急性颅脑损伤患者CT评分变化及血清乳酸、NSE、CRP的相关性分析

目的探讨急性颅脑损伤(ACI)患者计算机断层扫描(CT)评分变化与血清乳酸(LA)、神经元特异性烯醇化酶(NSE)及C-反应蛋白(CRP)水平的关系及其对预后的预测价值。方法选取2020年1月—2022年1月东台市人民医院收治的50例急性颅脑损伤患者作为疾病组,根据患者治疗后格拉斯哥预后评分(GOS)分为预后良好组(32例)和预后不良组(18例);选取50例行健康体检受试者作为健康组。受试者工作特征曲线(ROC)评估血清乳酸、NSE、CRP水平与CT评分对急性颅脑损伤患者预后的评估价值。结果疾病组血清乳酸、NSE、CRP水平均高于健康组(P<0.05);预后不良组乳酸、NSE、CRP水平和CT评分均高于预后良好组;经Spearman相关分析,急性颅内损伤患者血清中乳酸、NSE、CRP水平与CT评分呈正相关(r=0.431、r=0.345、r=0.226,均P<0.05);ROC曲线分析显示,血清乳酸、NSE、CRP水平、CT评分联合预测急性颅内感染预后的曲线下面积(AUC)高于单一指标检测(P<0.05)。结论急性颅脑损伤患者CT评分与患者入院血清乳酸、NSE、CRP水平呈正相关,联合诊断对患者预后评估有一定价值。

水厂全分布式管控一体化网络前端智能节点与NeuronC程序设计

目前,国内大多数自来水厂采用的是一种基于PLC的集散式(DCS,Distributed Control System)控制系统。这里介绍构建基于Lorworks的水厂管控一体化网络的方法和途径,包括前端测控设备的配置、智能节点的配置和Neuron C编程。最后给出输入输出控制程序,供参考。这是一种真正全分布式管控一体化网络的前端智能节点配置与设计方案。

龟羚帕安丸对帕金森病大鼠血清NSE、Cys-C、5-HT、5-HIAA及NE水平的影响

目的观察龟羚帕安丸对帕金森病(Parkinson’s disease,PD)大鼠血清神经元特异性烯醇化酶(Neuron-specific enolase,NSE)、胱抑素C(Cystatin C,Cys-C)、5-羟色胺(5-Hydroxytryptamine,5-HT)、5-羟基吲哚乙酸(5-Hydroxyindoleacetic acid,5-HIAA)及去甲肾上腺素(Norepinephrine,NE)水平的影响。方法采用6-羟基多巴胺(6-OHDA)立体定向注射法制作PD大鼠模型,造模成功的PD大鼠随机分为模型组,西药组,中药高、中、低剂量组,中西药合用组,每组15只,另设假手术组15只。模型组及假手术组给予等容积生理盐水灌胃,其余组给予相应药物灌胃,连续给药28 d。大鼠腹主动脉取血,用酶联免疫吸附测定法(Enzyme linked immunosorbent assay,ELISA)检测各组大鼠血清NSE、Cys-C、5-HT、5-HIAA及NE的水平。结果模型组大鼠血清NSE及Cys-C水平均明显升高,血清5-HT、5-HIAA及NE水平均明显降低;中药各剂量组、中西药合用组、西药组血清NSE及Cys-C水平均明显降低,5-HT、5-HIAA及NE水平均明显升高。结论龟羚帕安丸具有明显神经保护作用,作用机制与降低NSE及Cys-C水平,增加5-HT、5-HIAA及NE水平,降低脑实质损伤、神经炎症损伤及提高单胺类神经递质有关。

NEURON C语言与事件驱动编程

介绍了LonWorks网络系统中节点的主要开发语言NEURONC的特点，着重阐明了该语言对事件驱动编程的支持，在说明事件调度策略的基础上，提出一种“链式激发”的事件驱动编程方法。

Role of Mitochondria in Neuron Apoptosis during Ischemia-Reperfusion Injury

To investigate the role of mitochondria in neuronal apoptosis, ischemia-reperfusion mediated neuronal cell injury model was established by depriving of glucose, serum and oxygen in media. DNA fragmentation, cell viability, cytochrome C releasing, caspase3 activity and mitochondrial transmembrane potential were observed after N2a cells suffered the insults. The results showed that N2a cells in ischemic territory exhibited survival damage, classical cell apoptosis change, DNA ladder and activation of caspase3. Apoptosis-related alterations in mitochondrial functions, including release of cytochrome C and depression of mitochondrial transmembrane potential (△Ψm) were testified in N2a cells after mimic ischemia-reperfusion. Moreover, activation of caspase3 occurred following the release of cytochrome C. However, the inhibitor of caspase3, Ac-DEVD-CHO, couldn't completely rescue N2a cells from apoptosis. Administration of cyclosporine A, an inhibitor of mitochondria permeability transition pore only partly inhibited caspase3 activity and reduced DNA damage. Interestingly, treatment of Z-IETD-FMK, an inhibitor of caspase8 could completely reverse DNA fragmentation, but can't completely inhibit caspase3 activity. It was concluded that there were caspase3 dependent and independent cellular apoptosis pathways in N2a cells suffering ischemia-reperfusion insults. Mitochondria dysfunction may early trigger apoptosis and amplify apoptosis signal.

Underlying mechanism of protection from hypoxic injury seen with n-butanol extract of Potentilla anserine L. in hippocampal neurons

The alcohol and n-butanol extract of Potentilla anserine L. significantly protects myocardium from acute ischemic injury. However, its effects on rat hippocampal neurons and the mechanism of protection remain unclear. In this study, primary cultured hippocampal neurons from neonatal rats were incubated in 95% N2 and 5% CO2 for 4 hours. Results indicated that hypoxic injury decreased the viability of neurons, increased the expression levels of caspase-9 and caspase-3 mRNA, as well as cytochrome c, Caspase-9, and Caspase-3 protein. Pretreatment with 0.25, 0.062 5, 0.015 6 mg/mL n-butanol extract of Potentilla anserine L. led to a significant increase in cell viability. Expression levels of caspase-9 and caspase-3 mRNA, as well as cytochrome c, Caspase-9, and Caspase-3 protein, were attenuated. The neuroprotective effect of n-butanol extract of Potentilla anserine L. was equivalent to tanshinone IIA. Our data suggest that the n-butanol extract of Potentilla anserine L. could protect primary hippocampal neurons from hypoxic injury by deactivating mitochondrial cell death.

MANUAL ACUPUNCTURE PRODUCES LONG TERM INHIBITION OF THE NOCICEPTIVE TRANSMISSION TO WIDE DYNAMIC RANGE NEURONS IN THE SPINAL CORD OF THE RAT

singe unit discharge recordings were made from 42 WDR neurons in spinal dorsal horn in the rat. These neurons could he driven by electrical stimull activiting innocuous and noxious afferent fibres in the ipsilateral plantar nerve. Traditional manual acupuncture delivered at the local acupoints Zusanli, Chengshan, Kunlun and Yongquan induced a strong inhibition or the C-fiber response. in 19 of 42 neurons obtained but did not after the A-fibre response of the neurons. The inhibition of the fibre response outlasted the period of acupuncture for more than 30 min. Neither Anor C-fibre responses in the remaining 23 neurous could be affected by manual acupuncture. These results suggest that the acupuncture stimulation specifically influences nociceptive nociceptive transmission,maybe through a presynaptic action,Furthermore, the fact that the inhibitory effect outlasts the stimulation by more than 30 min indicates that either a neuromodulatory ,presumably peptidergic action is at hand or that a temporary synaptic modification occurs in the spinal dorsal horn.

Long-term adenosine A1 receptor activation-induced sortilin expression promotes α-synuclein upregulation in dopaminergic neurons

Prolonged activation of adenosine A1 receptor likely leads to damage of dopaminergic neurons and subsequent development of neurodegenerative diseases.However,the pathogenesis underlying long-term adenosine A1 receptor activation-induced neurodegeneration remains unclear.In this study,rats were intraperitoneally injected with 5 mg/kg of the adenosine A1 receptor agonist N6-cyclopentyladenosine(CPA)for five weeks.The mobility of rats was evaluated by forced swimming test,while their cognitive capabilities were evaluated by Y-maze test.Expression of sortilin,α-synuclein,p-JUN,and c-JUN proteins in the substantia nigra were detected by western blot analysis.In addition,immunofluorescence staining of sortilin andα-synuclein was performed to detect expression in the substantia nigra.The results showed that,compared with adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine(5 mg/kg)+CPA co-treated rats,motor and memory abilities were reduced,surface expression of sortin andα-synuclein in dopaminergic neurons was reduced,and total sortilin and totalα-synuclein were increased in CPA-treated rats.MN9D cells were incubated with 500 nM CPA alone or in combination with 10μM SP600125(JNK inhibitor)for 48 hours.Quantitative real-time polymerase chain reaction analysis of sortilin andα-synuclein mRNA levels in MN9D cells revealed upregulated sortilin expression in MN9D cells cultured with CPA alone,but the combination of CPA and SP600125 could inhibit this expression.Predictions made using Jasper,PROMO,and Alibaba online databases identified a highly conserved sequence in the sortilin promoter that was predicted to bind JUN in both humans and rodents.A luciferase reporter assay of sortilin promoter plasmid-transfected HEK293T cells confirmed this prediction.After sortilin expression was inhibited by sh-SORT1,expression of p-JUN and c-JUN was detected by western blot analysis.Long-term adenosine A1 receptor activation levels upregulatedα-synuclein expression at the post-transcriptional level by affecting sortilin expression.The online tool Raptor-X-Binding and Discovery Studio 4.5 prediction software predicted that sortilin can bind toα-synuclein.Co-immunoprecipitation revealed an interaction between sortilin andα-synuclein in MN9D cells.Our findings indicate that suppression of prolonged adenosine A1 receptor activation potently inhibited sortilin expression andα-synuclein accumulation,and dramatically improved host cognition and kineticism.This study was approved by the University Committee of Animal Care and Supply at the University of Saskatchewan(approval No.AUP#20070090)in March 2007 and the Animals Ethics Committee of University of South China(approval No.LL0387-USC)in June 2017.

Mitochondrial protective and anti-apoptotic effects of Rhodiola crenulata extract on hippocampal neurons in a rat model of Alzheimer's disease

In our previous study, we found that the edible alcohol extract of the root of the medicinal plant Rhodiola crenulata（RCE） improved spatial cognition in a rat model of Alzheimer＇s disease. Another study from our laboratory showed that RCE enhanced neural cell proliferation in the dentate gyrus of the hippocampus and prevented damage to hippocampal neurons in a rat model of chronic stress-induced depression. However, the mechanisms underlying the neuroprotective effects of RCE are unclear. In the present study, we investigated the anti-apoptotic effect of RCE and its neuroprotective mechanism of action in a rat model of Alzheimer＇s disease established by intracerebroventricular injection of streptozotocin. The rats were pre-administered RCE at doses of 1.5, 3.0 or 6.0 g/kg for 21 days before model establishment. ATP and cytochrome c oxidase levels were significantly decreased in rats with Alzheimer＇s disease. Furthermore, neuronal injury was obvious in the hippocampus, with the presence of a large number of apoptotic neurons. In comparison, in rats given RCE pretreatment, ATP and cytochrome c oxidase levels were markedly increased, the number of apoptotic neurons was reduced, and mitochondrial injury was mitigated. The 3.0 g/kg dose of RCE had the optimal effect. These findings suggest that pretreatment with RCE prevents mitochondrial dysfunction and protects hippocampal neurons from apoptosis in rats with Alzheimer＇s disease.

Scutellaria baicalensis stem-leaf total flavonoid reduces neuronal apoptosis induced by amyloid beta-peptide (25-35)

Scutellaria baicalensis stem-leaf total flavonoid might attenuate learning/memory impairment and neuronal loss in rats induced by amyloid beta-peptide. This study aimed to explore the effects of Scutellaria baicalensis stem-leaf total flavonoid on amyloid beta-peptide-induced neuronal apoptosis and the expression of apoptosis-related proteins in the rat hippocampus. Male Wistar rats were given intragastric administration of Scutellaria baicalensis stem-leaf total flavonoid, 50 or 100 mg/kg, once per day. On day 8 after administration, 10 pg amyloid beta-peptide （25-35） was injected into the bilateral hippocampus of rats to induce neuronal apoptosis. On day 20, hippocampal tissue was harvested and probed with the terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay. Scutellaria baicalensis stem-leaf total flavonoid at 50 and 100 mg/kg reduced neuronal apoptosis induced by amyloid beta-peptide （25-35） in the rat hippocampus. Immunohistochemistry and western blot assay revealed that expression of the pro-apoptotic protein Bax, cytochrome c and caspase-3 was significantly diminished by 50 and 100 mg/kg Scutellaria baicalensis stem-leaf total flavonoid, while expression of the anti-apoptotic protein Bcl-2 was increased. Moreover, 100 mg/kg Scutellana baicalensis stem-leaf total flavonoid had a more dramatic effect than the lower dosage. These experimental findings indicate that Scutellaria baicalensis stem-leaf total flavonoid dose-dependently attenuates neuronal apoptosis induced by amyloid beta-peptide in the hippocampus, and it might mediate this by regulating the expression of Bax, cytochrome c, caspase-3 and Bcl-2.

Inosine inhibits apoptosis and cytochrome C mRNA expression in rat neurons after cerebral ischemia/reperfusion

BACKGROUND: It has been demonstrated that adenosine can induce glial cell to release cytochrome C, enhance expression of apoptotic gene bax, inhibit anti-apoptotic gene bcl-2, and activate caspase-3 to apoptosis; Whereas inosine can inhibit neuronal apoptosis which is similar to bcl-2. OBJECTIVE: To observe the effects of inosine on neuronal apoptosis and expression of cytochrome C mRNA in rats after focal cerebral ischemia/reperfusion, and analyze the pathway of its neuroprotective effect. DESIGN: A randomised controlled animal trial. SETTINGS: Department of Neurology, Rongcheng Second People's Hospital; Department of Neurology, Affiliated Union Hospital, Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: Sixty-eight rats, weighing 230-280 g and clean grade, were used. TdT-mediated dUTP-biotin nick end labeling (TUNEL) and cytochrome C mRNA in situ hybridization kits and DAB staining kit were purchased from Wuhan Boster Biological Co., Ltd.; Inosine injection [200 mg (2 mL) each] from Qingdao First Pharmaceutical Factory. METHODS: The experiment was accomplished in the animal experimental center in Tongji Medical College of Huazhong University of Science and Technology from December 2003 to June 2005. ① Sixty-four rats were made into focal ischemia by middle cerebral artery occlusion (MCAO) with a nylon monofilament suture. The successfully induced rats were assigned to inosine group (n =32) and model group (n =32) at random. Rats in the inosine group were intraperitoneally administrated with inosine in dose of 100 mg/kg preoperatively, twice a day, 7 days in all. The rats in the control group were injected with the same dose of saline solution by the similar way preoperatively. Each group was randomized into ischemia /reperfusion 2, 6, 12, 24 hours, 2, 3, 7 and 14 days subgroups consisted of 4 rats. The other 4 rats were taken as the sham-operated group, the rats were given the same treatment except for not introduced the filament into the external carotid artery stump, and brain tissue was removed at 2 hours of reperfusion. ② In situ hybridization was performed to examine the expression of cytochrome C mRNA while TUNEL staining was made to characterize apoptosis. ③ The t test was used to compare the difference of measurement data. MAIN OUTCOME MEASURES: ① Neuronal apoptosis in the different regions of the ischemic brain tissue; ② Expression of cytochrome C mRNA in the different regions at different time points after MCAO. RESULTS: All the 68 rats were involved in the analysis of results. ① Neuronal apoptosis: A small number of TUNEL-positive cells were detected in the sham-operated brain and non-ischemic brain. The number of apoptotic cells in the ischemic cortex peaked at 24 hours of reperfusion [(72.00±1.98) cells] and that in the striatum peaked at 2 days [(94.75±3.57) cells], then decreased to the level of sham-operated group at 14 days. Inosine could reduce apoptotic cells from 12 hours to 7 days of reperfusion as compared with the model group (t =6.19-26.67, P < 0.01). ② Cytochrome C mRNA expression: There was weak expression of cytochrome C mRNA in both sham-operated brain and contralateral brain. Cytochrome C was detected at 2 hours of reperfusion in ischemic brain [(25.75±3.50), (39.75±2.49) cells], and strongly increased to a peak at 12 hours and 24 hours of reperfusion in cortex and striatum [(122.50±6.69), (119.25±5.12) cells], respectively. Furthermore, inosine could significantly decrease cytochrome C expression in cortex at 12 hours to 14 days of reperfusion after ischemic reperfusion and that in striatum at 12 hours to 3 days (t =8.67-43.26, P < 0.01). CONCLUSION: Inosine can exert a neuroprotective effect by inhibiting apoptosis and cytochrome C mRNA expression.

Valproic acid protects neurons and promotes neuronal regeneration after brachial plexus avulsion

Valproic acid has been shown to exert neuroprotective effects and promote neurite outgrowth in several peripheral nerve injury models. However, whether valproic acid can exert its beneficial effect on neurons after brachial plexus avulsion injury is currently unknown. In this study, brachial plexus root avulsion models, established in Wistar rats, were administered daily with valproic acid dis-solved in drinking water （300 mg/kg） or normal water. On days 1, 2, 3, 7, 14 and 28 after avulsion injury, tissues of the C 5-T 1 spinal cord segments of the avulsion injured side were harvested to in-vestigate the expression of Bcl-2, c-Jun and growth associated protein 43 by real-time PCR and western blot assay. Results showed that valproic acid significantly increased the expression of Bcl-2 and growth associated protein 43, and reduced the c-Jun expression after brachial plexus avulsion. Our findings indicate that valproic acid can protect neurons in the spinal cord and enhance neuronal regeneration fol owing brachial plexus root avulsion.

血清BDNF、NSE、PCT和CRP在小儿热性惊厥中的表达及意义

目的研究血清脑源性神经营养因子(BDNF)、神经元特异性烯醇化酶(NSE)、降钙素原(PCT)及C反应蛋白(CRP)4项指标水平在小儿热性惊厥中的表达及意义。方法选取2019年1月至2022年9月在徐州市肿瘤医院儿科(下称该院)就诊患有热性惊厥的患儿155例作为热性惊厥组,按照患儿的抽搐频率、持续时间与精神状态将其分为轻度热性惊厥组(n=77)和重度热性惊厥组(n=78)。同时,选取该院同期77例无惊厥的上呼吸道感染患儿作为对照组。对比3组的BDNF、NSE、PCT及CRP 4项指标的评分差异,选用Logistic回归分析影响患有热性惊厥儿童的独立危险因素。最后,再建立受试者工作特征(ROC)曲线分析BDNF、NSE、PCT、CRP各项及4项指标联合检测热性惊厥发生的价值。结果轻度热性惊厥组和重度热性惊厥组的BDNF、NSE、PCT及CRP 4项指标水平均高于对照组,差异有统计学意义(P<0.05)。重度热性惊厥组的BDNF、NSE、PCT及CRP 4项指标水平均高于轻度热性惊厥组,差异有统计学意义(P<0.05)。通过单因素分析,发现BDNF、NSE、PCT及CRP的差异具有统计学意义(P<0.05)。通过多因素分析,发现BDNF、NSE、PCT、CRP 4项水平是影响小儿热性惊厥的独立危险因素(P<0.05)。4项联合检测灵敏度最高。通过ROC曲线分析,4项联合检测曲线下面积值最高。结论BDNF、NSE、PCT及CRP项指标在患有热性惊厥的儿童患者体内明显升高,4项指标联合检测能更有效地对疾病的发生进行评估。

Astragalus injection inhibits c-Jun N terminal kinase mRNA expression following oxygen-glucose deprivation and reintroduction in rat hippocampal neurons

BACKGROUND： In studies concerning cell injury induced by cerebral ischemia-reperfusion, current experiments have primarily focused on altered protein levels. In addition, the apoptotic proteins Bax and Bcl-2 have been thoroughly studied with regard to initiating neuronal apoptosis. OBJECTIVE： To establish an in vitro model of oxygen-glucose deprivation and reintroduction in the rat hippocampus to simulate cerebral ischemia-reperfusion injury; to observe c-Jun N-terminal kinase 3 （JNK3） mRNA expression in hippocampal neurons following Astragalus injection; and thus to determine changes in the signaling and downstream pathways of neuronal apoptosis at the cellular and molecular level. DESIGN, TIME AND SETTING： A randomized, controlled, cellular and molecular experiment was performed at the Department of Central Laboratory, Chengde Medical College from February to June 2008. MATERIALS： Astragalus injection, the main ingredient of astragaloside, was purchased from Chengdu Di＇ao Jiuhong Pharmaceutical Manufactory, China. JNK3 mRNA probe and in situ hybridization kit were purchased from Tianjin Haoyang Biological Technology, China, and JNK3 RT-PCR primers were designed by Shanghai Bio-engineering, China. METHODS： Primary cultures of hippocampal neurons derived from Sprague Dawley rats, aged 1 2 days, were established. After 8 days, the hippocampal neurons were assigned to the following interventions： model group, Astragalus group, and vehicle control group, cells were subjected to oxygen-glucose reintroduction after oxygen-glucose deprivation for 30 minutes in sugar-free Earle＇s solution and a hypoxia device, which contained high-purity nitrogen. The normal control group was subjected to primary culture techniques and was not treated using above-mentioned interventions. In addition, the Astragalus and vehicle control groups were treated with Astragalus injection （0.5 g/L raw drug） or sterile, deionized water at 2 hours prior to oxygen-glucose deprivation, respectively. MAIN OUTCOME MEASURES： JNK3 mRNA expression was measured by in situ hybridization and RT-PCR at 0, 0.5, 2, 6, 24, 72, and 120 hours after oxygen-glucose reintroduction. RESULTS： Hippocampal neuronal morphology was normal in the normal control group. Hippocampal neurons exhibited apparent apoptosis-like pathological changes in the model, as well as the vehicle control, groups. The apoptosis-like pathological changes in the hippocampal neurons were less in the Astragalus group. Results from in situ hybridization and RT-PCR showed that JNK3 mRNA expression significantly increased in hippocampal neurons from model group, as well as the vehicle control group, compared with the normal control group （P 〈 0.05）. In addition, JNK3 mRNA expression significantly decreased in hippocampal neurons of the Astragalus group, compared with the model group and vehicle control group （P 〈 0.05）. CONCLUSION： Astragalus injection inhibited apoptosis-related JNK3 mRNA expression following oxygen-glucose deprivation and reintroduction, and accordingly played a role in inhibiting hippocampal neuronal apoptosis.

Human Embryo Neuronal Culture <i>in Vitro</i>: A Model to Study Cellular Physiology, Receptors, Power and Toxicity of Cytostatic Drugs for Human Use

Neural cells cultures from human embryo brain of 9° - 11°W gestational age have been used to study ERα (Estrogens Receptor α) and to perform toxicity test for Mitomycin C and Methotrexate. Histochemical confirmation of cellular neuronal phenotype was based on histochemical evidence of NSE (Neuron Specific Enolase).The detection of ERα in neuronal cells was performed with a rabbit Monoclonal Antibody. ERα was absent both on neurons grown in vitro and on tissue brain specimens. This finding is apparently in contrast with the positive immunoreactivity of ERα and ERβ reported by other Authors on foetal and adult CNS (Central Nervous System). The absence of nuclear ERα on neurons in culture and in brain tissue specimens in our experiment is not in contrast with the relevant physiologic role of estrogens on nervous central system, but it could be correlated to the embryonic period of life and could represent a protection of male brain from an undue estrogens imprinting. The mitomycin C, alkylation agent, has shown in our experiment a major neurotoxic and cytostatic power in comparison with methotrexate. Our conclusion is that human embryo neuronal culture in vitro is a powerful instrument for physiology and human therapy for cancer and neurodegenerative diseases.

GPER agonist G1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after cerebral ischemia/reperfusion injury

Studies have confirmed a strong association between activation of the endoplasmic reticulum stress pathway and cerebral ischemia/reperfusion(I/R) injury.In this study,three key proteins in the endoplasmic reticulum stress pathway(glucose-regulated protein 78,caspase-12,and C/EBP homologous protein) were selected to examine the potential mechanism of endoplasmic reticulum stress in the neuroprotective effect of G protein-coupled estrogen receptor.Female Sprague-Dawley rats received ovariectomy(OVX),and then cerebral I/R rat models(OVX+ I/R) were established by middle cerebral artery occlusion.Immediately after I/R,rat models were injected with 100 μg/kg E2(OVX + I/R +E2),or 100 μg/kg G protein-coupled estrogen receptor agonist G1(OVX + I/R + G1) in the lateral ventricle.Longa scoring was used to detect neurobehavioral changes in each group.Infarct volumes were measured by 2,3,5-triphenyltetrazolium chloride staining.Morphological changes in neurons were observed by Nissl staining.Terminal dexynucleotidyl transferase-mediated nick end-labeling staining revealed that compared with the OVX + I/R group,neurological function was remarkably improved,infarct volume was reduced,number of normal Nissl bodies was dramatically increased,and number of apoptotic neurons in the hippocampus was decreased after E2 and G1 intervention.To detect the expression and distribution of endoplasmic reticulum stress-related proteins in the endoplasmic reticulum,caspase-12 distribution and expression were detected by immunofluorescence,and mRNA and protein levels of glucose-regulated protein 78,caspase-12,and C/EBP homologous protein were determined by polymerase chain reaction and western blot assay.The results showed that compared with the OVX+ I/R group,E2 and G1 treatment obviously decreased mRNA and protein expression levels of glucose-regulated protein 78,C/EBP homologous protein,and caspase-12.However,the G protein-coupled estrogen receptor antagonist G15(OVX + I/R + E2 + G15) could eliminate the effect of E2 on cerebral I/R injury.These results confirm that E2 and G protein-coupled estrogen receptor can inhibit the expression of endoplasmic reticulum stress-related proteins and neuronal apoptosis in the hippocampus,thereby improving dysfunction caused by cerebral I/R injury.Every experimental protocol was approved by the Institutional Ethics Review Board at the First Affiliated Hospital of Shihezi University School of Medicine,China(approval No.SHZ A2017-171) on February 27,2017.

血清动态神经元特异性烯醇化酶、C反应蛋白水平与脑震荡患者病情严重程度相关性分析

目的:探究脑震荡患者血清动态神经元特异性烯醇化酶(NSE)、C反应蛋白(CRP)水平与病情严重程度的关系。方法:选取右江民族医学院附属梧州医院2019年1月-2021年3月收治的脑震荡患者60例作为研究对象,根据脑震荡评分将患者分为轻、中、重度组,并分别于脑震荡发生后4~8h、24h以及72h应用化学发光法、生物化学法对血清中NSE、CRP水平进行检测,分析NSE、CRP与脑震荡的相关性。结果:伤后4~8 h,不同脑震荡分级患者的NSE与CRP水平比较,差异无统计学意义(P>0.05),伤后24 h以及72 h时,NSE与CRP水平较伤后4~8 h有所降低,且其水平随着患者脑震荡分级的严重性升高,差异有统计学意义(P<0.05)。经过Pearson分析,NSE、CRP与脑震荡呈正相关(P<0.05)。结论:脑震荡分级患者的NSE、CRP水平随着病情严重程度增加而升高,可通过NSE与CRP水平反映脑震荡患者的病情严重情况。

血清NSE、S-100β、CRP/PA预测重度脑挫裂合并脑疝患者院内短期死亡的价值

目的分析血清神经元特异性烯醇化酶(NSE)、S-100β、C反应蛋白(CRP)/前白蛋白(PA)预测重度脑挫裂合并脑疝患者院内短期死亡的价值。方法回顾性分析2020年5月至2023年5月在西安高新医院接受去骨瓣减压术治疗的130例重度脑挫裂合并脑疝患者的临床资料,男85例,女45例,年龄(55.13±10.33)岁;入院时格拉斯哥昏迷量表(GCS)评分3~8分56例,>8分74例;脑挫伤部位:单发79例,多发51例。记录术后30 d患者生存情况并进行分组,26例(20.00%)于院内死亡为死亡组,104例(80.00%)治疗后顺利出院为存活组。收集两组年龄、性别等基线资料,入院时采用酶联免疫吸附法和电化学发光法检测血清NSE、S-100β、CRP、PA水平,并计算CRP/PA水平。采用t检验和χ^(2)检验,采用多因素logistic回归分析法分析重度脑挫裂合并脑疝患者院内短期死亡的危险因素,以受试者操作特征曲线(ROC)观察血清NSE、S-100β、CRP/PA水平预测重度脑挫裂合并脑疝患者院内短期死亡的价值。结果死亡组入院时格拉斯哥昏迷量表(GCS)评分3~8分、多发脑挫伤、入院前1周使用抗凝药物的患者占比以及血清NSE、S-100β、CRP/PA水平均高于存活组(均P<0.05);多因素logistic回归分析显示,入院时GCS评分、脑挫伤部位、入院前1周使用抗凝药物及血清NSE、S-100β、CRP/PA水平均为重度脑挫裂合并脑疝患者院内短期死亡的危险因素(均P<0.05);ROC分析证实血清NSE、S-100β、CRP/PA水平均可用于预测重度脑挫裂合并脑疝患者院内短期死亡,曲线下面积分别为0.795、0.753、0.801(均P<0.05)。结论入院时GCS评分、脑挫伤部位、入院前1周使用抗凝药物、血清NSE、S-100β、CRP/PA水平均为重度脑挫裂合并脑疝患者院内短期死亡的危险因素,临床应结合以上指标对高危患者进行重点筛查,及时采取干预措施。

缺氧缺血性脑病外周血CysC、NSE、CK-BB、乳酸水平相关分析

目的探讨缺氧缺血性脑病胱抑素C(cystatin C)、神经元特异性烯醇化酶(NSE)、肌酸激酶脑型同工酶(CK-BB)、乳酸水平变化,并分析与脑损伤程度的相关性。方法回顾性分析2019年1月至2023年10月收治的98例缺氧缺血性脑病患儿为研究组,研究组中根据脑损伤严重程度神经评分(NBNA)分为轻度组36例,中度组32例,重度组30例,另选30例健康新生儿为对照组。检测受试者CysC、NSE、CKBB、乳酸水平,Pearson分析各指标与脑损伤程度的相关性;受试者工作特征曲线(ROC)分析CysC、NSE、CK-BB、乳酸对脑损伤严重程度的预测价值。结果病例组CysC、NSE、CK-BB、乳酸水平高于对照组(P<0.05)。重度组CysC、NSE、CK-BB、乳酸水平高于中度组、轻度组,中度组外周血CysC、NSE、CK-BB、乳酸水平明显高于轻度组(P<0.05)。Pearson分析CysC、NSE、CK-BB、乳酸各指标与脑损伤严重程度呈正相关关系(r=0.479、0.642、0.655、0.618,P<0.05)。ROC分析显示CysC、NSE、CK-BB、乳酸联合预测脑损伤严重程度诊断准确性最高。结论缺氧缺血性脑病患儿外周血CysC、NSE、CK-BB、乳酸水平与脑损伤病情严重程度密切相关,是早期反映新生儿脑损伤严重程度的敏感生化指标。

Specific effects of c-Jun NH2-terminal kinaseinteracting protein 1 in neuronal axons

c-Jun NH2-terminal kinase（JNK）-interacting protein 3 plays an important role in brain-derived neurotrophic factor/tropomyosin-related kinase B（Trk B） anterograde axonal transport. It remains unclear whether JNK-interacting protein 1 mediates similar effects, or whether JNK-interacting protein 1 affects the regulation of Trk B anterograde axonal transport. In this study, we isolated rat embryonic hippocampus and cultured hippocampal neurons in vitro. Coimmunoprecipitation results demonstrated that JNK-interacting protein 1 formed Trk B complexes in vitro and in vivo. Immunocytochemistry results showed that when JNK-interacting protein 1 was highly expressed, the distribution of Trk B gradually increased in axon terminals. However, the distribution of Trk B reduced in axon terminals after knocking out JNK-interacting protein 1. In addition, there were differences in distribution of Trk B after JNK-interacting protein 1 was knocked out compared with not. However, knockout of JNK-interacting protein 1 did not affect the distribution of Trk B in dendrites. These findings confirm that JNK-interacting protein 1 can interact with Trk B in neuronal cells, and can regulate the transport of Trk B in axons, but not in dendrites.