Real-time analysis of inflammatory cytokines and regulatory gene expression in tissues surrounding the hematoma after intracerebral hemorrhage

BACKGROUND: Secondary lesions can occur in tissues surrounding the hematoma following intracerebral hemorrhage, with the presence of inflammatory reactions, cytokine expression and apoptosis. These have been confirmed in animal studies. Our study sought to determine whether these could be detected in human tissues surrounding the hematoma following intracerebral hemorrhage. OBJECTIVE: To investigate expression of inflammatory cytokines, Bax and Bcl-x, and identify neural cell apoptosis in tissues surrounding the hematoma, and to analyze the correlation between them and pathological damage in intracerebral hemorrhage patients. DESIGN, TIME AND SETTING: This histopathology, controlled study was performed at the Department of Neurosurgery, Sichuan People's Hospital, China, from January 2003 to January 2005. PARTICIPANTS: Brain tissues I cm from the hematoma in 30 intracerebral hemorrhage patients sewed as the experimental group. Brain tissues located away from the hematoma in 7 patients served as the control group. METHODS: TUNEL was used to detect neural cell apoptosis, lmmunohistochemistry (labeled dextran polymer) and RT-PCR were used to measure tumor necrosis factor-α , interleukin-1β, interleukin-6, Bax and Bcl-x protein and mRNA expression. Pathological changes in brain tissues surrounding the hematoma were observed following HE staining. MAIN OUTCOME MEASURES: Neural cell apoptosis, inflammatory cytokines, Bax and Bcl-x protein and mRNA expression, pathological changes in brain tissues surrounding the hematoma. RESULTS: Brain tissues surrounding the hematoma were mildly damaged within 6 hours, severely damaged at 24-72 hours, and significantly improved 1 week following intracerebral hemorrhage. Expression of tumor necrosis factor-α protein and mRNA, interleukin-1 β and interleukin-6 mRNA was not significant in tissues surrounding the hematoma, which was identical to the control group within 6 hours after intracerebral hemorrhage. This expression was significantly higher compared with the control group from 12-72 hours, and gradually decreased after 72 hours. The number of apoptotic neural ceils reached a peak between 12-72 hours. Tumor necrosis factor-α protein and mRNA, interleukin-1β and interleuldn-6 mRNA levels were positively correlated with apoptosis, Bax protein and mRNA levels (P < 0.01). CONCLUSION: Tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels are highly correlated with apoptosis. With the decrease in tumor necrosis factor-α, interleukin-1β and interleukin-6 levels, the number of apoptotic cells gradually reduced.     

Association between p75 neurotrophin receptor gene expression and cell apoptosis in tissues surrounding hematomas in rat models of intracerebral hemorrhage

Animal models of intracerebral hemorrhage were established by injection of autologous blood into the caudate nucleus in rats. Cell apoptosis was measured by flow cytometry and immunohistochemical staining of the p75 neurotrophin receptor. p75 neurotrophin receptor protein was detected by immunohistochemistry. p75 neurotrophin receptor mRNA was examined by quantitative real-time polymerase chain reactions. At 24 hours after modeling, cellular apoptosis occured around hematoma with upregulation of p75 neurotrophin receptor protein and mRNA was observed, which directly correlated to apoptosis. This observation indicated that p75 neurotrophin receptor upregulation was associated with cell apoptosis around hematomas after intracerebral hemorrhage.     

Mild hypothermia effects on matrix metalloproteinase-9 expression in the perihematomal region of rats following experimental intracerebral hemorrhage**☆

BACKGROUND： Matrix metalloproteinase-9 （MMP-9） expression increases with intracerebral hemorrhage, and participates in the pathophysiological processes of secondary brain injury after intracerebral hemorrhage.
OBJECTIVE： To investigate the effects of mild hypothermia on MMP-9 expression and brain edema in the perihematomal region of experimental intracerebral hemorrhage rats.
DESIGN, TIME AND SETTING： The randomized, controlled experiment was performed at the Central Laboratory of Shandong Provincial Hospital between May and September 2007.
MATERIALS： Seventy-two, Wistar, male rats, 12-weeks old, were used for this study. Rabbit anti-MMP-9 primary antibody was purchased from Boster, China.
METHODS： Wistar rats were equally and randomly divided into normothermia and mild hypothermia groups. The two groups each comprised control, 6-hour intracerebral hemorrhage, 24-hour intracerebral hemorrhage, 48-hour intracerebral hemorrhage, 72-hour intracerebral hemorrhage, and l-week intracerebral hemorrhage subgroups, with six rats in each subgroup. Rat models of intracerebral hemorrhage were established by injecting 100 μL of autologous blood into the rat caudate nucleus. Rats in the mild hypothermia group received four hours of local mild hypothermia immediately following the injection. lntracerebral temperature was maintained at （33 ± 0.5） ℃. Subsequently, intracerebral temperature was spontaneously recovered at 25 ℃. Rats in the control subgroup were not injected with autologous blood and received only with intracerebral hemorrhage.
MAIN OUTCOME MEASURES： Brain water content and MMP-9 expression surrounding the hematoma region. RESULTS： MMP-9 expression increased at 6 hours, and brain edema reached a peak at 48 hours after intracerebral hemorrhage. MMP-9 expression was significantly decreased in the mild hypothermia group compared with the normothermia group at each time point （P 〈 0.05）.
CONCLUSION： Mild hypothermia can significantly inhibit MMP-9 overexpression and reliev     

Effects of minocycline on apoptosis and angiogenesis-related protein expression in a rat model of intracerebral hemorrhage

In the present study, a rat model of non-traumatic intracerebral hemorrhage was established by type IV collagenase injection into the right globus pallidus. Bax and Bcl-2 expression in tissues surrounding hematomas was significantly increased within 14 days after injury, and it then gradually decreased. Vascular endothelial growth factor, Flk-1 and Flt-1 mRNA expression gradually increased over time. After intraperitoneal injection with minocycline, Bax expression was decreased 1 day after intracerebral hemorrhage. Flk-1 and Flt-1 mRNA expression was decreased after minocycline injection, but Bcl-2 expression was increased, and vascular endothelial growth factor mRNA expression was decreased between 4-14 days. These results indicated that protective effects of minocycline on nerve tissues were associated with increased Bcl-2 expression and decreased Bax expression in the early stage after intracerebral hemorrhage. In the late stage, minocycline downregulated vascular endothelial growth factor and its receptor expression to inhibit brain tissue self-repair.     

人脑出血血肿周围组织中神经生长因子前体-神经营养因子受体p75-sortilin通路与细胞凋亡

This study demonstrated that brain areas surrounding the site of hematoma following intracerebral hemorrhage are characterized by significantly increased apoptosis and expression of neurotrophin receptor p75 and sortilin. However, as detected by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemical staining, there was no significant change in nerve growth factor precursor expression levels. The appearance of neurotrophin receptor p75 expressing cells was positively correlated with cells that were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. These findings confirm that the nerve growth factor precursor-neurotrophin receptor p75-sortilin heterotrimeric complex-mediated apoptosis pathway may play an important role in cellular apoptosis following intracerebral hemorrhage.     

Electrocardiogram changes during hematoma enlargement in intracerebral hemorrhage patients**☆

BACKGROUND： It has been reported that cerebrovascular disease causes changes in electrocardiogram results. OBJECTIVE： To investigate changes in electrocardiogram results in patients with intracerebral bematoma enlargement. DESIGN, TIME AND SETTING： The present case-retrospective analysis study was performed at the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology from January 2005 to October 2006. PARTICIPANTS： A total of 225 intracerebral hemorrhage patients （142 males and 83 females） that were hospitalized at the Department of Neurology were enrolled the present study. The patient selection was in accordance with diagnostic criteria from the Fourth National Cerebrovascular Disease Congress of China in 1995, and diagnosis was confirmed using computed tomography. All patients underwent computed tomography twice within 24 hours following intracerebral hemorrhage, and were subjected to electrocardiogram examination after admission. METHODS： According to hematoma enlargement following intracerebral hemorrhage, all patients were divided into hematoma enlargement （n = 20） and non-hematoma enlargement （n = 205） groups. Because of the large patient number difference between the two groups, the hematoma enlargement group was matched with the non-hematoma enlargement group. Patients meeting these conditions were included in the non-hematoma enlargement group. Finally, 75 patients were included in the final analysis, 19 in the hematoma enlargement group and 56 in the non-hematoma enlargement group. Clinical data from the two groups were statistically analyzed. MAIN OUTCOME MEASURES： The incidence of electrocardiographic abnormalities between the hematoma enlargement and non-hematoma enlargement groups. RESULTS： In the hematoma enlargement group, 15 patients （79%） developed electrocardiographic abnormafities. In the non-hematoma enlargement group, 24 patients （43%） presented with electrocardiographic abnormalities. There were sig     

Apoptosis-related protein expression in rabbits with blast brain injury following early hyperbaric oxygen therapy

We treated detonator-explosion-induced craniocerebral injury in rabbits with hyperbaric oxygen 1-24 hours post-injury.Expression of the apoptosis-regulating protein cytochrome c,the pro-apoptotic protein Bax and the apoptosis marker caspase-3 in the tissues surrounding the area of injury was significantly reduced,while that of the anti-apoptotic protein Bcl-2 was significantly increased.Our findings indicate that the curative effects of early hyperbaric oxygen on cortical cell apoptosis is associated with suppression of cytochrome c release from mitochondria.This mechanism underlies the observed reduction in Bax expression and upregulation of Bcl-2 expression.     

MicroRNA-181c provides neuroprotection in an intracerebral hemorrhage model

Apoptosis is an important factor during the early stage of intracerebral hemorrhage.MiR-181 c plays a key regulatory role in apoptosis.However,whether miR-181 c is involved in apoptosis of prophase cells after intracerebral hemorrhage remains unclear.Therefore,in vitro and in vivo experiments were conducted to test this hypothesis.In vivo experiments:collagenase type VII was injected into the basal ganglia of adult Sprague-Dawley rats to establish an intracerebral hemorrhage model.MiR-181 c mimic or inhibitor was injected in situ 4 hours after intracerebral hemorrhage.Neurological functional defects(neurological severity scores)were assessed 1,7,and 14 days after model establishment.Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and western blot assay were conducted 14 days after model establishment.In vitro experiments:PC12 cells were cultured under oxygen-glucose deprivation,and hemins were added to simulate intracerebral hemorrhage in vitro.MiR-181 c mimic or inhibitor was added to regulate miR-181 c expression.3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay,luciferase reporter system,and western blot assay were performed.Experimental results revealed differences in miR-181 c expression in brain tissues of both patients and rats with cerebral hemorrhage.In addition,in vitro experiments found that miR-181 c overexpression could upregulate the Bcl-2/Bax ratio to inhibit apoptosis,while inhibition of miR-181 c expression could reduce the Bcl-2/Bax ratio and aggravate apoptosis of cells.Regulation of apoptosis occurred through the phosphoinositide 3 kinase(PI3 K)/Akt pathway by targeting of phosphatase and tensin homolog deleted on chromosome ten(PTEN).Higher miR-181 c overexpression correlated with lower neurological severity scores,indicating better recovery of neurological function.In conclusion,miR-181 c affects the prognosis of intracerebral hemorrhage by regulating apoptosis,and these effects might be directly mediated and regulated by targeting of the PTEN\PI3 K/Akt pathway and Bcl-2/Bax ratio.Furthermore,these results indicated that miR-181 c played a neuroprotective role in intracerebral hemorrhage by regulating apoptosis of nerve cells,thus providing a potential target for the prevention and treatment of intracerebral hemorrhage.Testing of human serum was authorized by the Ethics Committee of China Medical University(No.2012-38-1)on February 20,2012.The protocol was registered with the Chinese Clinical Trial Registry(Registration No.ChiCTR-COC-17013559).The animal study was approved by the Institutional Animal Care and Use Committee of China Medical University(approval No.2017008)on March 8,2017.     

Oxidized low-density lipoprotein receptor 1:a novel potential therapeutic target for intracerebral hemorrhage

Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal apoptosis.OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke.Therefore,OLR1 is likely involved in the progress of intracerebral hemorrhage.In this study,we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model.OLR1 small interfering RNA(10μL;50 pmol/μL)was injected into the right basal ganglia to knock down OLR1.Twenty-four hours later,0.5 U collagenase type VII was injected to induce intracerebral hemorrhage.We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma,neuron loss,inflammatory reaction,and oxidative stress in rat brain tissue.We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway.Therefore,silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage.These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.     

早年创伤对认知功能影响的研究进展

早年创伤是一个全球普遍存在的问题,严重影响儿童、青少年的大脑发育,继而导致认知功能、人格水平、社会行为的改变。早年创伤主要是父母、监护人或其他年长者对孩子施加躯体虐待、躯体忽视、情感虐待、情感忽视或性虐待。美国一项调查显示：儿童虐待事件的发生率高达1．2％[1]。早年创伤影响认知功能的多个领域,包括学习／工作记忆、视觉空间能力、执行功能、言语智能、复杂推理搜决策、学业表现等比]。创伤造成的认知功能改变是目前国内外神经科学和精神医学领域研究的热点,但其发病机制仍不明确,鉴于早年创伤与认知功能的关系问题,现就早年创伤对大脑发育、神经认知的影响加以综述。     

Brain network markers of abnormal cerebral glucose metabolism and blood flow in Parkinson＇s disease

Neuroimaging of cerebral glucose metabolism and blood flow is ideally suited to assay widely-distributed brain circuits as a result of local molecular events and behavioral modulation in the central nervous system. With the progress in novel analytical methodology, this endeavor has succeeded in unraveling the mechanisms underlying a wide spectrum of neurodegenerative diseases. In particular, statistical brain mapping studies have made significant strides in describing the pathophysiology of Parkinson＇s disease （PD） and related disorders by providing signature biomarkers to determine the systemic abnormalities in brain function and evaluate disease progression, therapeutic responses, and clinical correlates in patients. In this article, we review the relevant clinical applications in patients in relation to healthy volunteers with a focus on the generation of unique spatial covariance patterns associated with the motor and cognitive symptoms underlying PD. These characteristic biomarkers can be potentially used not only to improve patient recruitment but also to predict outcomes in clinical trials.     

Differential cognitive responses to guqin music and piano music in Chinese subjects： an event-related potential study

Objective To compare the cognitive effects of guqin （the oldest Chinese instrument） music and piano music. Methods Behavioral and event-related potential （ERP） data in a standard two-stimulus auditory oddball task were recorded and analyzed. Results This study replicated the previous results of culture-familiar music effect on Chinese subjects： the greater P300 amplitude in frontal areas in a culture-familiar music environment. At the same time, the difference between guqin music and piano music was observed in NI and later positive complex （LPC： including P300 and P500）： a relatively higher participation of right anterior-temporal areas in Chinese subjects. Conclusion The results suggest that the special features of ERP responses to guqin music are the outcome of Chinese tonal language environments given the similarity between Guqin＇s tones and Mandarin lexical tones.     

Effect of Ganoderma lucidum spore on expression of insulin-like growth factor-1, nuclear factor-kappa B, and neuronal apoptosis in the epileptic rat brain*★

BACKGROUND：It has been reported that Ganoderma lucidum spore powder, a very well known Chinese traditional medicine, can affect immunoregulation, free radical scavenging, and anti-hypoxia responses. OBJECTIVE： To investigate the effect of Ganoderma lucidum spore powder on expression of insulin-like growth factor-1 （IGF-1）, nuclear factor-κB （NF-κB） and neuronal apoptosis in rats with pentylenetetrazol （PTZ）-induced epilepsy. DESIGN, TIME AND SETTING： A cellular and molecular biology experiment with randomized controlled study design was performed at the Central Laboratory of Basic Medical College of Jiamusi University from June to August 2005. MATERIALS： Thirty healthy, adult, male, Wistar rats were selected and randomly divided into 3 groups （10 rats per group）： control, epilepsy model, and Ganoderma lucidum spore powder. A sub-eclampsia PTZ dose （35 mg/kg） was intraperitoneally injected to induce epilepsy in the latter two groups. Wild Ganoderma lucidum spore powder （30 g/L） was provided by the wild Ganoderma lucidum plant nursery at Jiamusi, China. Immunohistochemical detection and terminal deoxynucleotidyl transferase-mediate dUTP nick end-labeling （TUNEL） kits were purchased from Wuhan Boster Biological Technology Co., Ltd., China. METHODS： Ganoderma lucidum spore powder was intragastrically administered at a dose of 10.0 mL/kg, once a day for 28 days. In the epilepsy and control groups, an equivalent volume of normal saline was intragastrically administered. MAIN OUTCOME MEASURES： Immunoreactivity for IGF-1 and NF-κB/P65 were detected by immunohistochemical staining. Neuronal apoptosis was detected using TUNEL methods. RESULTS： The hippocampus and cerebral cortex of rats with PTZ-induced epilepsy exhibited a higher number of apoptotic cells at high magnification （×400）, compared with the control group. Expression of IGF-1 and NF-κB were higher in the epilepsy group, compared with the control group （P 〈 0.01）. In Ganoderma lucidum spore-treated rats,     

Naoxintong dose effects on inflammatory factor expression in the rat brain following focal cerebral ischemia

BACKGROUND： Certain components of tetramethylpyrazine, a traditional Chinese medicine, exhibit protective effects against brain injury. OBJECTIVE： To investigate the effects of different Naoxintong doses on expression of nuclear factor-kappa B （ kB）, interleukin-6, tumor necrosis factor-α, and complement 3 in rats following focal cerebral ischemia. DESIGN, TIME AND SETTING： The randomized experiment was performed at the Laboratory of Neurology, Second Hospital of Hebei Medical University from June 2004 to June 2006. MATERIALS： A total of 150 adult, healthy, male, Sprague Dawley rats, weighing 280-320g, were selected. Naoxintong powder （mainly comprising szechwan lovage rhizome, milkvetch root, danshen root, and radix angelicae sinensis） was obtained from Buchang Pharmacy Co., Ltd. in Xianyang City of Shanxi Province of China, lot number 040608. METHODS： The rats were randomly assigned into sham operation, saline, high-dose Naoxintong, moderate-dose Naoxintong, and low-dose Naoxintong groups, with 30 rats in each group. Rat models of middle cerebral artery occlusion were established using the suture method, with the exception of the sham operation group. Rats in the high-dose, moderate-dose and low-dose Naoxintong groups received 4, 2, and 1 g/kg Naoxintong respectively, by gavage. Rats in the saline group were treated with 1 mL saline by gavage All rats were administered by gavage at 5 and 23 hours following surgery, and subsequently, once per day. MAIN OUTCOME MEASURES： At 6, 24, 48, 72 hours, and 7 days following model establishment, brain water content was measured. Histopathological changes in brain tissues were detected using hematoxylin-eosin staining. Expression of nuclear factor- kB, interleukin-6, tumor necrosis factor- α, and complement 3 was examined by immunohistochemistry. RESULTS： A total of 150 rats were included in the final analysis with no loss. Brain water content was significantly increased in the ischemic hemisphere of rats from the saline, as well as the high-dose, mo     

Effect of bilobalide B on cholinergic hippocampal neurons exposed to cholesterol and apolipoprotein E4*☆

BACKGROUND： Extracts of ginkgo biloba leaves have been reported to improve nerve function and activity in Alzheimer＇s disease, which is associated with reduced secretion of cholinergic neurotransmitter in hippocampal neurons. OBJECTIVE： To validate the protective effect of bilobalide B against in vitro injury of cholinergic neurons of the hippocampus induced by combined cholesterol and apoE4 DESIGN, TIME AND SETTING： This randomized, controlled animal experiment was performed in the Pathology Laboratory, Tianjin University of Traditional Chinese Medicine from July 2003 to July 2006. MATERIALS： Neonatal Wistar rats, 1-day-old, both male and female, and mean body mass of 5 g were selected for this study. Cholesterol and apolipoprotein E4 （apoE4） were purchased from Sigma Company （USA）, bilobalide B was purchased from Tianjin Zhongyi Pharmaceutical Factory, batch number 20050312. METHODS： Hippocampal neurons were divided into three groups： a normal control group （routinely added media）, a model group （exposed to media containing 40 mg/L cholesterol and 30 mg/L apoE4 for 24 hours） and a bilobalide B group （exposed to media containing 160 mg/L bilobalide B for 16 hours, and then with addition of 40 mg/L cholesterol and 30 mg/L apoE4 for an additional 24 hours）. MAIN OUTCOME MEASURES： Levels of acetylcholine （ACh） and activity of acetylcholinesterase （ACHE） and choline acetyltransferase （CHAT） in hippocampal neurons were determined by microdosage hydroxylamine colorimetry, hydroxylamine colorimetry and radiological chemistry, respectively. RESULTS： The ACh level was significantly lower in the model group than that in the normal control group （P 〈 0.01）, while it was markedly higher in the bilobalide B group than in the model group （P 〈 0.05）. Activity of AChE was significantly decreased in the model group compared with the normal control group （P 〈 0.05）. However, there was no significant difference between the model group and the bilobalide B group ?     

Changes of 5-hydroxytryptamine and tryptophan hydroxylase expression in the ventral horn of spinal cord

Objective To investigate changes of 5-hydroxytryptamine （5-HT） and its synthesis rate-limiting enzyme tryp-tophan hydroxylase （TPH） in the ventral horn of spinal cord after exercise-induced fatigue, and to further discuss the mecha- nism of exercise-induced central fatigue at spinal level. Methods Sixteen healthy adult Wistar rats were randomly divided into 2 groups： exercise-induced fatigue group and control group. Immunohistochemical staining for 5-HT and TPH in the ventral horn were performed and analysized quantitatively. The mean optic densities of 5-HT and TPH positive fibers or terminals were measured by computerized image analyzer. Results Both 5-HT and TPH positive fibers/terminals decreased in the exercise-induced fatigue group. The immunohistochemical staining was weaker and the mean optic densities decreased obviously in the fatigue group compared with those in the control group （P 〈 0.05）. Conclusion 5-HT and TPH in the ventral horn of spinal cord might be involved in exercise-induced fatigue.     

Effects of realgar on stress proteins, inflammatory mediators, and complement in brain tissue and serum of rats with inflammatory brain injury*☆

BACKGROUND：The Chinese herbal compound realgar exerts detoxification effects as an adjuvant. It is suggested that realgar exerts detoxification via the following pathways： in the pathological state, realgar corrects the oxidative stress state by increasing stress levels, activating some endogenous protective factors and antagonizing the excessive release of inflammatory factors, as well as inhibiting complement activation. OBJECTIVE： To observe the changes in stress proteins, inflammatory mediators, and complement in the brain tissue and serum of rats with inflammatory brain injury, which have been treated with the Chinese herbal compound Angong Niuhuang, and to compare the efficacy of Angong Niuhuang with that of realgar, to verify the mechanism of action of realgar. DESIGN, TIME AND SETTING： Randomized, controlled, cytological experiment, performed in the Institute of Clinical Pharmacology, Guangzhou University of Traditional Chinese Medicine in March 2006. MATERIALS： Thirty-six healthy, male, Sprague Dawley rats received 250 U/kg Bordetella pertussis via the common carotid artery within 15 seconds to induce inflammatory brain injury. Reagents and kits were as follows： Realgar and Angong Niuhuang powder （Foshan Second Pharmaceutical Factory, China）, Bordetella pertussis diagnostic antigen （National Institute for the Control of Pharmaceutical and Biological Products, China）, heat shock protein 70 （HSP70） enzyme-labeled immunosorbent assay （ELISA） kit （Stressgen, USA）, tumor necrosis factor-α （TNF-α） ELISA kit （Biosource, USA）, nitric oxide synthase （NOS） kit, Coomassie brilliant blue protein kit （Nanjing Jiancheng Bioengineering Co.,Ltd., China）, and complements C3 and C4 （Shanghai Kehua Dongling Diagnositic Products Co.,Ltd., China）. METHODS： Thirty-six rats were randomly and evenly divided into the following six groups： normal control, model, high-, middle-, and low-dose realgar-treated, and Angong Niuhuang-treated groups. At one hour prior to establish     

癫癇社区防控策略可使更多农村地区癫癇患者受益

癫癇是一种临床常见的神经系统疾病。常于儿童和青少年期发病,若不接受正规治疗可反复发作,甚至迁延终身。该病不仅严重影响患者本人身体和心理健康,也给其家庭带来巨大痛苦和沉重的经济负担。据估计,全球约有逾50×106例癫癇患者,其中80%在发展中国家,发展中国家癫癇患病率是发达国家的2~3倍,且60%~90%的患者未接受治疗或仅接受非正规治疗[1-2]。癫癇的高患病率、高病死率及其对患者身心造成的严重不良影响已引起社会各界的重视,针对癫癇的各方面研究正在不断加强,     

阿尔茨海默病免疫治疗:对攻克神经变性疾病的几点启示

<正>阿尔茨海默病(AD)也称老年期痴呆,是老年人群高发的一种痴呆症,为临床常见的神经变性疾病,给社会和家庭带来巨大的经济负担和人文问题。临床常用的胆碱酯酶抑制药[多奈哌齐(donepezil)、加兰他敏(galantamine)、卡巴拉汀(rivastigmine)]和非竞争性N-甲基-D-天冬氨酸(NMDA)受体阻断药[美金刚(memantine)]均属于对症治疗,可短期缓解临床症状与体征,但不能达根治目的。因此,研制和发现能够阻断阿尔茨海默病进程并逆转其发病的治疗方法,即显得至关重要。20世纪80年代中期,有研究者发现了神经炎性斑[NPs,亦称老年斑([1]SPs)]的主要成分是β-淀粉样蛋白(Aβ);随后,又克隆出位于第21号染色体的β-淀粉样前体蛋白(APP)基因[2],该基因突变被认为是导致家族性阿尔茨海默病的原因[3]。藉此"淀