检索结果-南通市图书馆

Pain management of hemiplegic shoulder pain post stroke in patients from Nanjing,China

Neural Regeneration Research 2013年第25期8卷 2389-2398页

作者： Yi Zhu Bin Su Ning Li Hongzhu Jin Teaching and Research Department of Rehabilitation Treatment Second Clinical MedicineNanjing University of Traditional Chinese Medicine Wuxi Tongren International Rehabilitation Hospital Department of Rehabilitation Second Xiangya Hospital of Central South University Second Clinical Medicine Nanjing University of Traditional Chinese Medicine

We selected 106 hemiplegic patients with shoulder pain hospitalized after stroke from three hospi- tals in Nanjing, China between February 2007 and January 2012. All patients had complete clinical data sets and accounted for 45.5% of the inpatients because of stroke. Results showed that the number of patients with hemiplegic shoulder pain post stroke increased yearly, attacking mainly males 50-69 years of age. Of 106 patients, there were 60 cases （56.6%） of adhesive capsulitis, 19 （17.9%） of shoulder subluxation, 14 （13.2%） of complex regional pain syndrome, and 13 （12.6%） of central pain. The main symptoms were shoulder pain （100%）, limit of shoulder mobility （98.1%）, and adhesion of the scapula （56.6%）. MRI of the shoulder showed tendon and ligament lesions （57.1%） and rotator cuff tear （38.1%）. 53.8% of central pain was related to the thalamus, in addition to the basal ganglia, brain stem, and cerebellopontine angle. Shoulder pain, upper limb motor function, and function independence were significantly improved after comprehensive rehabilitation. In par- ticular, electroacupuncture based on basic physical therapy exhibited efficacy on shoulder subluxa- tion and complex regional pain syndrome. Multiple linear regression results showed a negative re- lationship of efficacy of pain management with the attack period of shoulder pain, involvement of the posterior limb of the internal capsule, and duration between onset and rehabilitation treatment, but a positive correlation with pain-related education, pain regression period, and pain diagnosis.

关键词： neural regeneration brain injury hemiplegia post stroke shoulder pain adhesive capsulitis shoulder subluxation complex regional pain syndrome grants-supported paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Effects of different frequencies of repetitive transcranial magnetic stimulation on the recovery of upper limb motor dysfunction in patients with subacute cerebral infarction

引用

Neural Regeneration Research 2016年第10期11卷 1584-1590页

作者： Jiang Li Xiang-min Meng Ru-yi Li Ru Zhang Zheng Zhang Yi-feng Du Shandong Provincial Hospital of Shandong University Jinan Shandong Province China Affiliated Hospital of Qingdao University Qingdao Shandong Province China

Studies have confirmed that low-frequency repetitive transcranial magnetic stimulation can decrease the activity of cortical neurons, and high-frequency repetitive transcranial magnetic stimulation can increase the excitability of cortical neurons. However, there are few studies concerning the use of different frequencies of repetitive transcranial magnetic stimulation on the recovery of upper-limb motor function after cerebral infarction. We hypothesized that different frequencies of repetitive transcranial magnetic stimulation in patients with cerebral infarction would produce different effects on the recovery of upper-limb motor function. This study enrolled 127 patients with upper-limb dysfunction during the subacute phase of cerebral infarction. These patients were randomly assigned to three groups. The low-frequency group comprised 42 patients who were treated with 1 Hz repetitive transcranial magnetic stimulation on the contralateral hemisphere primary motor cortex （M1）. The high-frequency group comprised 43 patients who were treated with 10 Hz repetitive transcranial magnetic stimulation on ipsilateral M1. Finally, the sham group comprised 42 patients who were treated with 10 Hz of false stimulation on ipsilateral M1. A total of 135 seconds of stimulation was applied in the sham group and high-frequency group. At 2 weeks after treatment, cortical latency of motor-evoked potentials and central motor conduction time were significantly lower compared with before treatment. Moreover, motor function scores were significantly improved. The above indices for the low- and high-frequency groups were significantly different compared with the sham group. However, there was no significant difference between the low- and high-frequency groups. The results show that low- and high-frequency repetitive transcranial magnetic stimulation can similarly improve upper-limb motor function in patients with cerebral infarction.

关键词： nerve regeneration brain injury repetitive transcranial magnetic stimulation cerebral infarction low-frequency stimulation high-frequency stimulation upper-limb motor function cerebral cortex stroke rehabilitation motor-evoked potential central motor conductiontime primary motor cortex neuroplasticity neural reorganization neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

L-3-n-butylphthalide protects against vascular dementia via activation of the Akt kinase pathway

引用

Neural Regeneration Research 2013年第19期8卷 1733-1742页

作者： Yaping Huai Yanhong Dong Jing Xu Nan Meng Chunfeng Song Wenbin Li Peiyuan Lv Department of Neurology Hebei Medical University Department of Neurology Hebei General Hospital Electron Microscope Center Hebei Medical University Department of Pathophysiology Hebei Medical University

As a neuroprotective drug for the treatment of ischemic stroke, 3-n-butylphthalide, a celery seed ex- tract, has been approved by the State Food and Drug Administration of China as a clinical therapeutic drug for ischemic stroke patients. L-3-n-butylphthalide possesses significant efficacy in the treatment of acute ischemic stroke. The activated Akt kinase pathway can prevent the death of nerve cells and exhibit neuroprotective effects in the brain after stroke. This study provides the hypothesis that I-3-n- butylphthalide has a certain therapeutic effect on vascular dementia, and its mechanism depends on the activation of the Akt kinase pathway. A vascular dementia mouse model was established by cere- bral repetitive ischemia/reperfusion, and intragastrically administered I-3-n-butylphthalide daily for 28 consecutive days after ischemia/repedusion, or 7 consecutive days before ischemia/reperfusion. The Morris water maze test showed significant impairment of spatial learning and memory at 4 weeks after operation, but intragastric administration of I-3-n-butylphthalide, especially pretreatment with I-3-n- butylphthalide, significantly reversed these changes. Thionine staining and western blot analylsis showed that preventive and therapeutic application of I-3-n-butylphthalide can reduce loss of pyrami- dal neurons in the hippocampal CA1 region and alleviate nerve damage in mice with vascular demen- tia. In addition, phosphorylated Akt expression in hippocampal tissue increased significantly after I-3-n- butylphthalide treatment. Experimental findings demonstrate that I-3-n-butylphthalide has preventive and therapeutic effects on vascular dementia, and its mechanism may be mediated by upregulation of phosphorylated Akt in the hippocampus.

关键词： neural regeneration brain injury ischemia/reperfusion Akt phosphorylated Akt Morris water maze cog-nitive function 3-n-butylphthalide hippocampus learning memory dementia grants-supported paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Hypoxic preconditioning stimulates angiogenesis in ischemic penumbra after acute cerebral infarction

引用

Neural Regeneration Research 2013年第31期8卷 2895-2903页

作者： Sijie Li Yanbo Zhang Guo Shao Mingfeng Yang Jingzhong Niu Guowei Lv Xunming Ji Institute of Hypoxic Medicine Xuanwu Hospital Capital Medical University Department of Neurology Affiliated Hospital of Taishan Medical University Research Center of Biology and Medicine Baotou Medical College

Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute cerebral infarction, but the mechanisms underlying this protection remain unclear. To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis, we in- duced a photochemical model of cerebral infarction in an inbred line of mice （BALB/c）. Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment. Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction, mainly in neurons and vascular endothelial cells. Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31. Moreover, hypoxic preconditioning reduced the infarct volume and improved neu- rological function in mice. These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra, which promoted angiogenesis.

关键词： neural regeneration brain injury hypoxic preconditioning acute cerebral infarction ischemicpenumbra vascular endothelial growth factor CD31 angiogenesis neuroprotection grants-supported paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model

引用

Neural Regeneration Research 2013年第25期8卷 2327-2335页

作者： Jinnan Zhang Wei Lu Qiang Lei Xi Tao Hong You Pinghui Xie Department of Neurology Second Xiangya HospitalCentral South University

Stroke remains a worldwide health problem. Salvianolate exerts a protective effect in various mi- crocirculatory disturbance-related diseases, but studies of the mechanisms underlying its protective action have mainly focused on the myocardium, whereas little research has been carried out in brain tissue following ischemia-reperfusion. We assessed the neuroprotective effects of salvianolate in a rat model of cerebral ischemia-reperfusion injury induced using the suture method. At onset and 24 and 48 hours after reperfusion, rats were intraperitoneally injected with salvianolate （18 mg/kg） or saline. Neurological deficit scores at 72 hours showed that the neurological functions of rats that had received salvianolate were significantly better than those of the rats that had received saline. 2,3,5-Triphenyltetrazolium chloride was used to stain cerebral tissue to determine the extent of the infarct area. A significantly smaller infarct area and a significantly lower number of apoptotic cells were observed after treatment with salvianolate compared with the saline treatment. Expression of heat shock protein 22 and phosphorylated protein kinase B in ischemic brain tissue was significantly greater in rats treated with salvianolate compared with rats treated with saline. Our findings suggest that salvianolate provides neuroprotective effects against cerebral ischemia-reperfusion injury by upregulating heat shock protein 22 and phosphorylated protein kinase B expression.

关键词： neural regeneration traditional Chinese medicine brain injury salvianolic acid B salvianolate heatshock protein 22 protein kinase B cerebral ischemia-reperfusion injury apoptosis neuroprotection neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Buyang Huanwu Decoction fraction protects against cerebral ischemia/reperfusion injury by attenuating the inflammatory response and cellular apoptosis

引用

Neural Regeneration Research 2013年第3期8卷 197-207页

作者： Yulian Jin Liuyi Dong Changqing Wu Jiang Qin Sheng Li Chunyan Wang Xu Shao Dake Huang Department of Pharmacology Key Laboratory of Anti-inflammatory and ImmunopharmacologyMinistry of Education Key Laboratory of Chinese Medicine Research and Development State Administration of Traditional Chinese MedicineAnhui Medical University Anhui Provincial Children's Hospital Anhui Institute of Materia Medica Hefei Qi-xing Medicine and Technology Co. Ltd. Synthetic Laboratory of Basic Medicine College Anhui Medical University

Buyang Huanwu Decoction fraction extracted from Buyang Huanwu Decoction contains saponins of Astragalus, total paeony glycoside and safflower flavones. The aim of this study was to demonstrate the neuroprotective effect and mechanism of Buyang Huanwu Decoction fraction on ischemic injury both in vivo and in vitro. In vivo experiments showed that 50-200 mg/kg Buyang Huanwu Decoction fraction reduced infarct volume and pathological injury in ischemia/reperfusion rats, markedly inhibited expression of nuclear factor-KB and tumor necrosis factor-a and promoted nestin protein expression in brain tissue. Buyang Huanwu Decoction fraction （200 mg/kg） exhibited significant effects, which were similar to those of 100 mg/kg Ginkgo biloba extract. In vitro experimental results demonstrated that 10-100 mg/L Buyang Huanwu Decoction fraction significantly improved cell viability, decreased the release of lactate dehydrogenase and malondialdehyde levels, and inhibited the rate of apoptosis in HT22 cells following oxygen-glucose deprivation. Buyang Huanwu Decoction fraction （100 mg/L） exhibited significant effects, which were similar to those of 100 mg/L Ginkgo biloba extract. These findings suggest that Buyang Huanwu Decoction fraction may represent a novel, protective strategy against cerebral ischemia/reperfusion injury in rats and oxygen-glucose deprivation-induced damage in HT22 cells in vitro by attenuating the inflammatory response and cellular apoptosis.

关键词： neural regeneration traditional Chinese medicine Buyang Huanwu Decoction fraction ischemia/reperfusion injury brain injury hippocampus neurons apoptosis inflammatory reactionoxidation traditional Chinese herbal medicines neuroprotection grants-supported paper photographs-containing paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Reducing LncRNA-5657 expression inhibits the brain inflammatory reaction in septic rats

引用

Neural Regeneration Research 2021年第7期16卷 1288-1293页

作者： Yi-An Zhan Xin-Liang Qiu Xu-Zhen Wang Ning Zhao Ke-Jian Qian Department of Critical Care Medicine the First Affiliated Hospital of Nanchang UniversityNanchangJiangxi ProvinceChina Department of Critical Care Medicine Xingguo County People’s HospitalGanzhouJiangxi ProvinceChina

Our preliminary study found that the long noncoding RNA(LncRNA)-5657 can reduce the expression of inflammatory factors during inflammatory reactions in rat glial cells.However, the role played by LncRNA-5657 during septic brain injury remains unclear.In the present study, rat models of septic encephalopathy were established by cecal ligation and puncture, and then the rats were treated with a hippocampal injection small hairpin RNA(sh RNA) against LncRNA-5657(sh-LnCRNA-5657).The sh-LncRNA-5657 treatment reduced the level of neuronal degeneration and necrosis in the rat hippocampus, reduced the immunoreactivities of aquaporin 4, heparanase, and metallopeptidase-9, and lowered the level of tumor necrosis factor-alpha.Glial cells were pre-treated with sh-LncRNA-5657 and then treated with 1 μg/mL lipopolysaccharide.Sh-LncRNA-5657 transfection decreased the expression of LncRNA-5657 in lipopolysaccharide-treated glial cells and decreased the mRNA and protein levels of tumor necrosis factor-alpha, interleukin-1β, and interleukin-6.These findings suggested that LncRNA-5657 expression can significantly reduce the inflammatory reaction during septic encephalopathy and induce protective effects against this disease.This study was approved by the Institutional Ethics Committee at the First Affiliated Hospital of Nanchang University of China(approval No.2017-004) in 2017.

关键词： brain injury glial cells inflammation injury lipopolysaccharide long noncoding RNA repair sepsis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons

引用

Neural Regeneration Research 2013年第2期8卷 121-126页

作者： Jinbao Yin Lijuan Xu Shuling Zhang Yuanyin Zheng Zhichao Zhong Hongling Fan XiLi Quanzhong Chang Department of Physiology Zhuhai Campus of Zunyi Medical College Department of Pathology Dongguan Campus of Guangdong Medical College

Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2＇-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2＇-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly（adenosine diphosphate-ribose）polymerase-1 and apoptosis-inducing factor.

关键词： neural regeneration brain injury chloride channel 3-morpholinosydnonimine hippocampus poly（adenosine diphosphate-ribose）polymerase-1 apoptosis inducing factor neuronal apoptosis grants-supported paper photographs-containing paper neuroregeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Neuroprotective effects of tadalafil on gerbil dopaminergic neurons following cerebral ischemia

引用

Neural Regeneration Research 2013年第8期8卷 693-701页

作者： Kwang Taek Kim Kyung Jin Chung Han Sae Lee Il Gyu Ko Chang Ju Kim Yong Gil Na Khae Hawn Kim Department of Urology Gachon University Gil Medical CenterGachon University Department of Physiology College of MedicineKyung Hee University Department of Urology Chungnam National University HospitalChungnam National University School of Medicine

Impairment of dopamine function, which is known to have major effects on behaviors and cognition, is one of the main problems associated with cerebral ischemia. Tadalafil, a long-acting phosphodiesterase type-5 inhibitor, is known to ameliorate neurologic impairment induced by brain injury, but not in dopaminergic regions. We investigated the neuroprotective effects of treatment with tadalafil on cyclic guanosine monophosphate level and dopamine function following cerebral ischemia. Forty adult Mongolian gerbils were randomly and evenly divided into five groups （n = 8 in each group）： Sham-operation group, cerebral ischemia-induced and 0, 0.1, 1, and 10 mg/kg tadalafil-treated groups, respectively. Tadalafil dissolved in distilled water was administered orally for 7 consecutive days, starting 1 day after surgery. Cyclic guanosine monophosphate assay and immunohistochemistry were performed for thyrosine hydroxylase expression and western blot analysis for dopamine D2 receptor expression. A decrease in cyclic guanosine monophosphate level following cerebral ischemia was found with an increase in thyrosine hydroxylase activity and a decrease in dopamine D2 receptor expression in the striatum and substantia nigra region. However, treatment with tadalafil increased cyclic guanosine monophosphate expression, suppressed thyrosine hydroxylase expression and increased dopamine 92 receptor expression in the striatum and substantia nigra region in a dose-dependent manner. Tadalafil might ameliorate cerebral ischemia-induced dopaminergic neuron injury. Therefore, tadalafil has the potential as a new neuroprotective treatment strategy for cerebral ischemic injury.

关键词： neural regeneration brain injury cerebral ischemia Tadalafil phosphodiesterase type-5 inhibitor dopamine dopamine D2 receptor cyclic guanosine monophosphate grants-supported paper photographs-containing paper neuroregneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Electroacupuncture reduces apoptotic index and inhibits p38 mitogen-activated protein kinase signaling pathway in the hippocampus of rats with cerebral ischemia/reperfusion injury

引用

Neural Regeneration Research 2017年第3期12卷 409-416页

作者： Xiao Lan Xin Zhang Guo-ping Zhou Chun-xiao Wu Chun Li Xiu-hong Xu School of Traditional Chinese Medicine Southern Medical University College of Acupuncture Moxibustion and TuinaHunan University of Chinese Medicine

Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling pathway.We established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa＇s method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture group.Terminal deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemia/reperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves.

关键词： nerve regeneration brain injury electroacupuncture cell apoptosis cerebral ischemia/reperfusion injury neurological impairment score morphological changes immunohistoehemical assay p38 mitogen-activated protein kinases phosphorylated p38 hippocampus neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：