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Objective To explore the effect of enriched environment on the level of NR2A and NR2B subunits of N-mehyl-D-aspartate (NMDA) receptors which belong to glutamate receptors with excitability at the 17th area of the visual cortex in amblyopia rats after the critical period,and to understand the possible mechanism of synaptic plasticity of the visual cortex in adult amblyopia rats.Methods Eighty Wistar rats were divided into normal group and experimental group by random number table.Right eyelids of all rats were sutured through the whole critical period in order to establish monocular deprivation (MD) amblyopia model.The rats in experimental group were divided into the amblyopia group,standard environment (SE) group and environmental enrichment (EE) group on P45 in random.The sutured right eyelids were opened on P46 in the SE group and EE group.All rats were sacrificed to get the 17th area of the left visual cortex on P60,P75 and P105.Three rats were used at different time points from each group.The Ⅰ-Ⅵ layers of the visual cortex area 17 were observed by using hematoxylin-eosin staining.The expression of NMDA-NR2A and NMDA-NR2B was detected by immunohistochemistry.Integrated optical density of NMDA-NR2A and NMDA-NR2B was detected by using special image analysis software (Image-Pro Plus 6.0).The use of animals complied with Regulation on the Managenment Experimental Ainimals from Shandong Eye Institute and Association for Research in Vision and Ophthalmology (ARVO).Results The positive expression of NMDA-NR2A and NMDA-NR2B were observed in the visual cortex.The positive cells were mostly round or elliptical and mainly expressed in cell membrane.The expression of NMDA-NR2A in P60,P75 and P105 from four groups had statistical differences (all at P＜0.05).There were less positive cells in amblyopia group and EE group than normal control group on P60,P75 and P105,while there were more positive cells in EE group than amblyopia group.Amblyopia can lead to reduced NMDA-NR2A expression in the visual cortex.The expression of NMDA-NR2A was stronger than that in the amblyopia group by intervention 15 days,30 days,and 60 days with the rich environments,but did not reach the normal level (all at P＜0.05).The expression of NMDA-NR2B in P60,P75 and P105 from four groups also had statistical difference (all at P＜0.05).There were more positive cells in amblyopia group than those in normal control group on P60,P75 and P105.There were more positive cells in EE group than normal control group on P60,while there were equal positive cells in EE group and normal control group on P75 and P105.Amblyopia can lead to increase NMDA-NR2B expression in the visual cortex.The expression of NMDA-NR2B was weaker than that in the amblyopia group by intervention 15 days with the rich environments,but did not reach the normal level (all at P＜ 0.05).The expression of NMDA-NR2B after intervention 30 days and 60 days reached the normal levels (all at P＞ 0.05).Conclusions The plasticity of visual cortex exists not only in the critical period but also after the critical period of visual development.EE,as a non-invasion method,can improve and recover the synaptic plasticity in visual cortex of adult rats by the expression of NMDA-NR2A and NMDA-NR2B.
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Objective To evaluate the effect of electroacupuncture ( EA) preconditioning on hipp-ocampal I-kappa B-α ( IκB-α)∕nuclear factor κB ( NF-κB)∕intercellular adhesion molecule-1 ( ICAM-1) signaling pathway during cerebral ischemia-reperfusion ( I∕R) in mice. Methods A total of 120 healthy male C57BL∕6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups ( n=30 each) u-sing a random number table method: control group ( group C) , cerebral I∕R group ( group I∕R) , precondi-tioning with EA at non-acupoint+cerebral I∕R group ( group S+I∕R) and preconditioning with EA at Baihui acupoint + cerebral I∕R group ( group E+I∕R) . The cerebral I∕R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I∕R. Group S+I∕R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I∕R injury model was established. Group E+I∕R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz∕15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I∕R injury model was established. Neurobe-havioral score was assessed at 24 and 48 h of reperfusion. Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the patho-logical changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 ( IL-6) , IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly in-creased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1βprotein and mRNA was up-regulated in I∕R, S+I∕R and E+I∕R groups ( P<0. 05) . Compared with group I∕R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R (P<0. 05), and no significant change was found in the parameters mentioned above in group S+I∕R (P>0. 05). Compared with group S+I∕R, neu-robehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R ( P<0. 05) . Conclusion The mechanism by which EA preconditioning attenuates cerebral I∕R injury may be related to inhibiting activation of hippocampal IκB-α∕NF-κB∕ICAM-1 signaling pathway in mice.
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Objective To investigate the status quo of job-family and family-job conflicts among the nursing of the operating room nurses.Method A total of 190 nurses from an operating room participated in the survey by demographic questionnaire and work-family conflict scale.Results The average score on job-family was (3.15 ± 0.48) and there were significant differences between family-job conflict and job-family (2.75 ± 0.27 vs.3.55 ± 0.61) (t =-10.349,P＜0.05).There were significant differences in job-family conflict scores (P ＜0.05) in view of different age,working years,professional titles,number of night shifts per month,marital status and daily working hours.There were significant differences in family-job conflict subscale scores (P＜0.05).Conclusions The job-family conflicts of the nurses in the operating room is at the middle level.The perceived job-family conflict is higher than that of the family-job conflict.Such factors as age,length of work,professional tide,number of night shifts per month,marital status and daily working hours can lead to job-family conflict among the operating room nurses.The nursing administrative should displace nursing personnel and optimize the shifts so as to reduce the rate of job-family conflicts.
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Objective To evaluate the relationship between the level of AMP-activated protein kinase (AMPK) in hippocampus and cognitive dysfunction after splenectomy in aged rats.Methods Sixty-three male aged Sprague-Dawley rats,weighing 480-550 g,were randomly divided into 3 groups (n =21 each):control group (group C),anesthesia group (group A),and surgery group (group S).Morris water maze (MWM) test was performed to evaluate the spatial learning and memory ability before surgery and at 1,3 and 7 days after surgery.The escape latency and swimming distance were recorded.Seven rats were chosen after MWM test was performed at 1,3 and 7 days after surgery and sacrificed.Their hippocampi were removed for detection of the expression of AMPK and phosphorylated (p-AMPK) (by Western blot).Results Compared with the baseline,the escape latency and swimming distance were significantly prolonged at 1 and 3 days after surgery in group S (P ＜ 0.05).Compared with group C,the escape latency and swimming distance were significantly prolonged at 1 and 3 days after surgery,the expression of AMPK was up-regulated at 1,3 and 7 days after surgery,and the expression of p-AMPK was up-regulated at 1 and 3 days after surgery in group S (P ＜ 0.05),and no significant changes were found in the indices mentioned above in group A (P ＞ 0.05).Conclusion Increased AMPK level in hippocampus is the regulatory mechanism of the body adapting to the development of cognitive dysfunction after splenectomy in aged rats.