近年来,随着商业银行业务发展和信息技术的丰富,运用数字化信息对绩效考核进行有效的管理、评价和分析已上升到战略管理层面.绩效考核系统(MPI)作为银行经营管理的综合评价系统,通过引入数据仓库技术作为技术手段和管理工具,能够更加灵活地实现各项指标考核,并保持各项考核数据在不同管理层级之间能够相互协调一致、高效动作,在较短的时间内将准确的信息传递到正确的人,为管理层制定相关政策提供决策依据,同时也能将管理层的政策意图下达到各机构及相关责任人.

Background Acute ischemic stroke causes long-term neurological and neurobehavioral dysfunctions. With the development of clinical medicine, the importance of pre-ischemic exercise intervention has been gradually recognized, but its mechanism remains to be further explored. Objective This study investigates the effects of different exercise intensity preconditioning in changes of hippocampal neurons and the expression of Gadd45β and DNA-PKcs in the hippocampal region after cerebral ischemia-reperfusion in rats. Method 160 SD rats were divided into control group (n=40), cerebral ischemia reperfusion group (I/R group, n=40), middle intensity exercise preconditioning group (EI 1+I/R group, n=40), high intense exercise preconditioning group (EI 2+I/R group, n=40). Stroke was induced by improved Pulsinelli four blood vessel blocking after exercise preconditioning. Morphological changes of neurons in the hippocampal region of rats were observed by HE staining at 6 h, 1d, 3d and 7d after ischemia in each group. Immunohistochemistry method was used to detect the expression of Gadd45β and DNA-PKcs in hippocampus CA1. The mRNA level of Gadd45β and DNA-PKcs in hippocampal CA1 was detected by Real Time PCR. Results Compared with I/R group, the neuronal cell necrosis of was alleviated in EI 1+I/R group, but more serious in EI 2+I/R group; The expression of Gadd45β and DNA-PKcs were significantly higher in the EI 1+ I/R group, but lower in EI 2+I/R group (P<0.01). Conclusion Moderate intensity exercise preconditioning can improve the survival of neurons after cerebral ischemia-reperfusion injury in rats. However, high-intensity motor preconditioning increased the damage and loss of neurons, and its mechanism may be related to the regulation of the expression of Gadd45β and DNA-PKcs in the hippocampus of cerebral ischemia-reperfusion rats, thus protecting and promoting the function of DNA repair system.

Objective To observe the effect of Tomatis converted auditory training on the executive functioning of breast cancer patients undergoing chemotherapy.Methods Eighty breast cancer patients with the executive dysfunction who were undergoing chemotherapy were divided into a control group and an experimental group,each of 40.The experimental group was given Tomatis high and low frequency auditory training,while the control group was given ordinary music training.The patients in both groups were treated in 4 stages,each of 5 consecutive days with intervals of 21 days.The Chinese Version of the Behavioral Assessment of Dysexecutive Syndrome (BADS) was used to evaluate both groups before and after the intervention,including rule transformation ability,problem solving ability,planning ability,supervising ability and organizing ability.Results After the intervention,the experimental group had a significantly higher average score than before the intervention in the rule-switching card test,the action planning test,the key-finding test,and the modified six-element test.Their average BADS score was also significantly improved.The control group showed a significantly better average score only in the key-finding test and in its average BADS total score.After the intervention,the experimental group had a significantly higher average score than the control group in the rule-switching card test and the action planning and six-element tests.Its average BADS rating was also significantly better.Conclusion Tomatis high and low frequency auditory training can improve the executive function of patients undergoing chemotherapy for breast cancer.Its effect is better than that of ordinary music training.

目的:探讨2型糖尿病db/db小鼠肾脏动态病理特点,阐明其糖尿病肾病的发生发展机制,为糖尿病肾脏并发症的研究提供实验依据.方法:选取SPF级7～8周龄雄性db/db小鼠(模型组)和同龄雄性db/m小鼠(正常组)各16只,分别于8、16和32周龄时检测2组小鼠体质量和空腹血糖(FBG)水平,每组各处死小鼠8只,取肾组织行HE和Masson染色观察其病理形态表现,电镜下观察其超微结构.结果:与正常组比较,模型组小鼠8、16和32周龄时体质量增大(P＜0.01),FBG水平明显升高(P＜0.01),双肾指数明显降低(P＜0.01);32周时模型组小鼠双肾指数明显低于16周时(P＜0.05).HE和Masson染色,16周龄时模型组小鼠肾组织可见明显病理改变,主要是肾小球体积增大和肾小管上皮细胞明显水肿;32周龄时病变明显加重,肾组织中可见大量蓝染胶原物质.电镜观察,16周龄时模型组小鼠肾组织以肾小球基底增厚、足突融合、肾小管上皮细胞线粒体数目减少及形态肿胀为主;32周龄时病变明显加重,可见大量胶原纤维.结论:16周龄糖尿病db/db小鼠肾脏有明显病理改变,主要是肾小球基底增厚、足突融合,32周龄时小鼠肾组织呈明显纤维化.

干细胞是一类能够产生一种或多种特殊细胞类型的 、具有自我更新能力的原始细胞 . 根据来源不同 ,干细胞可分为胚胎干细胞(ESCs)和成体干细胞 (ASCs )[1] . 牙髓干细胞 (DP-SCs)位于牙髓组织内丰富的牙髓细胞中 ,是一种具有自我更新和多向分化潜能的成体干细胞 ,可在不同的培养条件下诱导其发生多向分化 ,进而受到组织工程和再生医学领域的广泛关注 . 本文主要就 DPSCs 的生物学特性及多向分化能力进行简单介绍 .

目的 探讨内皮素A受体拮抗剂BQ-123对蛛网膜下腔出血( SAH)大鼠学习记忆功能的改善作用及机制.方法 成年雄性SD大鼠随机分为Sham组、SAH组和BQ-123组;枕大池二次注血法建立SAH模型,BQ-123组经侧脑室注射BQ-123溶液给药剂量为18 μg;穿梭箱检测大鼠学习记忆功能;HE染色观察海马区神经细胞形态结构变化;免疫组织化学染色检测自噬相关因子Beclin-1和LC3-Ⅱ的表达水平.结果 与Sham组比较,SAH组学习记忆能力显著下降( P<0. 05),海马区神经细胞数量显著减少(P<0. 05),Beclin-1和LC3-Ⅱ的表达明显升高(P<0. 05);与SAH组相比,BQ-123组学习记忆能力得改明显改善(P<0. 05),海马区神经细胞丢失数量明显较少(P<0. 05),Beclin-1和LC3-Ⅱ的表达明显升高(P<0. 05).结论 BQ-123干预可减轻SAH损伤造成的学习记忆功能障碍,其机制与可能与调控海马区神经细胞自噬有关.

Objective:To observe the effect of different exercise intensity preconditioning on expression of growth associated protein-43 (GAP-43) and neurite outgrowth inhibitor-A (Nogo-A) in rats with cerebral ischemia/reperfusion (I/R).Methods:Global cerebral ischemia model was formed by improved Pulsinelli four-vessel occlusion.Totally 80 rats were divided into four groups randomly:sham group,I/R group,exercise intensity 1 preconditioning group and exercise internsity 2 preconditioning group.Rats were sacrificed at the time of 6 h,1 d,3 d and 7 d respectively after injury.Morphological changes of neural cells in hippocarnpal CA1 area were observed by hematoxylin-eosin staining.Expression of GAP-43 and Nogo-A were detected respectively by immunohistochemistry and RT-PCR.Results:Compared with those in the cerebral ischemia/reperfusion group,the number of necrosis neurons significantly decreased and the expression of GAP-43 significantly increased at different time points in exercise intensity 1 preconditioning group and decreased in exercise intensity 2 preconditioning group.Meanwhile,the expression of Nogo-A was significantly decreased in exercise intensity 1 preconditioning group and increased in exercise intensity 2 preconditioning group.Conclusion:Exercise intensity 1 preconditioning can aggravate the apoptosis of nerve cells after cerebral ischemia/reperfusion injury and exercise intensity 2 preconditioning can aggravate the damage and loss of nerve cells,which is related to the regulation of GAP-43 and Nogo-A.

Objective To observe the effect of TOMATIS auditory training on improving cognitive and post-traumatic stress disorder in patients after breast cancer chemotherapy. Methods Eighty invasive ductal carcinoma of breast cancer patients with cognition and psychological disorders were selected in the breast department of Tangshan People's Hospital from October 2016 to September 2017. All patients were randomly divided into control group ( n=40) and experimental group ( n=40) . The experimental group was given the TOMATIS high and low audio frequency auditory training,and the control group was given ordinary music training. Before and after the intervention, the Chinese version of the Montreal cognitive assessment scale ( MoCA) and the post-traumatic stress disorder scale ( PTSD-SS) were evaluated for both groups of pa-tients. Results After the intervention,the experimental group had significantly higher scores in visual struc-ture skills((3. 83±0. 71)vs(2. 68±0. 57)),executive function ((2. 23±0. 53)vs(1. 55±0. 50)),attention and concentration((1. 55±0. 78)vs(1. 23±0. 53)),language((1. 50±0. 75)vs(1. 08±0. 47)),calculation ((2. 00±0. 60)vs(1. 45±0. 75)),abstract thinking((1. 63±0. 54)vs(1. 00±0. 51)),memory((4. 68± 0. 47)vs(2. 70±0. 72)),directive force((5. 25±0. 54)vs(3. 90±0. 81)) and total score((22. 65±2. 89)vs (15. 58±2. 10))than the control group(all P<0. 05). After intervention,the scores of subjective assessment of traumatic events((2. 60±0. 63)vs(3. 98±0. 62)),repeated recurring experiences((24.05±2.72)vs (26. 70±2. 28)),avoidance symptoms((24. 35±1. 64)vs(26. 40±1. 19)),increased alertness((24. 23± 1. 80)vs(25. 45±1. 20)),impaired social function((7. 28±1. 01)vs(8. 68±0. 66)),and total scores((85. 85±5. 13)vs(94. 63±2. 92)) in the experimental group were significantly lower than those in the control group,and the differences were statistically significant ( all P<0. 01) . Conclusion TOMATIS auditory train-ing can effectively improve the cognitive function and psychological state in breast cancer chemotherapy pa-tients,which is worthy of popularization and application.

目的 探讨BQ-123对蛛网膜下腔出血(SAH)的治疗作用及其机制.方法 160只雄性SD大鼠,随机分为假手术(Sham)组、SAH组、雷帕霉素组、低剂量BQ-123组、高剂量BQ-123组.2次注血法复制SAH大鼠模型;光镜观察海马区形态结构变化;免疫组织化学法检测海马区雷帕霉素靶蛋白(mTOR)、自噬相关基因Beclin-1和微管相关蛋白1轻链(LC3)-Ⅱ的表达;实时逆转录聚合酶链反应(real-time RT-PCR)检测mTOR、Beclin-1和LC3的mRNA表达;抓力测定实验评价各时间点大鼠前肢拉力情况;穿梭箱实验测试动物的学习功能.结果 与Sham组比较,SAH组海马区mTOR、Beclin-1和LC3 mRNA表达增加,存活神经元细胞数量减少,大鼠的学习功能和拉力值下降,差异有统计学意义(P＜0.05);与SAH组比较,雷帕霉素组海马区mTOR mRNA表达降低、Beclin-1和LC3 mRNA表达增高,存活神经元细胞数量增多,大鼠的学习功能和拉力值改善,差异有统计学意义(P＜0.05);与SAH组比较,BQ-123组海马区mTOR mRNA降低、Beclin-1和LC3 mRNA表达增高,存活神经元细胞数量增多,动物学习功能指标和拉力值改善,差异有统计学意义(P＜0.05),且上述变化在高剂量BQ-123更为明显.结论 BQ-123可改善SAH大鼠神经功能缺陷,抑制mTOR激活,从而提高海马区神经细胞自噬程度.

Objective To investigate the relationship of extracellular regulated protein kinases activation and neural cells autophagy in rats after subarachnoid hemorrhage.Methods One hundred twenty male SD rats were randomly divided into sham operated group,SAH group,ERK1/2 inhibitor U0126 group,autophagy inducer rapamycin (Rap) group.The animal models were established by injecting the autologous blood into cisterna magna twice.U0126 (5μ g/μL) and Rap (10nmol/μL) were injected into lateral ventricles in U0126 group and Rap group 30min before SAH.The morphology of hippocampal nerve cells were examined by using light microscopy.The expression levels of phosphorylated ERK 1/2 (p-ERK 1/2),ERK 1/2mRNA and autophagy markers (Beclin-1 and Beclin-1 mRNA、LC3-Ⅱ and LC3mRNA) in the hippocampus were detected by using inmunohistochemistry and real-time fluorescence quantitative PCR.Result Compared with sham group,the rate of dead nerve cells,the mRNA levels of ERK1/2,Beclin-1 and LC3 as well as the levels of the p-ERK1/2,Beclin-1 and LC3-Ⅱ increased in SAH group (P＜0.05).Compared with SAH group,the rate of dead nerve cells increased(P＜0.05),the ERK1/2 mRNA,Beclin-1 mRNA and LC3 mRN A,and p-ERK1/2,Beclin-landLC3-Ⅱ in U0126 group decreased(P＜0.05);the rate of dead nerve cells decreased (P＜0.05),the Beclin-1 mRNA and LC3 mRNA,the Beclin-1and LC3-Ⅱ level increased in Rap group(P＜0.05),but ERK 1/2 mRNA and p-ERK 1/2 remained unchanged (P＞0.05).Conclusion Activation of the ERK1/2 signaling pathway after SAH,can induce nerve cells death by increasing Beclin-1 and LC3-Ⅱ expressions.

Objective To investigate the relationship between extracellular regulated protein kina-ses activation and neural cells autophagy in rats after subarachnoid hemorrhage. Methods 120 male SD rats were divided into sham operated group,SAH group,low dose ERK1/2 inhibitor U0126 group,and high dose ERK1/2 inhibitor U0126 group. The animal models were established by injecting the autolo-gous blood into cisterna magna twice. Two U0126 groups were injected U0126(5 g/L or 10 g/L)in lat-eral ventricles 30 min before modeling. The morphology of hippocampal neurons was observed by light microscopy. The behavioral differences were detected using water maze behavior test. The expression levels of phosphorylated ERK1/2(p-ERK1/2)and autophagy marker proteins(Beclin-1,LC3-Ⅱ)in hippo-campus were detected by immunohistochemistry and Western-blot. Results Compared with those in Sham group,SAH group of rats in 72 h escape latency time significantly prolonged,wear number de-creased significantly(P< 0.05),neuron survival rate at each time point were significantly lower,whereas the expressions of p-ERK1/2,Beclin-1,and LC3-Ⅱ increased in SA H group,and reached the peak at 24 h. Compared with those in SA H group,the latency time of both low and high dose of U 0126 groups at the same time points was prolonged and the times for crossing the platform significantly reduced (P<0.05),and at each time point neuron survival ratio was significantly decreased,and the expressions of p-ERK1/2,Beclin-1 and LC3-Ⅱ,and neuronal cell survival ratio decreased in two U 0126 groups (P<0.05). Compared with those in low dose U 0126 group,high dose group at the corresponding time points,the escape latency prolonged and the times for crossing the platform significantly decreased (P<0.05),and all the expressions of p-ERK1/2 and neuronal cell survival ratio decreased in high U 0126 group(P<0.05),while there was no statistically significant difference in Beclin-1 and LC3-Ⅱ between the two dose groups(P>0.05). Conclusions ERK1/2 activation had a protective effect on nerve cells after SA H,and this protective effect is partly related to enhancing neurons autophagy.

Objective To investigate the effect of MAPK activation on autophagy in the hippocampus of rats with subarachnoid hemorrhage.Methods A total of 100 male SD rats were divided into 5 groups randomly:sham operated group,SAH group,inhibitor U0126 group,inhibitor SB203580 group,SP600125 group.The animal model was established by injecting the autologous blood into cisterna magna twice.The morphological changes of hippocampus nerve cells of rat brain were detected with HE.The mRNA levels of ERK1/2,p38MAPK,JNK and LC3 in hippocampus were detected with quantitative real time PCR and the expression of phosphorylated ERK1/2,phosphorylated p38MAPK,phosphorylated JNK and LC3-Ⅱ in hippocampus of rat brain were detected by immunohistochemistry.Results Compared with the Sham group,the survival rate of neurons in SAH group decreased (6 h:(84.982 ± 5.723) ％,24 h:(74.383± 9.860) ％,48 h:(62.860± 10.820) ％,72 h:(52.260± 10.960) ％) (all P＜0.05).The levels of ERK1/2 mRNA,p38MAPK mRNA,JNK mRNA and LC3 mRNA in hippocampus increased (all P＜ 0.05) and the expression of p-ERK1/2,p-p38MAPK,p-JNK,LC3-Ⅱ proteins increased(all P＜0.05).Compared with the SAH group,the survival rate of neurons in U0126 group was decreased (6 h:(71.620±6.542) ％,24 h:(66.221±7.742)％,48 h:(55.208±8.802) ％,72 h:(46.242±7.782) ％),and the ERK1/2 and LC3 in hippocampus decreased both in mRNA level and in protein level(all P＜0.05).Compared with the SAH group,the survival rate of neurons in SB203580 groups was increased (6 h:(89.082±6.602)％,24 h:(85.840±9.726) ％,48 h:(74.96± 10.916) ％,72 h:(69.211 ± 10.745) ％),and the p38MAPK,LC3-Ⅱ in hippocampus decreased at both mRNA and protein levels (all P＜0.05).Compared with the SAH group,the survival rate of neurons in SP600125 groups was increased (6 h:(91.620± 7.542) ％,24 h:(86.221 ± 10.742) ％,48 h:(75.208±11.802) ％,72 h:(70.242± 11.782) ％).The expression of JNK was decreased while the LC3-Ⅱ was increased in hippocampus (P＜0.05).Conclusion MAPK activation is involved in the autophagy of hippocampal neurons after SAH,in which ERK1/2 activation plays a positive role in the regulation of autophagy in hippocampal neurons after SAH,while p38MAPK and JNK activation plays a negative role in autophagy.

Objective:To investigate the effect of extracellular regulated protein kinases (ERK1/2) and phosphatidylinositol 3-kinase (PI3-K) pathways on the regulation of autophagy in the hippocampus of rats with subarachnoid hemorrhage.Methods:Totally 160 male SD rats were divided into sham operated group,SAH group,inhibitor U0126 group,inhibitor LY294002 group.The animal models were established by injecting the autologous blood into cisterna magna twice.The animal models were established by injecting the autologous blood into cisterna magna twice.The neuronal morphological changes in hippocampus of rats were detected with HE staining;The expression of phosphorylated ERK1/2,PI3-K,Beclin-1 and LC3-Ⅱ in hippocampus of rat were detected with immunohistochemistry.The expression of ERK1/2、PI3-K.Beclin-1 and LC3 in hippocampus of rat were detecteel with RT-PCR.Results:The survival rate of neurons in SAH group was lower than sham group,and expression of ERK1/2,PI3-K,Beclin-1 and LC3 was higher than sham group (P ＜0.05).The survival rate of neurons in hippocampus of U0126 group and LY294002 group was higher than SAH group.The expression of ERK1/2,PI3-K,Beclin-1 and LC3 was lower than SAH group (P ＜0.05).The difference of survival rate of neurons between U0126 group and LY294002 group was not statistically significant (P ＞ 0.05).The expression of ERK1/2,Beclin-1 and LC3 in U0126 group was lower than LY294002 group (P ＜0.05).The expression of PI3-K was higher than LY294002 group (P ＜ 0.05).Conclusion:The both activation of ERK1/2 and PI3-K pathway is involved in the regulation of autophagy of neural cells after SAH,and the PI3-K pathway is more important.

目的：探讨血糖控制情况及血管神经病变等并发症对2型糖尿病（ T2 DM ）患者执行功能的影响。方法选取确诊的T2 DM 患者280例，采用执行功能缺陷综合征的行为学评价测验对患者进行执行功能的测评。结果 T2DM患者BADS测评总分平均为（10．62±2．30）分。血糖控制情况、血管神经病变及病程是影响执行功能的危险因素（P＜0．05）。结论控制血糖及血管神经病变等并发症可提高T2DM患者执行功能。

Objective To observe the effect of aerobic exercise preconditioning on growth-associated protein-43 (GAP-43) and Nogo-A in rats after cerebral ischemia/reperfusion. Methods Sprague-Dawley rats were equally divided into sham group (n=40), cerebral ischemia/reperfusion group (n=40) and aerobic exercise preconditioning group (n=40), and global cerebral ischemia model was formed with modified four-vessel occlusion. The rats was sacrificed six hours, one day, three days and seven days after ischemia, respectively. The hippocampus neural cells were observed in five rats with HE staining and immunohistochemistry of GAP-43 and Nogo-A, and the other five rats were test-ed with RT-PCR of GAP-43 and Nogo-A. Results Compared with those in the cerebral ischemia/reperfusion group, the apoptotic neurons and expression of GAP-43 significantly increased all the time points in the aerobic exercise preconditioning group (P<0.01), while the ex-pression of Nogo-A decreased (P<0.01). Conclusion Aerobic exercise preconditioning can promote the regeneration of neuronal cells and axon after cerebral ischemia/reperfusion injury, which is related to the regulation of GAP-43 and Nogo-A.

Objective To observe the effect of exhaustive exercise preconditioning on GAP?43 and Nogo?A in rats with cerebral ischemia reperfusion. Methods 90 rats were randomly divided into sham oper?ation group,group of cerebral ischemia reperfusion(I/R) and exhaustive exercise preconditioning group.Rats were sacrificed at 6 h,1 d,3 d and 7 d respectively after injury. Neural functions were detected by shuttle box. Morphological changes of hippocampal neural cells were observed by HE staining. Expressions of GAP?43 and Nogo?A were detected respectively by immunohistochemistry and RT?PCR technology. Re?sults Compared with the sham group,the death rate of apoptotic neurons in I/R group was decreased( 6 h:(30.97±2.09)%,1 d:(38.41±1.10)%,3 d:(46.81±2.04)%,1 d:(43.46±1.57)%),the index of learning and memory ability(AARR?7 d:(38.00±12.60)%,PAL?7 d:(27.90±1.79)s) and expression of GAP?43 were decreased(6 h:(2.89±0.85),1 d:(4.06±0.25),3 d:(4.78±0.98),7 d:(7.02±0.21)),the expression of Nogo?A was increased(6 h:(2.93±0.19),1 d:(5.47±0.32),3 d:(4.62±0.26),7 d:(4.12±1.11))(P<0.05).Compared with I/R group,the death rate of apoptotic neurons in exhaustive exercise preconditioning group were decreased,the index of learning and memory ability(AARR?7 d:(20.66±7.60)%,PAL?7 d:(35.53±2.41)s) and expression of GAP?43 were decreased(6 h:(2.03±0.14),1 d:(2.92±0.27),3 d:(3.35±0.34),7 d:(5.24±0.52)),the expression of Nogo?A were increased(6 h:(3.92±0.51),1 d:(6.90± 0.79),3 d:(5.87±0.48),7 d:(5.37±0.50))(P<0.05). Conclusion Exhaustive exercise preconditioning ag? gravates the injury of neurons and neural function,which is related to the regulation of GAP?43 and Nogo?A in the hippocampus of rats.

目的 探讨丁基苯酞对弥漫性脑损伤(DBI)后大鼠海马排斥性导向分子(RGMa)表达的影响.方法 160只成年雄性Sprague-Dawlley大鼠,随机分为正常对照组(n=40),模型组(n=40),低剂量丁基笨酞干预组(n=40,80mg/kg),高剂量丁基苯酞干预组(n=40,160mg/kg).参照Marmarou's法建立脑损伤模型,选取伤后1、2、7、14d作为时间点,干预组均在致伤后采用腹腔注射丁基苯酞,1次/24h,连续注射14d.通过行为学评分量表测评神经功能;光镜观察神经细胞形态结构变化,免疫组织化学观察RGMa的表达情况.结果 与对照组比较,模型组动物各时间点行为学评分降低(P＜0.05);死亡神经元数量升高(P＜0.05);各时间点RGMa阳性表达增加(P＜0.05).与模型组比较,高低剂量丁基苯酞干预组中1、2d时行为学评分差异无统计学意义(P＞0.05),7d和14d行为学评分升高(P＜0.05),但在7d和14d丁基苯酞高、低剂量组间差异无统计学意义(P＞0.05).与模型组比较,丁基苯酞高、低剂量组死亡神经元数量降低(P＜0.05);丁基苯肽高、低剂量组之间差异无统计学意义(P＞0.05).与模型组比较,丁基苯酞高、低剂量组中RGMA阳性表达1d差异无统计学意义(P＞0.05),2、7、14d时RGMa阳性表达明显减少(P＜0.05).但在2、7、14d丁基苯肽高、低剂量组间差异无统计学意义(P＞0.05).与对照组比较,模型组各时间点RGMamRNA表达水平增加.与模型组比较,丁基苯酞高、低剂量组中1d时差异无统计学意义(P＞0.05),2、7、14d时减少(P＜0.05).丁基苯酞高、低剂量组间各时间点差异无统计学意义(P＞0.05).结论 丁基苯酞可减少弥漫性脑损伤大鼠大脑海马区RGMa表达.

Objective To explore sleep state of urban and rural elderly stroke patients, and to provide the basis for countermeasures. Methods A total of 6 173 elder patients from July 2012 to May 2013 were selected by using the stratified cluster sampling method. The Pittsburgh Sleep Quality Index ( PSQI) was used for the sleep evaluation. Results The incidence of sleeping disorders was 12. 4% in the urban and 15. 4% in the rural elder patients, which was significantly different (χ2 =11. 154,P<0. 01). In addition, 1 641 patients had sleeping disorders, with an incidence of 26. 6%. Among them, the incidence of sleeping disorders was 34. 9% in the elder patients with stroke, and 25. 2%in the elder patients without stroke, which was significantly different (χ2 =35. 473, P<0. 01). There were significant differences in the sleep quality, sleep latency, terms of sleep time, sleep efficiency, the use of hypnotic drugs, daytime dysfunction, sleep disorders between patients with and without stroke (P <0. 05). Conclusions The incidence of sleeping disorders in elderly people is high, and stroke is one of the influential factors of sleep disorders, so we should pay more attention to it.

Objective To explore the effetc of different intensity of exercise on learning ablility and oxygen free radical metabolism in rats after cerebral ischemia-reperfusion (I/R). Methods 60 male Sprague-Dawley rats were randomly divided into sham group, I/R group, aerobic exercise preconditioning group and exhaustive exercise preconditioning group. The morphological changes of neural cells in hippo-campus were observed with HE staining, the learning ablility was assessed with shuttle box, the activity of superoxide dismutase and malo-ndialdehyde level in hippocampus were measured with hydroxylamine method and TBA method respectively 1, 3, 7 days after injury. Re-sults The number of survival neurons, active avoidance reaction and activity of superoxide dismutase decreased, and the latency of passive avoidance and malondialdehyde levels increased in all the other groups compare with the sham group (P<0.001). Further more, the number of surviving neurons, active avoidance reaction rate and the activity of superoxide dismutase were less in the I/R group than in the aerobic exercise preconditioning group (P<0.001), and more than in the exhaustive exercise preconditioning group (P<0.001), while the latency of passive avoidance and the level of malondialdehyde was more than in the aerobic exercise preconditioning group (P<0.001), and less than in the exhaustive exercise preconditioning group (P<0.001). Conclusion Regular aerobic exercise is beneficial to protect the learning ability from cerebral I/R in rats, but exhaustive exercise may be negative, which may associated with the metabolism of oxygen free radical in hip-pocampus impacted by exercise.