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Objective To investigate the effect of intravenous ultrafine superparamagnetic iron oxide nanoparticles feraheme (generic name:ferumoxytol) on cerebral infarction volume and inflammatory response in mice with permanent middle cerebral artery occlusion.Methods Thirty C57BL/6J mice were divided into sham operation group,saline control group,and feraheme group by the random number table (n =10 in each group).A permanent right middle cerebral artery occlusion model was induced by the modified suture method in the saline control group and the feraheme group,and no suture was inserted into the mice of the sham operation group.The intervention was performed by tail vein injection at 24 h after modeling.The sham operation group and the feraheme group were injected with 18 mg/kg feraheme,and the saline control group was injected with the same volume of normal saline.The neurobehavioral scores were conducted at 24 h (before the feraheme or saline injection) and 48 h (before the MRI exam) after modeling.MRI scans were performed at 48 h after modeling,and the cerebral infarction volume was calculated according to T2-weighted imaging.After the end of the scan,orbital blood was collected for the detection of serum tumor necrosis factor (TNF)-α,interleukin (IL)-1 β,and IL-6 levels.Then,the mice were sacrificed and the brain tissue was taken for HE staining and Ibal immunohistochemical staining.Results There were no significant differences in the infarct volume and neurological function score between the saline control group and the feraheme group.The serum levels of TNF-α,IL-1β,and IL-6 in the saline control group and the feraheme group were significantly higher than those in the sham operation group (P ＜0.05),but there was no significant difference between the saline control group and the feraheme group.Conclusion Intravenous injection of 18 mg/kg feraheme at 24 h after cerebral ischemia did not affect the infarct volume and inflammatory response,suggesting that this dose of feraheme can be used for molecular imaging studies of inflammatory response after cerebral ischemia.
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Objective@#To investigate the early intervention effects of metoprolol on connexin 43(Cx43) and phosphorylated Cx43 (p-Cx43) expression in rabbits with post myocardial infarction.@*Methods@#A total of 24 adult male New Zealand white rabbits were divided into sham group (n=6), early treatment group(n=6), routine treatment group(n=6), and myocardial infarction group(n=6) with a randomized block design blocked by weight. Myocardial infarction was induced by left anterior descending coronary artery (LAD) ligation. Rabbits in sham group received similar surgical procedure without LAD ligation. Metoprolol (12.5 mg/kg dissolved in 2 ml distilled water) was applied to rabbits in early treatment group and routine treatment group per gavage immediately after recovery from anesthesia and at 24 hours after myocardial infarction, respectively, then treated daily for 40 days. Rabbits in sham group and myocardial infarction group received 2 ml distilled water per gavage daily for 40 days. Plasma lactate dehydrogenase (LDH) and creatine kinase (CK) level were detected by automatic biochemistry analyzer after 6 hours in all rabbits. Ventricular fibrillation threshold (VFT) was measured in vivo by bipolar pacing electrodes at 40 days. Cx43 and p-Cx43 distribution in ventricular tissue was detected by immunofluorescence analyses. Cx43 and p-Cx43 protein level in ventricular tissue was determined by Western blot.@*Results@#(1) Plasma LDH ((851.7±85.9)U/L vs. (332.3±39.6)U/L, P<0.01) and CK ((1 192.7±105.3)U/L vs. (462.3±65.6)U/L, P<0.01) were significantly higher in myocardial infarction group than in sham group (both P<0.01). (2) VFT was significantly lower in myocardial infarction group than that in sham group ((470.0±91.0) beats per minute vs. (683.3±60.9) beats per minute, P<0.05), and VFT was significantly higher in early treatment group ((633.3±43.2) beats per minute) and routine treatment group ((645.0±30.8) beats per minute) than in the myocardial infarction group (both P<0.05). (3) Immunofluorescence analyses showed that Cx43 was mainly localized in the intercalated disk, which was perpendicular to the cell long axis with linear arrangement, and less lateral distribution in sham group, early treatment group and routine treatment group, which was significantly different as the case in the myocardial infarction group. The expression of p-Cx43 in myocardial infarction group was less than in sham group, which was significantly upregulated in in early treatment group and routine treatment group when compared with myocardial infarction group, and expression of p-Cx43 was significantly higher in early treatment group than in routine treatment group. (4)The p-Cx43/Cx43 ratio of protein was significantly lower in myocardial infarction group than in sham group (0.165±0.011 vs. 0.363±0.046, P<0.05), and significantly higher in early treatment group (0.720±0.063) and routine treatment group (0.364±0.030) than in myocardial infarction group (both P<0.05), and this ratio was significantly higher in early treatment group than in routine treatment group (P<0.05).@*Conclusion@#Metoprolol treatment, especially the early metoprolol treatment (within 24 hours after LAD ligation), could significantly improve VFT by ameliorating the distribution and dephosphorylation of myocardial Cx43 in rabbits with experimental myocardial infarction.
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Objective To investigate the effect of norepinephrine (NE) on the proliferation and migration capacity of endo‐thelial progenitor cells (EPCs) ,and bone marrow mobilization and to analyze its molecular mechanism .Methods The 8‐week old C57 mice were taken and randomly divided into 3 groups ,5 cases in each group :the blank control group(subcutaneous injection of normal saline without operaion) ,model group(subcutaneous injection of normal saline and ischemia in left lower extremity ) and NE group(subcutaneous injection of NE 100μmol/100 μL and ischemia in left lower extremity) .The limb ischemia model was prepared by adopting the femoral arterial ligation in mouse left lower extremity ,then NE was continuously pumped by the micro‐osmotic pump .The EPCs contents from bone marrow ,peripheral blood and spleen were assayed with the flow cytometric analyzer ;human peripheral blood EPCs were cultured and stimulated by NE .The proliferation and migration capacity ,and the activation situation of Akt and eNOS signal pathway were detected .Results NE could promote the mobilization of bone marrow EPCs in limb ischemia mice ,increased the EPCs quantity of peripheral blood and spleen ,comparing the NE group with the model group ,the EPCs quantity was increased for bone marrow [(3 .271 ± 0 .772)% vs .(1 .320 ± 0 .256)% ] ,peripheral circulation[(0 .261 ± 0 .041)% vs .(0 .110 ± 0 .028)% ] and spleen[(4 .671 ± 0 .345)% vs .(1 .880 ± 0 .0 .381)% ] ,the differences were statistically significant (P<0 .01) .NE could promote the proliferation and migration capacity ,moreover could activate the Akt‐eNOS signal pathway in EPCs with a dose dependent manner .Conclusion NE could promote the proliferation and migration of EPCs and mouse bone marrow mobilization via the Akt‐eNOS signal pathway .
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Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.
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Objective To observe CT features of ovarian thecofibroma and the clinical significance.Methods CT manifestations, clinical data and pathological diagnosis of 12 cases of ovarian thecofibroma proved by pathology were retrospectively analysed.Results The CT manifestation of ovarian thecofibroma was typical,which was showed as following:on one side of the attachment area tumor,single,ovoid or class circular shape,most boundary clear,equal or slightly low density solid masses,internal or boundary ar-ea accompanied by a small amount low density area,mild delay enhancement in solid ingredients or no obvious enhancement.Conclu-sion CT examination is important for qualitative diagnosis of ovarian thecofibroma and finding complications.
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Objective: To explore influence of long-term oral valsartan-angiotensin II type 1 receptor blocker on ventricular arrhythmia after myocardial infarction (MI) in rabbits and its possible mechanism. Methods: A total of 24 New Zealand rabbits were randomly divided into sham operation group (n=8), MI group (n=8) and valsartan group (n=8) according to number table. Sham operation group only received thoracotomy without ligation of anterior descending branch of left coronary artery (LAD), while MI group and valsartan group received ligation of anterior descending branch of LAD. Valsartan group received valsartan gavage (10 mg•kg-1•d-1) since the second day after operation, three groups all were fed for 12 weeks. Mono active potential (MAP) of left ventricular myocardial cells of subendocardial myocardium（inner layer myocardium）, subepicardial myocardium（outer layer myocardium）and middle layer myocardium were recorded before MI and 12 weeks after MI, and times of provocative malignant arrhythmias were recorded on 12 weeks after MI in three groups. Results: 1. Ventricular tachycardia or fibrillation (VT/ VF) episodes were markedly decreased in VAL group than that in MI group on 12 weeks after MI [(3.1±0.8) vs. (12.7±1.5), P＜0.05]; 2. After MI 12 w, the action potential duration to 90% repolarization (APD90) of three-layer ventricular myocytes in MI group was prolonged than that before MI [（259.2±22.1）ms,（288.0±25.8）ms,（244.6±22.6）ms vs.（230.1±23.2）ms,（244.2±23.4）ms,（229.0±21.7）ms, P＜0.05 or＜0.01]；but there were no significant difference in APD90 of three layers ventricular myocytes between before and after MI in valsartan group (P>0.05 all); Compared with sham operation group and valsartan group, there was significant prolonged in transmural dispersion of repolarization (TDR) [(18.8±6.2) vs. (23.9±7.7) vs. (37.2±10.2), P0.05). Conclusions: Long-term oral valsartan can significantly reduce malignant ventricular arrhythmia incidence in rabbits after MI, which may be related to improving TDR in rabbits after MI.
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Objective To investigate the effect of astaxanthin on the peripheral blood endothelial progenitor cells (EPCs) apop-tosis induced by oxidative stress in vitro and to explore its underlying mechanism .Methods Human peripheral blood EPCs were in vitro cultured and divided into the control group ,model group with 100 μmol/L tert-butyl hydroperoxide(tBHP) and the astaxan-thin plus tBHP group(with 0 .10 ,1 .00 ,10 .00 nmol/L astaxanthin pretreatment for 24 h ,then adding the final concentration of 100μmol/L tBHP for 6 h continuous culture) .The cell viability was measured by the MTT method .The level of reactive oxygen spe-cies (ROS) was determined by the DCFH-DA method .The changes of mitochondrial membrane potential(MMP) and the apoptosis ratio were detected by the JC-1 method and the DAPI method ,respectively .Results Compared with control group ,100μmol/L tB-HP could obviously caused the apoptosis of EPCs(P<0 .05) ,while astaxanthin could decrease tBHP induced apoptosis ,which man-ifested by the decrease of the apoptosis ratio (P<0 .05) and MMP increase .Conclusion Astaxanthin has the protective effect on the apoptosis of EPCs ,its mechanism may be related with the protection of the mitochondrial function .
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Objective To investigate the effect of astaxanthin( ASX)on endothelial progenitor cells( EPCs)injury induced by oxidative stress in vitro and to explore its underlying mechanism. Methods Cultured EPCs isolated from peripheral blood were randomly divided into 5 groups:normal control,model group[ tert-butyl hydroperoxide( tBHP)100μmol·L-1 ],and ASX+tBHPgroups(thecellswerepreconditionedwithASX0.1,1.0,and10.0nmol·L-1,respectively).Thecellviabilitywas measured by MTT method. The level of reactive oxygen species( ROS)was determined by DCFH-DA method. The changes of mitochondrial membrane potential( MMP)and apoptosis ratio were detected by JC-1 method and DAPI method,respectively. caspase-3 activity changes of EPCs were detected. Results The cell viability of EPCs was improved with the increasing concentration of ASX. Compared with the model group[(48. 5±4. 3)%],0. 1,1. 0,10. 0 nmol·L-1 ASX significantly increased the cell viabilities[(57. 6±8. 2)%,(77. 6±7. 5)%,and(85. 3±6. 1)%,P﹤0. 05]. The results of DAPI staining revealed that ASX pretreatment could significantly reduce the apoptotic rate of EPCs. The apoptotic rate of the model group was( 27. 8 ± 3. 2)%,while that of ASX+tBHP groups was[(20. 4±2. 9)%,(14. 9±1. 7)%,and(7. 8±0. 7)%,P﹤0. 05],respectively. The data from caspase-3 activity assay indicated that ASX precondition could also remarkably decrease the caspase-3 activity for EPCs. The caspase-3 activity of the model group was(0. 345±0. 018),while that of the ASX+tBHP group were[(0. 291± 0. 013),(0. 209±0. 004),and(0. 169±0. 013),P﹤0. 05],respectively. In addition,treatment with tBHP resulted in an increase of DCF fluorescence,while ASX precondition could decrease the DCF fluorescence,which suggested the accumulation of intercellular ROS for EPCs. Injury of michondrial membrane resulted in the loss of mitochondrial membrane potential( MMP). The MMP detected by JC-1 method revealed that compared with model group,pretreatment of ASX inversed the reduction of MMP. Conclusion Astaxanthin inhibits endothelial progenitor cell apoptosis induced by oxidative stress through inhibiting ROS production,improving the mitochondrial function and down-regulating caspase-3 activity.
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The first case of acquired syphilitic skull osteitis accompanied by syphilitic meningitis in China is reported.A 55-year-old female presented with a persistent distending pain of the frontal and occipital regions of the skull for two months.T1 weighted magnetic resonance imaging(MR1) showed muhiple lesions in the skull and linear enhancement of the meninge near the lesions.The serum and cerebrospinal fluid (CSF) were positive for Treponema pallidum particle agglutination assay (TPPA) and rapid plasma reagin circle card test(at the dilutions of 1∶32 and 1∶4 respectively).The levels of leukocyte and protein were 10 ×106/L and 0.82 g/L respectively in CSF.TP DNA was detected in the calvarial periosteum.Histopathological examination of the frontal bone showed focally destructive osteolytic lesions with obscure texture of the bone,hyperemia around the destructive bone tissue and in dura mater-like tissues,proliferation of interstitial fibrous tissue,swelling of endothelial cells and inflammatory infiltration predominantly composed of abundant plasma cells.After managed with routine treatment regimen for neurosyphilis,her headache was relieved 3 days later,nearly disappeared 15 days later,completely disappeared 30 days later.No similar headache recurred.A 5year follow up demonstrated a satisfactory long-term and short-term outcome.She was finally diagnosed with syphilitic skull osteitis complicated by syphilitic meningitis.
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BACKGROUND:A series of studies have demonstrated that ventral mesencephalic dopamine precursors may differentiate into considerable dopaminergic neurons (DNs) available for cell transplantation for Parkinson's disease.However,the detailed molecular characteristics of these cells remain undear.OBJECTIVE:To observe the expression of main marker genes of DNs cultured in vitro.DESIGN,TIME AND SETTING:This observation experiment was performed at the Brain Tumor Laboratory in the Second Affiliated Hospital of Soochow University and Shanghai Biochip Company from December 2005 to December 2008.MATERIALS:Inbred pregnant Wistar rats (F+36) weighing 300 g approximately were used for in vitro culture of mesencephalic cells.METHODS:Ventral mesencephalic cells from inbred pregnant Wistar rats were cultured with basic fibroblast growth factor,and were induced to differentiate in vitro with L-Ascorbic acid-2-phosphate sesquimagnesium salt.Total RNA were extracted before and 4,7 days after the induction.Affymetrix microarrays were utilized to detect the expression changes of main marker genes of DNs.MAIN OUTCOME MEASURES:Morphologic changes of differentiated ventral mesencephalic precursors;Expression of DN-ralated common marker genes before and after the induced differentiation.RESULTS:Rat ventral mesencephalic precursors differentiated into numerous tyrosine hydroxylase-positive cells,which expressed multiple marker genes of DNs,such as AHD2,calcium binding protein 1 (Cab1),DDC,DAT,Drd2,Girk2,VMAT-2,with variously degrees and with different tendencies.Among those genes,only Cab1 was significantly up-regulated and only Girk2 was significantiy down-regulated.CONCLUSION:Rat ventral mesencephalic precursors can be induced to differentiate into plenty of tyrosine hydroxylase-positive DNs,mainly originating in A10 regions.
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the incidence of the complication.
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Objective To observe the migration ability of different quantity of BMSCs labled with Resovist after transplanted in rat models with Parkinson disease (PD) with 1.5T MR scanner and micro-47 coil, in order to determine the optimal transplanted dosage of BMSCs and observation time in vivo. Methods Forty PD rats were randomly assigned to 5 groups (each n=8) including 1×10~5 BMSCs group, 1.5×10~5 BMSCs group, 2×10~5 BMSCs group, 2.5×10~5 BMSCs group and control group. FFE-T2WI were obtained immediately and 1 week, 4 weeks, 8 weeks after transplantation to measure and compare the volume of hypointense areas of different groups in different time with 1.5T and 47 mm inner diameter micro-coil. At the meantime, rotational behavior was assessed in each group. After MR scanning, the rats were executed and prepared for immunohistochemistry staining at 12 weeks after transplantation. Results Only the extent of the dark region became wider 4 weeks after transplantation in 2×10~5 BMSCs group (P=0.005). The therapeutic efficacy in 2×10~5 BMSCs group was the best confirmed by behaviour studies (P=0.02). Conclusion For the treatment of PD and evaluation of the migratory ability of BMSCs, the optimal transplanted dosage of BMSCs is 2×10~5, while the best observation time is 4 weeks after transplantation.
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Objective:To observe the effect of Jiedu Huoxue Prescription on gastrin of atrophic gastritis rats. Methods:The atrophic gastritis rats model was established by using combination of MNNG, sodium salicylate, hot saline water and irregular diet. The blood serum gastrin content was detected with RI. Results: Compared with model group, the contents of gastrin in Jiedu Huoxue Prescription group, sanjiu group and weimeisu group increased significantly (P
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Objective To study the way of measurement of both the thoracic width and height by roentgenography and its clinical significance.Methods The thoracic width and height in 158 healthy people and 30 cases with emphysema on chest plain X-ray films were measured and analysed statistically.The relationship among the width and height of the chest,height and weight of body in healthy people were studied.Results In normal group,the thoracic width and height were 26.59 cm and 23.84 cm in men,24.8 cm and 21.6 cm in women in average,respectively.In emphysema group,the average thoracic width and height were more than 27 cm and 26 cm in men,25 cm and 24 cm in women,respectively.The formulas calculated thoracic width and height relevant to height of body were 10.9403+0.0951 ?height of body and -0.6381+0.1462 ?height of body in men,11.0605+0.0864 ?height of body and -8.6428+0.1907?height of body in women normally.Therefore,the possibility of prompting emphysema was present when the thoracic width and height were more than 1 cm and 3 cm according to above calculating formulas.Conclusion The data of the calculated thoracic width and height based on the formulas mentioned adove are of significant value for diagnosing emphysema with imaging.
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Objective To investigate the optimal time points for transplantation with in vitro cultured dopaminergic neurons as a potential treatment of Parkinson’s disease. Methods After the ventral mesencephalic precursors from E11 rat embryos were expanded for 7 days in vitro, they were harvested respectively from day 0 to day 7 in the period of induced differentiation. Then the cells were seeded again and cultured for another 7 days. The final survival of dopaminergic neurons determined the optimal time points for moving cells in vitro and, possibly, for transplantation in vivo. Result The survival rate of dopaminergic neurons moved on day 0 and day 1 in the period of induced differentiation was significantly higher than that at other time points. Conclusion The optimal time points for transplantation are found possibly to be day 0 and day 1 in the period of differentiation after the expansion of ventral mesencephalic precursors from E11 rat embryos.