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Objective:To evaluate the role of aquaporin 4 (AQP4) in dexmedetomidine-induced reduction of blood-brain barrier permeability in mechanically ventilated mice and the relationship with protein kinase C (PKC).Methods:One hundred and fifty clean-grade healthy male C57BL6 mice, weighing 20-25 g, aged 8-12 weeks, were divided into 5 groups ( n=30 each) using a random number table method: control group (group C), mechanical ventilation group (group V), LY317615 group (group L), dexmedetomidine group (group D), and dexmedetomidine+ PMA group (group DP). Group C spontaneously breathed air for 6 h. The animals were mechanically ventilated for 6 h in group V. PKC inhibitor LY3176 15 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation in group L. Dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation in D and DP groups. PKC activator PMA 15 μg/kg was intraperitoneally injected at 60 min before mechanical ventilation in group DP. Mice were anesthetized at 1 day after mechanical ventilation, then sacrificed and hippocampal tissues were taken for microscopic examination of pathological changes in the hippocampal CA1 and CA3 areas (with a light microscope). Brain tissues were also taken to measure the water content and content of Evans blue (EB) and to detect the expression of PKC and AQP4 (by Western blot). The cognitive function was evaluated using a novel object recognition task at 3 days after mechanical ventilation. Results:Compared with group C, the water content and EB content of brain tissues were significantly increased after mechanical ventilation, the expression of PKC and AQP4 in brain tissues was up-regulated, the percentage of novel object exploration and discrimination index were decreased ( P<0.05), and the histopathological damage in the hippocampal CA1 and CA3 areas was aggravated in group V and group DP. Compared with group V, the water content and EB content of brain tissues were significantly decreased after mechanical ventilation, the expression of PKC and AQP4 in brain tissues was down-regulated, the percentage of novel object exploration and discrimination index were increased ( P<0.05), and the histopathological damage in the hippocampal CA1 and CA3 areas was significantly attenuated in group D and group L. Compared with group D, the water content and EB content of brain tissues were significantly increased after mechanical ventilation, the expression of PKC and AQP4 in brain tissues was up-regulated, the percentage of novel object exploration and discrimination index were decreased ( P<0.05), and the histopathological damage in the hippocampal CA1 and CA3 areas was aggravated in group DP. Conclusions:AQP4 is involved in dexmedetomidine-induced reduction of blood-brain barrier permeability in mechanically ventilated mice, and the mechanism is related to inhibiting activation of PKC.
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Objective:To evaluate the role of transient receptor potential vanillic acid 4 (TRPV4) in dexmedetomidine-induced improvement in cognitive function in mice with mechanical ventilator-caused brain injury.Methods:Ninety clean-grade healthy male C57BL6 mice, weighing 20-25 g, aged 8-12 weeks, were divided into 5 groups ( n=18 each) using a random number table method: control group (group C), mechanical ventilation group (group V), HC-067047 group (group H), dexmedetomidine group (group D), and dexmedetomidine+ GSK1016790A group (group DG). In group C, the animals breathed air spontaneously for 6 h without mechanical ventilation. In group V, the animals were mechanically ventilated for 6 h. In group H, TRPV4 blocker HC-067047 10 mmol was injected into the cerebral ventricle at 3 and 6 h of mechanical ventilation. In D and DG groups, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation. In group DG, TRPV4 agonist GSK1016790A 5 μmol was injected into the cerebral ventricle at 60 min before mechanical ventilation. Morris water maze test was performed on 6 mice in each group at 1 day before mechanical ventilation and 3 and 7 days after mechanical ventilation. Six mice in each group were randomly selected and sacrificed at 1 day after mechanical ventilation, and the brain tissue was taken for determination of the neuronal apoptosis in hippocampal CA1 area by TUNEL method, and the apoptosis index was calculated. Six mice in each group were randomly selected and sacrificed at 1 day after mechanical ventilation, and the hippocampal tissues were taken for determination of the expression of TRPV4, serine-threonine protein kinase (Akt), phosphorylated Akt (p-Akt), Bcl-2, Bax and caspase-3 by Western blot. Results:Compared with group C, the escape latency was significantly prolonged and the number of crossing the original platform was reduced at 3 and 7 days after mechanical ventilation, the expression of TRPV4 and caspase-3 was up-regulated, the ratio of Bcl-2/Bax was decreased, and the apoptosis index of neurons was increased in group V and group DG ( P<0.05). Compared with group V, the escape latency was significantly shortened and the number of crossing the original platform was increased at 3 and 7 days after mechanical ventilation, the expression of TRPV4 and caspase-3 was down-regulated, the expression of p-Akt was up-regulated, the ratio of Bcl-2/Bax was increased, and the apoptosis index of neurons was decreased in group D and group H ( P<0.05). Compared with group D, the escape latency was significantly prolonged at 3 and 7 days after mechanical ventilation, the number of crossing the original platform was reduced, the expression of TRPV4 and caspase-3 was up-regulated, the expression of p-Akt was down-regulated, the ratio of Bcl-2/Bax was decreased, and the apoptosis index of neurons was increased in group DG ( P<0.05). Conclusions:TRPV 4 is involved in dexmedetomidine-induced improvement in cognitive function, which is related to up-regulation of p-Akt expression and inhibition of apoptosis in hippocampal neurons in mice with mechanical ventilation-caused brain injury.
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Objective:To investigate the effect of baicalin on cognitive function of mice with brain injury induced by mechanical ventilation and its mechanism.Methods:Seventy two C57BL6 mice, weighing 20-25 g, aged 8-12 weeks, were randomly divided into control group (group C), mechanical ventilation group (group V), baicalin group (group B), baicalin+ Akt inhibitor MK-2206 group (group BM) according to random number table method, with 18 in each group.Mice in group C did not have mechanical ventilation and breathed air independently for 6 hours.Mice in group V received mechanical ventilation for 6 hours.Mice in group B and group BM were intraperitoneally injected with baicalin 100 mg/kg 30 minutes before mechanical ventilation, and mice in group BM were injected intraventricular with Akt inhibitor MK-2206 300 μg/kg 60 minutes before mechanical ventilation.Six mice in each group were randomly selected to test their learning and memory abilities by Morris water maze test 1st day before mechanical ventilation and 3rd day and 7th day after mechanical ventilation.One day after mechanical ventilation, six mice in each group were killed, and the brain tissue was taken.TUNEL method was used to detect the neuronal apoptosis in hippocampal CA1 area, and the apoptosis index was calculated.One day after mechanical ventilation, six mice in each group were killed, and the hippocampus was taken, Western blot was used to detect the protein expressions of caspase-3, caspase-9, Akt, p-Akt, GSK-3β and p-GSK-3β.SPSS 22.0 software was used for statistical analysis of data, repeated measure ANOVA and one-way ANOVA were used for comparison between multiple groups.LSD- t test was used for further pairwise comparison. Results:The results of water maze test showed that the time and group interaction of the four groups were not significant ( F=1.14, P>0.05), the main effect of time and group were both significant ( F=47.36, 59.65, both P<0.05). At 3rd day and 7th day after mechanical ventilation, the escape latencies of mice in group V were higher than those in group C (both P<0.05), and the numbers of platform crossing were lower than those in group C (both P<0.05). And 3 days and 7 days after mechanical ventilation, the escape latencies of mice in group B were lower than those in group V (both P<0.05) and the numbers of platform crossing were higher than those in group V (both P<0.05). The escape latenies of mice in BM group on the 3rd and 7th day were higher than those in group B (both P<0.05), and the numbers of platform crossing were lower than those in group B on the 3rd day and 7th day after mechanical ventilation(both P<0.05). TUNEL and Western blot results showed that apoptosis index of hippocampal neurons and expression levels of apoptosis-related proteins caspase-3 and caspase-9 were significant different in the four groups ( F=51.42, 41.21, 40.19, all P<0.05). The apoptosis index of hippocampal neurons ((40.6±3.9)%), the expression levels of caspase-3 (4.93±0.92) and caspase-9 (4.81±0.88) in the hippocampus of mice in group V were higher than those in group C ((13.7±1.4)%, (1.87±0.27), (1.71±0.25), all P<0.05), the apoptosis index of hippocampal neurons ((15.6±1.6)%), the expression levels of caspase-3 (1.95±0.30) and caspase-9 (1.76±0.28) in group B were lower than those in group V ((40.6±3.9)%, (4.93±0.92), (4.81±0.88), all P<0.05), the apoptosis index of hippocampal neurons ((27.8±2.7)%), the expression levels of caspase-3 (3.58±0.61) and caspase-9 (3.49±0.57) in BM group were higher than those in group B ((15.6±1.6)%, (1.95±0.30), (1.76±0.28), all P<0.05). Expression level of p-Akt, p-GSK-3β in hippocampal tissues of the four group of mice were significantly different ( F=37.54, 43.23, both P<0.05). The expression level of p-Akt (0.51±0.06) and p-GSK-3β (0.47±0.05) of hippocampal tissues of mice in group V were lower than those of group C ((1.07±0.10), (1.11±0.12), both P<0.05), the expression level of p-Akt (0.99±0.10) and p-GSK-3β (1.08±0.09) of hippocampal tissues of mice in group B were higher than those of group V (both P<0.05), the expression level of p-Akt (0.83±0.08) and p-GSK-3β (0.81±0.07) of hippocampal tissues of mice in group BM were lower than those in group B (both P<0.05). Conclusion:Baicalin can improve the cognitive function of mice with brain injury induced by mechanical ventilation, which is related with activation of Akt/GSK-3β signaling pathway and inhibition of hippocampal neuron apoptosis.
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Objective:To evaluate the effects of dexmedetomidine on alveolar epithelial barrier function in rats with ventilator-induced lung injury (VILI), and the role of protein kinase C (PKC).Methods:One hundred clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 5 groups ( n=20 each) using a random number table method: control group (group C), VILI group (group V), PKC inhibitor group (group B), dexmedetomidine group (group D), and dexmedetomidine plus PKC agonist group (DP group). The VILI model was developed by mechanical ventilation with a tidal volume of 40 ml/kg for 4 h in anesthetized animals.Group C breathed air autonomously for 4 h without mechanical ventilation.Group V was mechanically ventilated for 4 h. In group B, bisindolvlmaleimide I 0.12 mg/kg was injected intramuscularly 1 h before mechanical ventilation.In D and DP groups, dxmedetomidine 5.0 μg/kg was injected intravenously at 20 min before mechanical ventilation, and dexmedetomidine was intravenously infused at the rate of 5.0 μg·kg -1·h -1 during mechanical ventilation.In group DP, PKC agonist phorbol-12-myristic acid-13-acetate 15 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation.At 4 h of mechanical ventilation, oxygenation index (OI), lung permeability index (LPI) and wet/dry lung weight (W/D) ratio were measured, the pathological changes of lung tissues were observed, and lung injury was assessed and scored.The expression of PKC, occludin and ZO-1 protein was detected by Western blot, and the expression of PKC mRNA, occludin mRNA and ZO-1 mRNA was determined by real-time polymerase chain reaction. Results:Compared with group C, OI was significantly decreased, LPI, W/D ratio and lung injury score were increased, the expression of PKC protein and mRNA was up-regulated, and the expression of occludin and ZO-1 protein and mRNA was down-regulated in V and DP groups ( P<0.05), and no significant change was found in the parameters mentioned above in B and D groups ( P>0.05). Compared with group V, OI was significantly increased, LPI, W/D ratio and lung injury score were decreased, the expression of PKC protein and mRNA was down-regulated, and the expression of occludin and ZO-1 protein and mRNA was up-regulated in B, D and DP groups ( P<0.05). Compared with group D, OI was significantly decreased, LPI, W/D ratio and lung injury score were increased, the expression of PKC protein and mRNA was up-regulated, and the expression of occludin and ZO-1 protein and mRNA was down-regulated in group DP ( P<0.05). Conclusions:Dexmedetomidine can reduce the damage to alveolar epithelial barrier function in rats with VILI, and the mechanism is related to inhibition of PKC activation and up-regulation of the expression of occludin and ZO-1.
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Objective:To evaluate the role of transient receptor potential vanilloid receptor 1 (TRPV1)/nuclear factor-κB (NF-κB) signaling pathway in dexmedetomidine-induced alleviation of ventilator-induced lung injury (VILI) in rats.Methods:One hundred clean-grade healthy male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 5 groups ( n=20 each) using a random number table method: control group (group C), VILI group (group V), AMG9810 group (group A), dexmedetomidine group (group D), and dexmedetomidine + RTX group (group DR). VILI model was prepared by mechanical ventilation with a tidal volume of 40 ml/kg for 4 h. In group A, TRPV1 inhibitor AMG9810 30 mg/kg was intraperitoneally injected at 1 h before mechanical ventilation.Dexmedetomidine 5.0 μg/kg was intravenously infused at 20 min before mechanical ventilation, and dexmedetomidine was intravenously infused at the rate of 5.0 μ g·kg -1·h -1 during ventilation in group D and group DR.In group DR, RTX 70 μ g/kg was intraperitoneally injected for 3 consecutive days before mechanical ventilation.At 4 h of mechanical ventilation, the concentrations of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and IL-6 in bronchoalveolar lavage fluid (BALF) were detected, oxygenation index (OI) and wet/dry lung weight (W/D) ratio were measured, the histopathological changes of lung tissues were observed, and lung injury was assessed and scored.The expression of TRPV1 and NF-κB in lung tissues was detected by Western blot, and real-time polymerase chain reaction was used to detect the expression of TRPV1 and NF-κB mRNA. Results:Compared with group C, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly increased, OI was decreased, the W/D ratio and lung injury scores were increased, and the expression of TRPV1 and NF-κB protein and mRNA was up-regulated in group V ( P<0.05). Compared with group V, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly decreased, OI was increased, the W/D ratio and lung injury scores were decreased, and the expression of TRPV1 and NF-κB protein and mRNA was down-regulated in A, D and DR groups ( P<0.05). Compared with group D, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly increased, OI was decreased, the W/D ratio and lung injury scores were increased, and the expression of TRPV1 and NF-κB protein and mRNA was up-regulated in group DR ( P<0.05). Conclusions:The mechanism by which dexmedetomidine alleviates VILI is partially related to inhibition of the activation of TRPV1/NF-κB signaling pathway and inhibition of the inflammatory responses in lung tissues of rats.
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OBJECTIVE:To in vestigate the effects of dexmedetomidine (Dex)on SIRT 1/Akt/GSK3β/β-catenin signaling pathway in cerebral injury of sepsis model rats ,and explore the mechanism of its protecitve effect on cerebral injury. METHODS : A total of 80 male SD rats were randomly divided into sham operation group (Sham group ),sepsis group (CLP group ),CLP+Dex group(10 μg/kg Dex),CLP+Dex+Sirtinol group (10 μg/kg Dex+2 μL/100 g SIRT 1 inhibitor sirtinol ),with 20 mice in each group. Two hours before modeling ,CLP+Dex+Sirtinol group was injected with sirtinol via lateral ventricle. Sepsis model was induced by cecal ligation and perforation in each group (in sham group ,only operation was performed but no ligation was performed). At 0,3,6 h after modeling ,CLP+Dex group and CLP+Dex+Sirtinol group were given Dex (10 μg/kg) intraperitoneally,Sham group and CLP group were given constant volume of normal saline intraperitoneally. Cerebral tissue water content,Evans blue (EB)content,apoptosis in cerebral cortex ,the levels of IL- 1β and TNF-α in cerebral tissue as well as the protein expression of SIRT 1,p-Akt,p-GSK3β and β-catenin in hippocampus were detected 24 h after last medication. RESULTS : Compared with Sham group ,cerebral tissue water content ,EB content ,the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were increased significantly(P<0.05),while the protein expression of SIRT 1, p-Akt,p-GSK3β and β-catenin in hippocampus were decreased significantly (P<0.05). Compared with CLP group ,cerebral tissue water content ,EB content ,the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were decreased significantly in CLP+Dex group (P<0.05),while the protein expression of SIRT 1,p-Akt,p-GSK3β and β-catenin in hippocampus were increased significantly (P<0.05). Sirtinol could significantly reverse the above-mentioned cerebral protection and factor regulation effects of Dex (P<0.05). CONCLUSIONS :Dex can protect the cerebral tissue of sepsis model rats,which may play an anti-inflammatory and anti-apoptotic role by activating SIRT 1/Akt/GSK3β/β-catenin signaling pathway ,so as to reduce cerebral edema ,protect blood-brain barrier and reduce cerebral injury.
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Objective To establish a reliable pretreatment method for the detection of mequindox and its metabolite in pork luncheon meat by ultra-performance liquid chromatography/triple qudrupole tandem mass spectrometry. Methods Samples were extracted with ethyl acetate, and the results of purification and enrichment by PAX and PEP solid-phase extraction columns were analyzed. Acetonitrile/methanol (3:11) - 0.1% formic acid water was used as the mobile phase, and Shimadzu Inertsil ODS-3-column (3µm, 2.1 × 100mm) chromatographic columns were used for qualitative and quantitative analysis using the multi-reaction detection positive ion mode. Results The results showed that PEP cartridge had good recovery rate. The detection limit of mequindox was 0.10µg/kg, and limit of quantitation was 0.30µg/kg. The average recoveries for spiked levels of 0.33, 0.83, and 1.65µg/kg were 127%, 72.0%, and 60.1%, respectively. The detection limit of 2-quinoxalinecarboxylic acid was 0.10µg/kg, and limit of quantitation was 0.40µg/kg. The average recoveries for spiked levels of 0.42, 1.05, and 2.1µg/kg were 125%, 99.0%, and 60.9%, respectively. Conclusion This method is suitable for the determination of mequindox and its metabolite 2-quinoxalinecarboxylic acid in luncheon meat.
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Objective:To evaluate the effect of dexmedetomidine on the extracellular signal-regulated kinase(ERK)/sodium-potassium ATPase(Na + -K + -ATPase)signaing pathway in lung tissues of rats with mechanical ventilation-induced lung injury (VILI). Methods:Forty-eighty clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 4 groups ( n=12 each) using a random number table method: control group (group C), VILI (alpha2-adrenergic receptor antagonist) group (group V), dexmedetomidine group (group D), and dexmedetomidine plus yohimbine group (group DY). Group C underwent no mechanical ventilation and breathed air spontaneously for 4 h. Mechanical ventilation (respiratory rate 40 breaths/min, tidal volume 40 ml/kg, inspiratory/expiratory ratio 1∶1, PEEP 0, fraction of inspired oxygen 21%) lasted 4 h in group V. Dexmedetomidine was infused intravenously in a dose of 5.0 μg/kg at 20 min before ventilation followed by an infusion of 5.0 μg·kg -1· h -1 throughout ventilation in group D. In group DY, yohimbine 0.1 mg/kg was injected intravenously at 10 min before dexmedetomidine, and the other treatments were similar to these previously described in group D. Blood samples and lung tissues were taken at 4 h of mechanical ventilation to determine the wet/dry weight ratio (W/D ratio), lung permeability index (LPI), alveolar fluid clearance rate (AFC), and expression of extracellular signal-regulated kinase (ERK), phosphorylated extracellular signal-regulated kinase (p-ERK), and Na + -K + -ATPase in lung tissues (by Western blot) and to observe pathological changes of lung tissues. Results:Compared with group C, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, and Na + -K + -ATPase expression was down-regulated in group V and group DY ( P<0.05), and no significant change was found in the incidence of the parameters mentioned above in group D ( P>0.05). Compared with group V, LPI and W/D ratio were significantly decreased, AFC was increased, p-ERK expression was down-regulated, Na + -K + -ATPase expression was up-regulated ( P<0.05), and the pathological changes of lung tissues were significantly attenuated in group D, and no significant change was found in the incidence of the parameters mentioned above in group DY ( P>0.05). Compared with group D, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, Na + -K + -ATPase expression was down-regulated ( P<0.05), and the pathological changes of lung tissues were accentuated in group DY. Conclusion:The mechanism by which dexmedetomidine alleviates VILI may be related to activating alpha2-adrenergic receptors and inhibiting ERK/Na + -K + -ATPase signaling pathway in rats.
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Objective To investigate the effectiveness of predicting the incidence of supine hy-potension syndrome (SHS)after spinal anesthesia measured by ultrasonic measurement of the varia-tion of brachial artery peak velocity in different positions of parturient.Methods Parturient scheduled for elective cesarean section,ASA physical status Ⅰ or Ⅱ,were divided into SHS group and no-SHS group (SBP in the upper extremity decreased by > 30 mm Hg or decreased to < 80 mm Hg)after spinal anesthesia.HR,SBP,DBP of supine position and left lateral position before anesthesia were re-corded,and brachial artery peak velocity were measured by Ultrasonic.The differences of the above indexs before and after the transformation position were calculated.The receiver operating characteris-tic curve (ROC)was plotted by indexs of which P values were less than 0.05,to evaluate the predic-tive effect of each index on SHS after spinal anesthesia.Results Among the 196 patients,89 cases (45.4%)developed SHS after spinal anesthesia.SBP,DBP,peak velocity of brachial artery (Vpmin) and brachial artery peak velocity variation (ΔVp)were different before and after the transformation position (P<0.05).The difference in SHS group was significantly higher than no-SHS group.The areas under ROC curve (AUC)of ΔSBP,ΔDBP,ΔVpmin,ΔΔVp were 0.711 (95%CI 0.575-0.846), 0.573 (95%CI 0.419-0.727),0.948 (95% CI 0.895-0.987),0.864 (95% CI 0.770-0.958),and the cut-off values were 17.5 mm Hg,7.6 mm Hg,17.8 cm/s,and 13.1%.Conclusion The differ-ence of brachial artery peak velocity measured by ultrasonic in different positions of parturient can ef-fectively predict the occurrence of SHS,in which ΔVpmin≥ 17.8 cm/s has better predictive effect.
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OBJECTIVE:To explore the effects and safety of atorvastatin combined with probucol on the vascular elasticity in patienits with hypertension. METHODS:246 hypertensive patients were randomly divided into control group and observation group,123 cases in each group. All patients received conventional antigypertensive treatment,based on it,control group was given 10 mg Atorvastatin tablet,qd;observation group was additionally given 0.25 g Probucol tablet,qd,on the basis of control group. They were treated for 1 year. Clinical efficacy,lipid levels(total cholesterol,triglyceride,low density lipoprotein cholesterol,high density lipoprotein cholesterol),cystatin C (Cys-C),C-reactive protein (CRP),elastic parameters of common carotid artery and lower limb artery(stiffness,pressure-strain elastic modulus,compliance,augmentation index,pulse wave velocity)before and af-ter treatment in 2 groups were observed,and the incidence of adverse reactions was compared. RESULTS:Before treatment,there were no significant differences in lipid levels,Cys-C,CRP and elastic parameters of common carotid artery and lower between 2 groups (P>0.05);after treatment,the above-mentioned indexes were significantly improved,and the improvement degree in ob-servation group was superior to control group,the differences were statistically significant(P<0.05). And there were no severe ad-verse reactions during treatment in both 2 groups. CONCLUSIONS:Atorvastatin combined with probucol can improve lipid level and elasticity of common carotid artery and lower limb artery,with good safety.
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The research of the secondary damage remote from middle cerebral artery territory infarction has made significant progress in recent years.More animal experiments from the cellular,biochemical and molecular levels have been performed for in-depth and detailed research on remote site damage. The injury mechanisms such as oxidative damage and β amyloid deposition have been found.The new imaging detection technologies,such as magnetic resonance diffusion tensor imaging(DTI),have gradually been applied to the diagnosis of remote site damage.
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Objective To study clinical efficacy on cesarean scar pregnancy (CSP) treated by transvaginal surgery.Methods From Jan.2008 to Mar.2011,31 cases with CSP were managed by transvaginal surgery in Anshan Women and Children Hospital.Based on ultrasonograpy examination and intraoperative exposure of lesion,variable surgical options were executed.Fifteen cases in group A were treated by debridement resection and vaginal repair of uterine wall,7 cases in group B were treated by transvaginal uterine artery ligation and curettage,9 cases were treated by cutting the anterior wall in the lower uterine segment and repairing uterine.The intraoperative blood loss,operation time,hospital stay,hCG fluctuation at postoperative period and complications were analyzed among those groups.Results Allcases in 3 groups were cured well in one time.( 1 ) The intraoperative blood loss were (41 ±21 ) ml in group A,(27 ±7) ml in group B and ( 148 ± 132) ml in group C.There was no statistically different blood loss between group A and group B ( P > 0.05 ),however,the amount blood loss in group C was significantly more than those in group A and group B ( P < 0.05 ).( 2 ) The average surgical time,the mean hospital stay,postoperative recovery time of blood hCG were (40 ± 11 ) minutes,(4.7 ± 0.8 ) days and ( 2.7 ± 1.0) weeks in group A,(44 ± 5 ) minutes,(4.0 ± 0.8) days and (2.9 ± 1.0) weeks in group B,(40 ± 12) minutes,(4.9 ± 1.0) days and (2.8 ±0.9) weeks in group C.Those clinical index were no statistically different among those 3 groups(P >0.05).(3) No bladder injury and other complications were observed in those groups.Conclusions Transvaginal surgery is efficacy,easy to operate,to keep the uterus,safe and economy in treatment of CSP.Surgery in group A is suitable to treat early and exogenous lesions; surgery in group B is suitable to treat endogenous lesions; surgery in group C is suitable to treat failure cases in group A and B,however,the injury is greater than those in group A and B.
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Objective To investigate the effects of electric stimulation on motor function and expression of Rho kinase following cerebral infarction in rats. Methods Acute cerebral infarction was modeled in adult male Sprague-Dawley ( SD) rats using the permanent middle cerebral artery occlusion ( PMCAO) technique. The rats were randomly divided into sham operation, control, unilateral electric stimulation and bilateral electric stimulation groups ( each group had 36 rats). Electric stimulation was applied to the paralyzed ( unilateral or bilateral) limbs in the last two groups. Motor function recovery and the expression of Rho kinase were examined using a beam walking test ( BWT) and immunohistochemistry respectively at the 3rd, 7th, 14th and 21st day after stimulation. In addition, the cerebral infarction volume was also determined by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining at different time points. Results Motor function improved significantly in the electric stimulation groups compared with the control group, and the effect in the bilateral electric stimulation group was better than that in the unilateral electric stimulation group. The expression of Rho kinase decreased remarkably in the electric stimulation groups, and it was significantly lower in the bilateral group than in the unilateral electric stimulation group. No difference in cerebral infarction volume was found at the 3rd day. At the 21st day, the cerebral infarction volume had decreased significantly in both stimulation groups compared with the control group, but no difference was seen between the unilateral and bilateral electric stimulation groups. Conclusions Early electric stimulation, especially bilateral electric stimulation, can improve motor function after cerebral infarction and reduce cerebral infarction volume, which may be associated with down-regulation of the expression of Rho kinase in the border zone of the infarction.
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Objective To investigate the effects of unilateral and bilateral electrical stimulation of the upper and lower limbs on motor function following cerebral infarction and the expressions of microtubule-associated protein-2 (MAP-2) and survivin in the infarction border zone of rats. Methods Adult male Sprague-Dawley (SD) rats were randomly divided into sham operation, control, impaired limb and bilateral limbs electrical stimulation groups (each group included 32 rats). Acute cerebral infarction was mimicked using a middle cerebral artery occlusion tech-nique. After cerebral infarction for 24 h, the rats were treated daily with or without electrical stimulation. A beam walking test (BWT) was used to measure limbs motor function and immunohistochemistry and HE staining were used to detect the expressions of MAP-2 and survivin in the border zone of infarcted area after electrical stimulation treat-ment for 3, 7, 14 and 21 d. Results Comparet with the control group treatment with electric stimulation led to BWT scores increasing significantly, and bilateral stimulation was more potent in ameliorating motor function thanstimulating the impaired limb only. The expression of MAP-2 was significantly higher in eleetrieal stimulation groups than in control group from the 7th of treatment, and it was higher in bilateral stimulation group than that in unilateral stimulation group from tbe 14th day of treatment. There was no significant difference in MAP-2 expression between bi-lateral stimulation group and sham operation group at the 21st day of treatment. In electrical stimulation groups, at every time point the expressions of survivin were obviously higher than that in sham operation group, and it was higher than that in control group and peaked at the 7tb and 14th day of treatment and in bilateral stimulation group it was no-tably higher than that in unilateral stimulation group. At the 21st d of treatment the level of survivin expression drop-per; however, there was no significant difference between unilateral and bilateral electrical stimulation groups. Con-clusions Treatment with electrical stimulation, particularly in bilateral limbs stimulation, could induce MAP-2 and survivin expressions in the infarction border zone of rats. It also could promote the recovery of motor function in para-lyzed limbs after cerebral infarction of rats. The improvement might involve the up-regulation of MAP-2 and survivin expressions.
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OBJECTIVE To standard operating room hospital infection monitoring management,to guarantee the management effect of perioperation hospital infection.METHODS Based on standardized,systematized,sequenced theory and idea.The operating room hospital infection supervisory system plan were for mulated.Including:hospital infection monitoring of operation room,test result analysis,and monthly report system.RESULTS We had grasped the key the link,during operating room scale expansion.The prompt establishment perfect special control system,monitoring the perioperation hospital infection effectively,received highly praise.CONCLUSIONS Sysmatic mornitoring and scientific control and good adaptive team.Can guarantec continualls improvement.
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Objective To investigate the risk factors of cerebral palsy in newborns with periventricular leukomalacia(PVL).Methods Sixty-one infants with sequela of cerebral palsy among 806 neonates born at the Second People'S Hospital of Liaocheng,Shandong,China,during December 2000 to November 2005 were studied for its etiology.Diagnosis of cerebral palsy in 26 of the 61 infants was established by type B ultrasonic scanning or magnetic resonance imaging(MRI)for the head at least twice and excluded of other diseases.Thirty-five infants without PVL hospitalized at the same hospital were enrolled as control group during the same period.Logistic regression analysis was performed for the risk factors of PVL. Results Twenty-six infants were diagnosed as PVL.accounting for 42.6%of those with cerebral palsy.Main high-risk factors of PVL included severe asphyxia(x3),low gestational age(x1),intraventricular hemorrhage(x14)and low blood pressure(x8),with odds ratios of 2.843,3.575,3.268 and 1.947,respectively,and a fitted regression model as logistic(P)=β0+0.7952 x3-1.428x1-1.328 x14+0.8256x8.Pregnant hypertension,neonate respiratory distress syndrome(NRDS),and intrauterine infection could also affect occurrence of PVL,all with statistical significance(P<0.05).Conclusion PVL is one of main causes of cerebral palsy,with severe asphyxia,low gestational age,intraventricular hemorrhage and low blood pressure as main high-risk factors.
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We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.
Subject(s)
Base Sequence , China , Cluster Analysis , Gene Components , Genetic Variation , Genome, Viral , Genotype , Molecular Sequence Data , Phylogeny , Reverse Transcriptase Polymerase Chain Reaction , Severe acute respiratory syndrome-related coronavirus , Genetics , Sequence Analysis, DNA , Severe Acute Respiratory Syndrome , GeneticsABSTRACT
Heme is a key cofactor in aerobic life, both in eukaryotes and prokaryotes. Because of the high reactivity of ferrous protoporphyrin IX, the reactions of heme in cells are often carried out through heme-protein complexes. Traditionally studies of heme-binding proteins have been approached on a case by case basis, thus there is a limited global view of the distribution of heme-binding proteins in different cells or tissues. The procedure described here is aimed at profiling heme-binding proteins in mouse tissues sequentially by 1) purification of heme-binding proteins by heme-agarose, an affinity chromatographic resin; 2) isolation of heme-binding proteins by SDS-PAGE or two-dimensional electrophoresis; 3) identification of heme-binding proteins by mass spectrometry. In five mouse tissues, over 600 protein spots were visualized on 2-DE gel stained by Commassie blue and 154 proteins were identified by MALDI-TOF, in which most proteins belong to heme related. This methodology makes it possible to globally characterize the heme-binding proteins in a biological system.
Subject(s)
Animals , Mice , Carrier Proteins , Genetics , Electrophoresis, Gel, Two-Dimensional , Electrophoresis, Polyacrylamide Gel , Heme , Chemistry , Hemeproteins , Genetics , Mass Spectrometry , Mice, Inbred ICR , Protein Binding , Proteins , Chemistry , Proteome , Proteomics , Methods , Sepharose , Chemistry , Tissue DistributionABSTRACT
Expressed Sequence Tag (EST) analysis has pioneered genome-wide gene discovery and expression profiling. In order to establish a gene expression index in the rice cultivar indica, we sequenced and analyzed 86,136 ESTs from nine rice cDNA libraries from the super hybrid cultivar LYP9 and its parental cultivars. We assembled these ESTs into 13,232 contigs and leave 8,976 singletons. Overall, 7,497 sequences were found similar to existing sequences in GenBank and 14,711 are novel. These sequences are classified by molecular function, biological process and pathways according to the Gene Ontology. We compared our sequenced ESTs with the publicly available 95,000 ESTs from japonica, and found little sequence variation, despite the large difference between genome sequences. We then assembled the combined 173,000 rice ESTs for further analysis. Using the pooled ESTs, we compared gene expression in metabolism pathway between rice and Arabidopsis according to KEGG. We further profiled gene expression patterns in different tissues, developmental stages, and in a conditional sterile mutant, after checking the libraries are comparable by means of sequence coverage. We also identified some possible library specific genes and a number of enzymes and transcription factors that contribute to rice development.
Subject(s)
Arabidopsis , Genetics , DNA, Complementary , Metabolism , Databases as Topic , Expressed Sequence Tags , Gene Library , Genome, Plant , Genomics , Methods , Multigene Family , Open Reading Frames , Oryza , Genetics , Quality Control , SoftwareABSTRACT
ObjectiveTo investigate the gene expression of Chk1 gene in cerebrum after brain ischemia-reperfusion,trying to provide evidence to elucidatethe molecular mechanism of brain injury. MethodsEighty-five male Wistar rats were divided into 3 groups. Group Ⅰ served as normal control. In group Ⅱ (non-ischemia group) animals underwent the whole experimental procedures except the occlusion of the bilateral vertebro-arteries and common carotid arteries. In group Ⅲ(ischemiareperfusion group) animals were further divided into 3 subgroups according to the duration of ischemia: 10min, 30min and 60min. Each subgroup was again further divided based on the duration of reperfusion: 30min, 2h and 6h. The cerebrum was immediately removed from rats after complete brain ischemiareperfusion. The RNA was isolated and the reverse-transcription-polymerase chain reaction (RT-PCR) was carried out . The cDNA was analyzed by automatic system and the parameters were assessed to define the status of Chk1 mRNA expression in different ischemia and reperfusion groups. ResultsThe quantity of Chk1 mRNA expression in the cerebral cortex of normal adult rat was about half of the glyceraldehyde-3-phosphatedehydrogenase. When reperfused for 30min, 2h or 6h following 10min, 30 min cerebral ischemia and reperfused for 30min or 2h following 60 min cerebral ischemia, the expression of Chk1 mRNA was not significantly different from that in non-ischemia group. Only reperfused for 6h following 60 min cerebral ischemia, Chk1 mRNA expression decreased significantly. ConclusionsThe results indicate that Chk1 gene might be involved in molecular mechanism of cerebrum damage during complete global brain ischemia- reperfusion.