre and Sev-Post groups.In group Sev-Pre,2％ sevoflurane was inhaled for 30 min,and then HS was induced.In group Sev-Post,2％ sevoflurane was inhaled for 30 min starting from the time point immediately after HS was induced.Immediately before establishment of the model and at 30,60,90,120,180 and 240 min of HS (T1-6),blood samples from the jugular vein were collected for determination of serum interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations by enzymelinked immunosorbent assay.At 4 h of HS,the rats were sacrificed,and brains were removed for microscopic examination of hippocampal CA1 region (using haematoxylin and eosin staining) and for determination of the expression of NF-κB in nucleoprotein (by Western blot).Results Compared with group Sham,the concentrations of serum IL-1β and TNF-α were significantly increased at T2-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was up-regulated in HS,Sev-Pre and Sev-Post groups (P＜0.05).Compared with group HS,the concentrations of serum IL-1β and TNF-α were significantly decreased at T3-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was down-regulated in Sev-Pre and Sev-Post groups (P＜0.05).There were no significant differences between group SevPre and group Sev-Post in concentrations of serum IL-1β and TNF-α and expression of NF-κB in nucleoprotein in hippocampal CA1 region (P＞0.05).The pathologic changes were significantly attenuated in SevPre and Sev-Post groups as compared with group HS.Conclusion The mechanism by which sevoflurane attenuates brain injury induced by HS may be related to inhibition of NF-κB activation and reduction of inflammatory responses in pigs.

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS).Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22-25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham) , group HS, and sevoflurane group (S group).In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured.The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated.The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40％ blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury.In group S, 2％ sevoflurane was inhaled for 30 min after successful establishment of the model.Immediately before establishment of the model (T0) , and at 30, 60,90, 120, 180 and 240 min after HS (T1-6) , blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method).Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P＜0.05).Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P＜ 0.05).Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses.

Objective To evaluate the effect of sevoflurane preconditioning on brain injury induced by cardiopulmonary bypass (CPB) in rats.Methods Forty adult male Sprague-Dawley rats,aged 6-8 months,weighing 350-450 g,were randomly divided into 5 groups (n=8 each) using a random number table:sham operation group (S group),CPB group,and preconditioning with different concentrations of sevoflurane groups (SP1,SP2 and SP3 groups).In SP1,SP2 and SP3 groups,sevoflurane with the final concentrations of 1.2％,2.4％ and 3.6％,respectively,was inhaled for 1 h,and then CPB was started.After sevoflurane preconditioning and before CPB (T0),at 30 min of CPB (T1),at the end of CPB (T2),and at 1,2 and 3 h after termination of CPB (T3-5),venous blood samples were collected from the right internal jugular vein for determination of serum S100-β protein concentrations by enzyme-linked immunosorbent assay.Rats were sacrificcd at T5,and hippocampi were isolated for determination of neuronal apoptosis (by TUNEL) and NF-κB p65 expression (by immunohistochemistry).Results Compared with group S,the concentration of serum S100-β protein was significantly increased at T1-5,the number of apoptotic neurons was significantly increased,and the expression of NF-κB p65 was significantly up-regulated in CPB,SP1,SP2 and SP3 groups (P＜0.05).Compared with group CPB,the serum S100-β protein concentration was significantly decreased at T1-5,the number of apoptotic neurons was significantly decreased,and the expression of NF-κB p65 was significantly down-regulated in SP1,SP2 and SP3 groups (P＜ 0.05).Compared with group SP1,the serum S100-β protein concentration was significantly decreased at T1-5,the number of apoptotic neurons was significantly decreased,and the expression of NF-κB p65 was significantly down-regulated in SP2 and SP3 groups (P＜0.05).Compared with group SP2,the serum S100-β protein concentration was significantly decreased at T1-5,the number of apoptotic neurons was significantly decreased,and the expression of NF-κB p65 was significantly downregulated in group SP3 (P＜0.05).Conclusion Sevoflurane preconditioning can attenuate CPB-induced brain injury probably by inhibiting activation of NF-κB in hippocampal neurons of rats.