Neuron specific enolase,p53蛋白和proliferating-cell nuclear antigen在肺癌组织中的表达及意义

目的：研究神经元特异性烯醇化酶（neuronspecificenolase，NSE）的表达，与p53蛋白和增殖细胞核抗原（prolif－erating－cellnuclearantigen，PCNA）表达的关系及意义．方法：用特异性鼠抗人单克隆抗体，按LSAB免疫组织化学方法检测石蜡包埋的肺癌标本中NSE，p53蛋白和PCNA的表达．结果：在小细胞性肺癌（SmallCellLungCancer，SCLC）中，NSE阳性表达者，PCNA标记指数（LabellingIndex，LI）高于NSE阴性者，而p53蛋白的表达与NSE的表达无关．在非小细胞性肺癌（non－smallcelllungcancr，non－SCLC）中，p53蛋白的表达和PCNALI均与NSE的表达无关．结论：在SCLC的发生及发展过程中，神经内分泌功能可能起了部分作用．而p53抑癌基因在SCLC的发生中并不起着重要的作用．

Changes in plasma calcitonin gene-related peptide and serum neuron specific enolase in rats with acute cerebral ischemia after low-frequency electrical stimulation with different waveforms and intensities

Following acute cerebral ischemia in rats, plasma calcitonin gene-related peptide decreased and the level of serum neuron specific enolase and the volume of the infarction increased. Square-wave and triangular-wave electrical stimulation with low or high intensities could increase the plasma calcitonin gene-related peptide, decrease the serum neuron specific enolase and reduce the infarction volume in the brain in rats with cerebral ischemia. There was no significant difference between different wave forms and intensities. The experimental findings indicate that low-frequency electrical stimulation with varying waveforms and intensities can treat acute cerebral ischemia in rats.

Neuron-specific enolase expression in a rat model of radiation-induced brain injury following vascular endothelial growth factor-modified neural stem cell transplantation

BACKGROUND： Previous studies have shown that transplantation of vascular endothelial growth factor （VEGF）-modified neural stem cells （NSC） provides better outcomes, compared with neural stem cells, in the treatment of brain damage. OBJECTIVE： To compare the effects of VEGF-modified NSC transplantation and NSC transplantation on radiation-induced brain injury, and to determine neuron-specific enolase （NSE） expression in the brain. DESIGN, TIME, AND SETTING： The randomized, controlled study was performed at the Linbaixin Experimental Center, Second Affiliated Hospital, Sun Yat-sen University, China from November 2007 to October 2008. MATERIALS： VEGF-modified C17.2 NSCs were supplied by Harvard Medical School, USA. Streptavidin-biotin-peroxidase-complex kit （Boster, China） and 5, 6-carboxyfluorescein diacetate succinimidyl ester （Fluka, USA） were used in this study. METHODS： A total of 84 Sprague Dawley rats were randomly assigned to a blank control group （n = 20）, model group （n = 20）, NSC group （n = 20）, and a VEGF-modified NSC group （n = 24）. Rat models of radiation-induced brain injury were established in the model, NSC, and VEGF-modified NSC groups. At 1 week following model induction, 10 pL （5 ×10^4 cells/μL） VEGF-modified NSCs or NSCs were respectively infused into the striatum and cerebral cortex of rats from the VEGF-modified NSC and NSC groups. A total of 10μL saline was injected into rats from the blank control and model groups. MAIN OUTCOME MEASURES： NSE expression in the brain was detected by immunohistochemistry following VEGF-modified NSC transplantation. RESULTS： NSE expression was significantly decreased in the brains of radiation-induced brain injury rats （P 〈 0.05）. The number of NSE-positive neurons significantly increased in the NSC and VEGF-modified NSC groups, compared with the model group （P 〈 0.05）. NSE expression significantly increased in the VEGF-modified NSC group, compared with the NSC group, at 6 weeks following transplantation （P 〈 0.05）. CONCLUSION： VEGF-modified NSC transplantation increased NSE expression in rats with radiation-induced brain injury, and the outcomes were superior to NSC transplantation.

Plasma level of neuron specific enolase in patients with acute cerebral infarction:A case-control study

BACKGROUND： The plasma level of neuron specific enolase （NSE） can be used to diagnose and evaluate neuronal injury and predict early prognosis. OBJECTIVE： To observe the dynamic changes in plasma levels of NSE in patients with acute cerebral infarction, and to investigate its correlations with disease severity and prognosis. DESIGN, TIME AND SETTING： This non-randomized, concurrent case-control experiment was performed at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007. PARTICIPANTS： Eighteen patients with acute cerebral infarction, who received treatment at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007, were recruited into the patient group. An additional 10 healthy individuals, who received health examinations simultaneously, were included as controls. METHODS： Following admission （within 3 days） and at days 6, 12, and 30 subsequent to acute cerebral infarction attack, 3 mL venous blood was taken from each patient before the morning meal to determine the plasma level of NSE by enzyme-labeled immunosorbent assay. One-time blood extraction was performed in each healthy subject during the health examination for the same purpose as in patients. At 6 and 30 days following acute cerebral infarction attack, CT examination was performed for calculation of cerebral infarction volume according to the Tada formula. Following admission and at 30 days of disease invasion, all patients were scored by the National Institutes of Health Stroke Scale （NIHSS, 13 items）. MAIN OUTCOME MEASURES： Comparison of NSE plasma level between acute cerebral infarction patients and healthy individuals; correlations of NSE plasma level in acute cerebral infarction patients with cerebral infarction volume, NIHSS score, and prognosis. RESULTS： Following admission and at days 6 and 12 of disease invasion, the plasma level of NSE was significantly higher in the patient group than in the control group （P 〈 0.05）. Following admission and at day 30 of disease invasion, the NIHSS scores of the patient group were 17.706 and 11.222, respectively. Following admission and at day 6 of disease invasion, the plasma level of NSE was positively correlated with cerebral infarction volume （r = 0.503, 0.435, P 〈 0.05）, but it was negatively correlated with NIHSS score （r = -0.571, 0.368, P 〈 0.05）. The plasma level of NSE was mostly correlated with cerebral infarction volume, followed by NIHSS score, and lastly prognosis, with regression coefficients of 0.386, 0.343, and 0.340, respectively. CONCLUSION： The plasma level of NSE is higher in patients with acute cerebral infarction than in the healthy population. It can reflect infarct severity and predict early prognosis of acute cerebral infarction.

The diagnostic value of neuron specific enolase in patients with gliomas

Objective: In order ic look into the alterations and effects of neuron specific enolase (NSE) in cerebralspinal fluid (CSF ) and serum of foe paticnts with glioma and meningiomas. Methods: We studied CSF and serumlevels of NSE in 40 patients with gliomas and 10 with meningiomas;3 days before and after operation byradioimmunoassay. Results: Compared with the value of NSE: in CSF and serum from 10 control patients. samplesfrom patients with malignant gliomas contained abnormally high level of NSE before operation (P < 0. 05 ) butnormal level after operation (P >0. 05 ). However. samples from patients with low grade gliomas andmeningiomas were within normal range before and after operation (P >0. 05). Gliomas with totall refectionshowed normal NSE values but with sub lotal removal presented high levels of NSE after surgery (P < 0. 05).Conclusion: The increased value of NSE in patients with malignant gliomas may be associated with elevated rate of glucolysis. As one of the new tumor markers NSE Is postulated to play an important role in the diagnosi followup and monitoring of gliomas.

Flunarizine and lamotrigine prophylaxis effects on neuron-specific enolase, S-100, and brain-specific creatine kinase in a fetal rat model of hypoxic-ischemic brain damage

BACKGROUND： Calcium antagonists may act as neuroprotectants, diminishing the influx of calcium ions through voltage-sensitive calcium channels. When administered prophylactically, they display neuroprotective effects against hypoxic-ischemic brain damage in newborn rats. OBJECTIVE： To investigate the neuroprotective effects of flunarizine （FNZ）, lamotrigine （LTG） and the combination of both drugs, on hypoxic-ischemic brain damage in fetal rats. DESIGN AND SETTING： This randomized, complete block design was performed at the Department of Pediatrics, Shenzhen Fourth People＇s Hospital, Guangdong Medical College. MATERIALS： Forty pregnant Wistar rats, at gestational day 20, were selected for the experiment and were randomly divided into FNZ, LTG, FNZ ＋ LTG, and model groups, with 10 rats in each group. METHODS： Rats in the FNZ, LTG, and FNZ ＋ LTG groups received intragastric injections of FNZ （0.5 mg/kg/d）, LTG （10 mg/kg/d）, and FNZ （0.5 mg/kg/d） ＋ LTG （10 mg/kg/d）, respectively. Drugs were administered once a day for 3 days prior to induction of hypoxia-ischemia. Rats in the model group were not administered any drugs. Three hours after the final administration, eight pregnant rats from each group underwent model establishment hypoxia-ischemia brain damage to the fetal rats. Cesareans were performed at 6, 12, 24, and 48 hours later; and 5 fetal rats were removed from each mother and kept warm. Two fetuses without model establishment were removed by planned cesarean at the same time and served as controls. A total of 0.3 mL serum was collected from fetal rats at 6, 12, 24, and 48 hours, respectively, following birth. MAIN OUTCOME MEASURES： Serum protein concentrations of neuron-specific enolase and S-100 were measured by ELISA. Serum concentrations of brain-specific creatine kinase were measured using an electrogenerated chemiluminescence method. RESULTS： Serum concentrations of neuron-specific enolase, S-100, and brain-specific creatine kinase were significantly higher in the hypoxic-ischemic fetal rats, compared with the non-hypoxic-ischemic group. Serum concentrations of neuron-specific enolase, S-100, and brain-specific creatine kinase were significantly less in the FNZ, LTG, and FNZ ＋ LTG groups following ischemia, compared with the model group （P 〈 0.01）. However, these values were significantly greater in the FNZ and LTG groups, compared with the FNZ ＋ LTG group, following ischemia （P 〈 0.01）. CONCLUSION： Preventive antenatal use of oral FNZ and LTG has positive neuroprotective effects on intrauterine hypoxic-ischemic brain damage. The combined effect of these two drugs is superior.

Electrophoretic Determination of Aqueous and Serum Neuron-specific Enolase in the Diagnosis of Retinoblastoma

Purpose: Neuron-specific enolase (NSE) of containing γ-enolase is considered valuable in the diagnosis of tumours of neuroectodermal origin.Method : We used rapid electrophoretic method on cellulose acetate plate to determine the pattern of enolase isoenzymes in 21 aqueous humor and 23 serum specimens from retinoblastoma (Rb) and 21 aqueous and 25 serum specimens from 25 control cases to evaluate NSE in the diagnosis of Rb. The assay allowed assessment of all three major isoenzymes (aa,aγ and γγ),and NSE relative activity and its percentage in the total relative activity of the three enolase isoenzymes were assessed by means of fluorometer.Result: Aqueous from all patients with Rb contained aa,ar and rr isoenzymes and presented strong postitive, the positive rate of NSE being 100% and its relative activity accounting for 45 ± 9% of the total relative activity of the 3 enolase isoenzymes; No enolase was detectable in control aqueous with cataract, glaucoma and Coats's diseases (4 cases),but in two

THE EXTENSIVENESS AND SPECIFICITY OF EFFECT OF ELECTROACUPUNCTURE AT DIFFERENT ACUPOINTS ON NOCICEPTIVE RESPONSE OF CONVERGENT NEURONS IN TRIGEMINAL NUCLEUS CAUDALIS

Experiments were carried out on rats anaesthetized with uraethane. The sponta-neous discharges and nociceptive responses of convergent neurons in the right trigerninal nucleus cau-dalis(TNC) to noxious stimuli at receptive field (cheek) were recorded extracellularly with glass mi-cro-electrode. Electroacupuncture (EA ) was applied at bilateral " Xiaguan" (ST 7 on face ) or "Zusanli" (ST 36 on shank) acupoint with Iow (2V) and high (18V) intensity. The noclceptive re-sponse of convergent neurons in TNC could be inhihited by low intensity EA applied at "Xiaguan" butnot "Zusanlil", showing the specificity of acupoints. High intensity EA at either "Xiaguan" or "Zusan-li" also reduced the nociceptive responses, showing the analgesic extensiveness of acupoints. We sug-gest that "the gate of control" mechanism plays a main role in low intensity EA and "diffuse noxiousinhibitory controls" (DNIC) rnechanism does so in high intensity EA.The results suggest that we should pay attention to the location of acupoints,

Neuron-specific Enclose and Myelin Basic Protein in Cerebrospinal Fluid of Patients with First Episode Schizophrenia

In order to study whether patients with schizophrenia have cerebral injury, neuron-specific enolase （NSE） and myelin basic protein （MBP）in cerebrospinal fluid （CSF） of 33 patients with first episode schizophrenia and 9 from the control group were determined by double antibody sandwich enzyme immunoassay method. The results showed that there was significant difference in the NSE contents between the experimental group and control group （P〈0.01）. The NSE contents in CSF in the experimental group were positively correlated with MBP in schizophrenia patients （P〈 0.05）. These findings suggested that patients with schizophrenia had cerebral injury.

Key elements determining the intestinal region-specific environment of enteric neurons in type 1 diabetes

Diabetes,as a metabolic disorder,is accompanied with several gastrointestinal(GI)symptoms,like abdominal pain,gastroparesis,diarrhoea or constipation.Serious and complex enteric nervous system damage is confirmed in the background of these diabetic motility complaints.The anatomical length of the GI tract,as well as genetic,developmental,structural and functional differences between its segments contribute to the distinct,intestinal region-specific effects of hyperglycemia.These observations support and highlight the importance of a regional approach in diabetes-related enteric neuropathy.Intestinal large and microvessels are essential for the blood supply of enteric ganglia.Bidirectional morpho-functional linkage exists between enteric neurons and enteroglia,however,there is also a reciprocal communication between enteric neurons and immune cells on which intestinal microbial composition has crucial influence.From this point of view,it is more appropriate to say that enteric neurons partake in multidirectional communication and interact with these key players of the intestinal wall.These interplays may differ from segment to segment,thus,the microenvironment of enteric neurons could be considered strictly regional.The goal of this review is to summarize the main tissue components and molecular factors,such as enteric glia cells,interstitial cells of Cajal,gut vasculature,intestinal epithelium,gut microbiota,immune cells,enteroendocrine cells,prooxidants,antioxidant molecules and extracellular matrix,which create and determine a gut region-dependent neuronal environment in diabetes.

Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury

Spinal Cord Injury(SCI)is a debilitating condition characterized by damage to the spinal cord,resulting in loss of function,mobility,and sensation.Although increasingly prevalent in the US,no FDA-approved therapy exists due to the unfortunate complexity of the condition,and the difficulties of SCI may be furthered by the development of SCI-related complications,such as osteoporosis.SCI demonstrates two crucial stages for consideration:the primary stage and the secondary stage.While the primary stage is suggested to be immediate and irreversible,the secondary stage is proposed as a promising window of opportunity for therapeutic intervention.Enolase,a metabolic enzyme upregulated after SCI,performs non-glycolytic functions,promoting inflammatory events via extracellular degradative actions and increased production of inflammatory cytokines and chemokines.Neuron-specific enolase(NSE)serves as a biomarker of functional damage to neurons following SCI,and the inhibition of NSE has been demonstrated to reduce signs of secondary injury of SCI and to ameliorate dysfunction.This Viewpoint article involves enolase activation in the regulation of RANK-RANKL pathway and summarizes succinctly the mechanisms influencing osteoclast-mediated resorption of bone in SCI.Our laboratory proposes that inhibition of enolase activation may reduce SCI-induced inflammatory response and decrease osteoclast activity,limiting the chances of skeletal tissue loss in SCI.

Transcriptional regulation in the development and dysfunction of neocortical projection neurons

Glutamatergic projection neurons generate sophisticated excitatory circuits to integrate and transmit information among different cortical areas,and between the neocortex and other regions of the brain and spinal cord.Appropriate development of cortical projection neurons is regulated by certain essential events such as neural fate determination,proliferation,specification,differentiation,migration,survival,axonogenesis,and synaptogenesis.These processes are precisely regulated in a tempo-spatial manner by intrinsic factors,extrinsic signals,and neural activities.The generation of correct subtypes and precise connections of projection neurons is imperative not only to support the basic cortical functions(such as sensory information integration,motor coordination,and cognition)but also to prevent the onset and progression of neurodevelopmental disorders(such as intellectual disability,autism spectrum disorders,anxiety,and depression).This review mainly focuses on the recent progress of transcriptional regulations on the development and diversity of neocortical projection neurons and the clinical relevance of the failure of transcriptional modulations.

Neuron specific enolase is a potential target for regulating neuronal cell survival and death: implications in neurodegeneration and regeneration

Enolase is a multifunctional enzyme primarily involved in catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate during glycolysis and the reverse reaction during gluconeogenesis[1-4].Though typically expressed in the cytosol,enolase has been shown to migrate to the cell surface upon inflammatory signal[3].

Significance of serum neuron-specific enolase in patients with acute traumatic brain iniurv

Objective: To study the association between serum neuron-specific enolase (NSE) and the extent of brain damage and the outcome after acute traumatic brain injury (TBI). Methods: The release patterns of serum NSE in 78 patients after acute TBI were analyzed by using the enzyme linked immunosobent assay. The levels of NSE were compared with Glasgow coma scale, the category of brain injury and the outcome after 6 months of injury. Results: There were different NSE values in patients with minor (12.96 μg/L±2.39 μg/L), moderate (23.44 μg/L±5.33 μg/L) and severe brain injury (42.68 μg/L±4.57 μg/L). After severe TBI, the concentration of NSE in patients with epidural hematomas was 13.38 μg/L±4.01 μg/L, 24.03 μg/L±2.85 μg/L in brain contusion without surgical intervention group, 55.20 μg/L±6.35 μg/L in brain contusion with surgical intervention group, and 83.85 μg/L±15.82 μg/L in diffuse brain swelling group. There were close correlations between NSE values and Glasgow coma scale (r=-0.608, P<0.01) and the extent of brain injury (r=0.75, P<0.01). Patients with poor outcome had significantly higher initial and peak NSE values than those with good outcome (66.40 μg/L±9.46 μg/L, 94.24 μg/L±13.75 μg/L vs 32.16 μg/L±4.21 μg/L, 34.08 μg/L±4.40 μg/L, P<0.01, respectively). Initial NSE values were negatively related to the outcome (r=-0.501, P<0.01). Most patients with poor outcomes had persisting or secondary elevated NSE values. Conclusions: Serum NSE is one of the valuable neurobiochemical markers for assessment of the severity of brain injury and outcome prediction.

Effect of 8-bromo cyclic AMP on neuron specific enolase, heat shock protein, nitric oxide, nitric oxide synthase and nitric oxide synthase mRNA in human retinoblastoma HXO Rb44 cells and cell differentiation

Objective To study the effect of 8 bromo cyclic AMP (8 Br cAMP) on nitric oxide synthase (NOS) mRNA, NOS and nitric oxide (NO) product, heat shock protein (hsp)70 and neuron specific enolase (NSE) in human retinoblastoma HXO Rb44 cells and the effect related to cell differentiation Methods Cultured human retinoblastoma HXO Rb44 cells were divided into two aliquots One was cultured with 2×10 5 ?mol/L of 8 Br cAMP for 24 hours as the experiment group; the other was treated with no 8 Br cAMP as the control group The cell suspensions in concentration of 1×10 7/ml in both groups were dropped onto the nitrocellulose membrane (NCM) The NOS mRNA was detected with the biotin labeled NOS cDNA probe by RNA dot blot The NOS activity was detected by protein dot blot The immunoreactivity (IR) of hsp70 and NSE was detected by protein dot blot The NO was detected by nitrate reductase method NCM specimens were analyzed by a TLC scanner for detection of the dot blot signal intensity Results The signals of NOS mRNA, NOS activity, hsp70 IR, NSE IR, and NO content in the experiment group were higher than those in the control group ( P <0 05-0 01) Conclusions 8 Br cAMP could increase NO product and the expression of NOS mRNA, NOS , NSE and hsp70 The results indicate that 8 Br cAMP could facilitate synthesis of NO in the neuroblastoma HXO Rb44 cells which could have tendency toward neuron development, suggesting that the increased hsp70, NO and NOS may involve cell differentiation of the retinoblastoma HXO Rb44

卵圆孔未闭导致隐源性卒中患者血清cTn I,NSE水平检测及诊断价值研究

目的 探究卵圆孔未闭(PFO)导致隐源性卒中患者血清心肌钙蛋白I(cTn I)、神经元特异性烯醇化酶(NSE)蛋白表达及诊断价值。方法 选取2020年12月~2022年12月达州市中心医院收治的PFO患者108例,根据患者是否导致隐源性卒中分为隐源性卒中组(卒中组,n=32)和非隐源性卒中组(未卒中组,n=76)。根据美国国立卫生研究院卒中量表(NIHSS)评估神经功能缺损程度,分为轻度组(<4分,n=10)、中度组(4~15分,n=15)和重度组(>15分,n=7)。全自动生化分析仪检测所有患者纤维蛋白原(FIB)、C反应蛋白(CRP)和丙氨酸氨基转移酶(ALT)水平。采用ELISA检测血清中cTn I,NSE水平。ROC曲线分析血清cTn I,NSE对PFO导致隐源性卒中的诊断价值;Logistic回归分析影响PFO患者隐源性卒中发生的因素。结果 与未卒中组相比,卒中组患者FIB(3.20±0.36g/L vs 2.95±0.30g/L),CRP(73.58±7.43mg/L vs 62.52±7.11mg/L),ALT(68.58±6.82U/L vs 61.08±6.28U/L),cTn I(0.78±0.10ng/L vs 0.58±0.08ng/L)和NSE(37.52±3.82μg/L vs 30.35±3072μg/L)水平显著升高,差异具有统计学意义(t=3.722~10.994,均P <0.05)。与轻度组相比,中度组和重度组患者血清中cTn I,NSE水平显著升高(t=5.891,7.177;3.458,4.105),重度组cTn I,NSE水平显著高于中度组(t=2.474,1.336),差异具有统计学意义(均P<0.05)。二者联合诊断PFO患者隐源性卒中发生的AUC(95%CI)为[0.981(0.962~1.000)],高于cTn I[0.878(0.864~0.948)],NSE[0.911(0.850-0.972)]单独诊断(Z=8.621,6.477,均P <0.001)。Logistic回归分析显示,cTn I(OR=2.631,95%CI:1.508~4.591),NSE(OR=2.841,95%CI:1.514~5.330)是PFO患者隐源性卒中发生的影响因素(均P <0.05)。结论 PFO患者导致隐源性卒中患者血清中cTn I,NSEl水平显著升高,对PFO患者发生隐源性卒中具有一定的诊断价值。

通调心肾针刺法结合温阳补肾灸治疗血管性痴呆的疗效及对认知功能的影响

目的观察通调心肾针刺法结合温阳补肾灸治疗血管性痴呆(VD)的临床疗效及对事件相关电位P300、神经元特异性烯醇化酶(NSE)及乙酰胆碱酯酶(AChE)的影响。方法采用随机数字表法将60例VD患者分为针灸组和西药组各30例。2组均予调控血压、血糖、血脂等西医基础治疗;西药组予盐酸多奈哌齐片,每次5mg,每日1次,口服;针灸组在西药组治疗基础上,予通调心肾针刺法结合温阳补肾灸,每日1次,每周6次;2组均连续治疗4周。于治疗前后当日评估2组患者简易智力状态检查量表(MMSE)、日常生活能力量表(ADL)评分,检测血清NSE、AChE浓度,测定事件相关电位P300,并判定MMSE和P300的异常检出率变化。监测2组安全性指标。结果与本组治疗前比较,2组MMSE评分、ADL评分均显著提高(P<0.05),针灸组P300潜伏期下降、P300波幅升高(P<0.05),2组NSE、AChE水平降低(P<0.05);与西药组比较,针灸组治疗后MMSE评分、ADL评分及P300波幅升高,P300潜伏期下降,NSE、AChE水平下降(P<0.05)。患者P300潜伏期异常检出率明显高于MMSE评分异常检出率(P<0.05);与本组治疗前比较,针灸组患者P300潜伏期异常率和MMSE评分异常率降低(P<0.05)。2组均未见明显不良反应。结论通调心肾针刺法结合温阳补肾灸能提高患者认知功能及改善日常生活能力,其机制可能与降低NSE及AChE水平有关,事件相关电位P300在判断VD及认知能力方面较MMSE更为敏感。

病毒性脑膜炎患者脑脊液NSE、SAA、IP-10、IL-23水平与病情进展的关系

目的探讨病毒性脑膜炎患者脑脊液神经元特异性烯醇化酶(NSE)、血清淀粉样蛋白A(SAA)、干扰素诱导蛋白-10(IP-10)和白细胞介素(IL)-23水平与病情进展的关系。方法选取2022年1月至2024年4月在该院确诊的108例病毒性脑膜炎患者作为研究对象,根据患者病情严重程度将其分为轻度组(63例)和中重度组(45例)。采用酶联免疫吸附试验检测脑脊液NSE、IP-10、IL-23水平,采用免疫散射比浊法检测脑脊液SAA水平。比较轻度组和中重度组病毒性脑膜炎患者脑脊液NSE、SAA、IP-10、IL-23水平。所有患者均随访1个月,根据随访结果分为预后良好组和预后不良组,比较两组脑脊液NSE、SAA、IP-10、IL-23水平。绘制受试者工作特征(ROC)曲线分析脑脊液NSE、SAA、IP-10、IL-23单独及联合检测对病毒性脑膜炎严重程度的诊断价值。结果轻度组和中重度组年龄、性别、发热时间、低钾血症比例、感觉障碍比例比较,差异均无统计学意义(P>0.05)。轻度组脑脊液NSE、SAA、IP-10、IL-23水平均低于中重度组,差异均有统计学意义(P<0.05)。ROC曲线分析结果显示,脑脊液NSE、SAA、IP-10、IL-23单独及联合检测诊断病毒性脑膜炎严重程度的曲线下面积(AUC)分别为0.706、0.723、0.695、0.641、0.760,联合检测的AUC大于各项指标单独检测的AUC(P<0.05)。预后良好组纳入78例,预后不良组纳入30例。预后良好组脑脊液NSE、SAA、IP-10、IL-23水平均低于预后不良组,差异均有统计学意义(P<0.05)。结论脑脊液NSE、SAA、IP-10和IL-23水平显著升高与病情严重程度及预后效果有关,提示这些生物标志物可作为病毒性脑膜炎病情进展的重要预测因子。

Autologous cord blood vs individualized supplements in autistic spectrum disorder:CORDUS study results

BACKGROUND Cellular therapies have started an important new therapeutic direction in autistic spectrum disorder(ASD),and the ample diversity of ASD pathophysiology and the different types of cell therapies prompt an equally ample effort to employ clinical studies for studying the ASD causes and cell therapies.Stem cells have yielded so far mixed results in clinical trials,and at patient level the results varied from impressive to no improvement.In this context we have administered autologous cord blood(ACB)and a non-placebo,material intervention repre-sented by an individualized combination of supplements(ICS)to ASD children.METHODS CORDUS clinical study is a crossover study in which both oral ICS and intravenous ACB were sequentially administered to 56 children;ACB was infused as an inpatient procedure.Treatment efficacy was evaluated pre-treatment and post-treatment at 6 months by an independent psychotherapist with Autism Treatment Evaluation Checklist,Quantitative Checklist for Autism in Toddlers and a 16-item comparative table score,after interviewing the children’s parents and therapists.Before and after each intervention participants had a set of blood tests including inflammatory,metabolic and oxidative markers,and the neuronal specific enolase.RESULTS No serious adverse reactions were noted during and after cord blood or supplement administration.ACB improved evaluation scores in 78%of children with age 3–7-years(n=28),but was much less effective in kids older than 8 years or with body weight of more than 35 kg(n=28;only 11%of children improved scores).ICS yielded better results than ACB in 5 cases out of 28,while in 23 kids ACB brought more improvement than ICS(P<0.05);high initial levels of inflammation and ferritin were associated with no improvement.Ample individual differences were noted in children's progress,and statistically significant improvements were seen after ACB on areas such as verbalization and social interaction,but not on irritability or aggressive behavior.CONCLUSION ACB has superior efficacy to ICS in ASD;high inflammation,ferritin,age and body weight predict less improvement;more clinical studies are needed for studying ACB efficacy in ASD.

右美托咪定在老年患者冠状动脉旁路移植术围手术期疗效的Meta分析

目的评估右美托咪定在老年患者冠状动脉旁路移植术(CABG)中的安全性、有效性。方法检索PubMed、Cochrane Libary、Embase、Web of Science数据库、中国知网、维普数据库、万方数据库中有关右美托咪定用于老年患者CABG的随机对照试验研究文献。检索时间为建库至2022年12月,语种为中文和英文。由两位研究者独立进行文献筛选、资料提取和方法学质量评价,使用RevMan 5.3软件对收集的数据进行Meta分析。结果最终纳入18项研究。Meta分析结果显示,右美托咪定组与对照组CABG术中机械通气时间比较差异无统计学意义(P>0.05)。右美托咪定组CABG术后住院时间明显短于对照组(MD=-1.96,95%CI-3.43~-0.49,P=0.009)。右美托咪定组CABG术后神经元特异性烯醇化酶(NSE)水平明显低于对照组(MD=-2.42,95%CI-3.96~-0.88,P=0.002),术后1 d右美托咪定组NSE水平明显低于对照组(P<0.05)。右美托咪定组CABG术后S-100β蛋白水平明显低于对照组(MD=-0.18,95%CI-0.25~-0.11,P<0.00001),术后即刻右美托咪定组S-100β蛋白水平低于对照组(P<0.01)。右美托咪定组CABG患者简易智力状态检查量表(MMSE)评分明显高于对照组(MD=1.63,95%CI 1.05~2.21,P<0.00001),术后3 d、术后7 d右美托咪定组MMSE评分高于对照组(P<0.01)。两组低血压、心动过缓发生率比较差异无统计学意义(P>0.05)。右美托咪定组患者的谵妄发生率低于对照组(OR=0.40,95%CI 0.29~0.56,P<0.00001),且体外循环右美托咪定组、非体外循环右美托咪定组患者的谵妄发生率均低于相应对照组(OR=0.34,95%CI 0.19~0.61,P=0.0003;OR=0.44,95%CI 0.29~0.66,P<0.0001)。右美托咪定组患者术后死亡率低于对照组(OR=0.32,95%CI 0.11~0.95,P=0.04)。结论老年患者CABG术中使用右美托咪定可改善其术后认知功能、降低术后谵妄发生率和术后死亡率、缩短住院时间。