Role Of Neuron-specific Enolase Research Articles

The Role of Neuron Specific Enolase, S100B, Glial Fibrillary Acidic Protein, and Myelin Basic Protein as Prognostic and Survival Values in Traumatic Brain Injury: Systematic Review and Meta-analysis

The Role of Neuron Specific Enolase, S100B, Glial Fibrillary Acidic Protein, and Myelin Basic Protein as Prognostic and Survival Values in Traumatic Brain Injury: Systematic Review and Meta-analysis

Neuron-specific enolase as a prognostic biomarker in acute ischemic stroke patients treated with reperfusion therapies.

Ischemic stroke is a significant global health concern, with reperfusion therapies playing a vital role in patient management. Neuron-specific enolase (NSE) has been suggested as a potential biomarker for assessing stroke severity and prognosis, however, the role of NSE in predicting long-term outcomes in patients undergoing reperfusion therapies is still scarce. To investigate the association between serum NSE levels at admission and 48 h after reperfusion therapies, and functional outcomes at 90 days in ischemic stroke patients. This study conducted a prospective cross-sectional analysis on consecutive acute ischemic stroke patients undergoing intravenous fibrinolysis and/or endovascular thrombectomy. Functional outcomes were assessed using the modified Rankin Scale (mRS) at 90 days post-stroke and two groups were defined according to having unfavorable (mRS3-6) or favorable (mRS0-2) outcome. Demographic, clinical, radiological, and laboratory data were collected, including NSE levels at admission and 48 h. Spearman's coefficient evaluated the correlation between analyzed variables. Logistic regression analysis was performed to verify which variables were independently associated with unfavorable outcome. Two ROC curves determined the cut-off points for NSE at admission and 48 h, being compared by Delong test. Analysis of 79 patients undergoing reperfusion treatment following acute stroke revealed that patients with mRS 3-6 had higher NIHSS at admission (p < 0.0001), higher NIHSS at 24 h (p < 0.0001), and higher NSE levels at 48 h (p = 0.008) when compared to those with mRS 0-2. Optimal cut-off values for NSE0 (>14.2 ng/mL) and NSE48h (>26.3 ng/mL) were identified, showing associations with worse clinical outcomes. Adjusted analyses demonstrated that patients with NSE48h > 26.3 ng/mL had a 13.5 times higher risk of unfavorable outcome, while each unit increase in NIHSS24h score was associated with a 22% increase in unfavorable outcome. Receiver operating characteristic analysis indicated similar predictive abilities of NSE levels at admission and 48 h (p = 0.298). Additionally, a strong positive correlation was observed between NSE48h levels and mRS at 90 days (r = 0.400 and p < 0.0001), suggesting that higher NSE levels indicate worse neurological disability post-stroke. Serum NSE levels at 48 h post-reperfusion therapies are associated with functional outcomes in ischemic stroke patients, serving as potential tool for patient long-term prognosis.

Role of Neuron-Specific Enolase, D-Dimer and C-Reactive Protein in the Cranial Nerve Injury After Surgery of Posterior Fossa Tumor

Cranial nerve injury after posterior cranial fossa tumor surgery (PCFTS) is a common symptom in clinic. Intracranial pressure (ICP) monitoring has been widely used in patients with severe posterior cranial fossa injuries. By establishing a rat model of PCFT, we explore the correlation between neuron-specific enolase (NSE), D-Dimer (D-D) and C-reactive protein (CRP) and provide the better clinical reference to cranial fossa injury treatment. 30 SD female rats aged 20–22 months; randomly divided them into control groups and experimental groups and experimental rats were further divided into 12 for moderately increased group (21–40 mmHg) and 8 for severely increased group (&gt;40 mmHg) to measure NSE, D-D, and CRP and analyze their relationship. NSE, DD, and CRP in severely increased group and moderately increased group were significantly higher than those in control group. NSE (103.69±7.84) μg/L, DD (1.52±0.25) mg/L, CRP (47.63)±8.59) mg/L in severely increased group was significantly higher than moderately increased group (NSE (61.77±30.11) μg/L, DD (0.97± 0.37) mg/L, CRP (30.65± 9.56) mg/L) (P &lt; 0.05). ICP is positively correlated with NSE, DD and CRP (r = 0.775, P = 0.000, intracranial pressure=18.589+0.254NSE; r =0.872, P =0.000, IC=10.564+0.254 DD; r =0.825, P =0.000, ICP = 9.73+0.774CRP). There is a positive correlation between cranial nerve injury and NSE, D-dimer and CRP after PCFTS. It can be evaluated by detecting the above values to assess the degree of cranial nerve injury so as to predict the patient’s condition.

The role of neuron-specific enolase (NSE) and S100B protein in the incidence of acute postoperative cognitive dysfunction (POCD) in geriatric patients receiving general anesthesia

Introduction: Postoperative cognitive dysfunction (POCD) following general anesthesia is frequent among geriatric patients worldwide. Neuroinflammation and neuronal injury have been associated with the incidence of POCD. Some biomarkers of brain damage including neuron-specific enolase (NSE) and S100B protein have been widely studied; however, their association with the incidence of POCD is still controversial. This study aimed to assess the correlation of serum NSE and S100B levels with the incidence of POCD among geriatric patients receiving general anesthesia. Methods: A prospective cohort study was conducted among geriatric patients receiving general anesthesia at Dr. Soetomo Hospital, Surabaya from July to October 2022. The Montreal Cognitive Assessment (MoCA) INA instrument was used to assess POCD, and enzyme-linked immunosorbent assay (ELISA) was used to quantify the levels of serum NSE and S100B. Spearman’s rank correlation was implemented to identify the correlation of MoCA INA scores with the levels of NSE and S100B. Mann-Whitney analysis was used to determine the association between NSE and S100B levels with the incidence of POCD. A p-value of ≤0.05 was considered statistically significant. Results: A total of 48 patients were enrolled in the study and 16.7% of them had POCD. Spearman’s correlation test suggested no significant correlation between MoCA INA score with serum NSE level (rs:-0.095; p=0.522) and S100B level (rs:-0.213; p=0.146). Mann-Whitney analysis indicated no significant difference in the NSE and S100B levels of patients with and without POCD (p=0.3470 and p=0.097, respectively). Conclusion: There was no significant association between NSE and S100B levels with the incidence of POCD among geriatric patients receiving general anesthesia during elective surgeries at Dr. Soetomo Hospital, Surabaya.

Role of Neuron-Specific Enolase in the Diagnosis and Disease Monitoring of Sarcoidosis.

Sarcoidosis is a systemic granulomatous disease of unknown etiology. The diagnosis of sarcoidosis is based on clinicopathologic findings accompanied by the formation of granulomas in multiple organs, including the lung. Although angiotensin-converting enzyme (ACE) and soluble interleukin 2 receptor (sIL-2R) are traditionally used for the diagnosis of sarcoidosis, specific diagnostic markers remain to be determined. In the current study, we found that serum neuron-specific enolase (NSE) levels were elevated in patients with sarcoidosis. Serum NSE levels were positively correlated with serum ACE and sIL-2R levels. The sensitivity of NSE alone was modest, but its combination with sIL-2R and ACE had the highest sensitivity compared to those of each single marker. When comparing serum NSE and pro-gastrin-releasing peptide (ProGRP) levels in SCLC patients with those in patients with sarcoidosis and nonsarcoidotic benign diseases, serum NSE could be used to distinguish SCLC from sarcoidosis and nonsarcoidosis by setting at a cutoff value of 17.0 ng/ml with a sensitivity of 73.5% and a specificity of 90.2%, which were comparable to those of ProGRP. Serum NSE levels were associated with organ involvement and were higher in sarcoidosis patients who had been treated with oral corticosteroid (OCS) than in those who had never received OCS therapies; there was a positive association between elevated serum NSE levels and OCS use. Increased concentrations of serum NSE in patients at the nonremission phase decreased after spontaneous remission, whereas serum NSE levels fluctuated in accordance with serum ACE or sIL-2R levels during the follow-up period in patients with sarcoidosis. These findings suggest that NSE could be a marker for the diagnosis and monitoring of the clinical outcome of patients with sarcoidosis.

Role of neuron-specific enolase, glial fibrillar acidic protein and NR2-antibodies in early diagnostic of ischemic stroke

Background. Application of a biomarker panel during the acute period of the ischemic stroke (IS) can contribute to a more accurate and prompter diagnostics and verification of the optimal approach to a patients’ management.Objective. We aimed to clarify values of neuron-specific enolase (NSE), glial fibrillar acidic protein (GFAP) and antibodies for NMDA receptor’s NR2-subunit (NR2-antibodies) in the acute period of IS, to compare with such values in patients without IS, to assess their relationship with severity of neurological deficit and short-term outcome and also to establish sensitivity and specificity of the biomarker panel.Design and methods. 63 patients with IS and 31 people (11 with chronic brain ischemia and 20 healthy individuals) as controls were included. Results. NSE and GFAP values in IS group exceeded reference values at the onset of disease, lowering significally by 10-14 day, while NR2-antibodies’ values were lower at the onset of the disease compared with controls, rising by 10-14 day. In patients with unfavourable short-term outcome higher levels of NSE, GFAP and NR2-antibodies were found. A panel of such biomarkers has higher sensitivity and specificity than each of them individually.Conclusion. Researched substances can be used in a biomarker panel for IS diagnostics, brain damage monitoring, patient’s condition evaluation and short outcome prognosing.

Role of neuron specific enolase as a biomarker in Parkinson’s disease

Parkinson’s disease (PD) is thought to be the most common neurodegenerative disease with movement disorder. The key motor symptoms are rigidity, tremor, akinesis/hypokinesia/bradykinesia, and postural instability. However, in our day-to-day clinical practice we tend to see several other symptoms which may be motor or non-motor. Non-motor symptoms (NMS) are quite common and debilitating. The pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta (SNPc) and accumulation of unfolded or misfolded alpha-synuclein. Diagnosis of PD is difficult in the pre-motor stage. Late diagnosis renders a substantial loss of dopaminergic neurons in SNPc and spread of disease in other parts of the brain. This may manifest as either full blown symptoms requiring multiple medications or may even lead to life threatening condition due to lack of early diagnostic tools and techniques. Biomarkers are required to diagnose PD at a very early stage when prevention is possible. Hence, we see a lot of interest among researchers involved in finding a biomarker specific to the disease. Biomarkers may be clinical, image based, genetic, and biochemical. Cerebrospinal fluid (CSF) and serum markers which may correlate with disease pathophysiology are of great significance. One such molecule which recently gained a lot of attention is neuron-specific enolase (NSE). The main aim of this paper is to highlight the role of NSE in predicting neurodegeneration and neuroinflammation ultimately reflecting damage of brain cells in PD.

The Possible Role of Neuron Specific Enolase and Neurofilament Light Protein as Markers for Organophosphorus-induced Neurotoxicity

Background: Acute organophosphorus (OP) poisoning is a common toxic emergency all over the worldespecially in the developing countries as Egypt. Neurological damage occurs after exposure to thesecompounds can lead to respiratory failure and death. Thus, it is important to identify the severity of poisoningand predict the need to ventilation support or death.Methods: A prospective study that included 50 adult patients presented with neurological manifestationsafter acute OP poisoning admitted to the ICU of Poison Control Center of Ain shams university (PCC-ASU),and 25 healthy volunteers. Meusering levels of Neuron Specific Enolase (NSE) and Neurofilament Light(NFL) protein and correlate this with severity according to APACHE II score and outcome of patients.Conclusion: There was a significant difference between cases and controls among levels of NSE and NFLprotein, also there was a significant correlation between NSE and NFL protein levels and prediction of bothM.V. need and mortality, so NSE and NFL protein can be used as markers for neurological damage afterexposure to OP compounds.

Neuropsychiatric sequelae of acute carbon monoxide poisoning: The predictive role of neuron specific enolase and glial fibrillary acidic protein

BackgroundAcute carbon monoxide (CO) poisoning is one of the most common poisons worldwide and neuropsychiatric sequelae (NS) are the most frequent form of its morbidity. ObjectivesThis study aimed to measure the percentage of patients liable to NS, to evaluate the cognitive profile of patients with NS and to assess the role of neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) in predicting the development of NS after acute CO poisoning. MethodsThis prospective study included 50 patients with acute CO poisoning presented to the Poison Control Center, Ain Shams University Hospitals during the period from beginning of November 2015 till the end of January 2017. Patients’ demographic characteristics, clinical manifestations and blood carboxyhemoglobin levels were recorded. Serum levels of NSE and GFAP were determined on admission. Every patient was invited to participate in a follow-up visit at a dedicated outpatient clinic one month after CO exposure. During the visit, a complete neurological examination, as well as a psychiatric evaluation using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders version 4 Axis-I were performed for detection of neurological and psychiatric disorders. Wechsler memory scale test was administrated for detection of cognitive deficits. The patients were divided into two groups based on the presence or absence of NS. ResultsCognitive impairment was found in 38 % of patients in the NS group. The serum levels of NSE and GFAP were significantly high in the NS group in comparison to the non-NS group. Receiver operating characteristic curves (ROC) determined the cut-off level of NSE at 39 ng/mL achieved 100 % sensitivity with 88.64 % specificity to predict the development of NS after acute CO poisoning while GFAP had 95.24 % sensitivity and 69.23 % specificity at a cut-off value of 2.8 ng/mL. ConclusionNSE and GFAP could be useful in the early identification of patients at risk of developing NS after CO poisoning helping in treatment plans and thus improving quality of care.

NSE, positively regulated by LINC00657-miR-93-5p axis, promotes small cell lung cancer (SCLC) invasion and epithelial-mesenchymal transition (EMT) process.

Background: Neuron specific enolase (NSE) is a specific biomarker for SCLC. However, the biological roles and aberrant expression of NSE in SCLC have not been well illustrated.Methods: The expression of NSE, miR-93-5p and LINC00657 in SCLC tissues and cell lines were detected using real time quantitative PCR (qRT-PCR) or immunohistochemistry. CCK8 assay was performed to detect cell proliferation. Cell migration and invasion capabilities were investigated by transwell assay. Epithelial-mesenchymal transition (EMT) process was verified by detecting epithelial marker E-cadherin and mesenchymal marker N-cadherin. The direct interactions between miR-93-5p and NSE or LINC00657 were predicted by bioinformatics tools and verified using dual luciferase reporter assay.Results: Upregulated expression of NSE in SCLC tumor tissues were positively associated with advanced tumor stage, distant metastasis and poor overall survival. Overexpression of NSE promoted cell proliferation, migration, invasion and EMT in SCLC cells, while silence of NSE inhibited these effects. Mechanically, NSE expression was positively correlated with LINC00657, and negatively correlated with miR-93-5p. Moreover, NSE was positively regulated by LINC00657 through sponging of miR-93-5p. LINC00657 and miR-93-5p promoted SCLC cell migration, invasion and EMT by NSE-mediated manner.Conclusion: Overall, our study revealed a novel role of NSE in SCLC. NSE was positively regulated by LINC00657 through competitively interacting with miR-93-5p, which may be potential targets for SCLC patients.

Knockdown of neuron-specific enolase suppresses the proliferation and migration of NCI-H209 cells.

Neuron-specific enolase (NSE) is generally considered as a marker for diagnosis and evaluation of the response to therapy in small cell lung cancer (SCLC). However, the role of NSE in the progression of SCLC remains to be elucidated. In the present study, the functions of NSE in SCLC, in addition to the potential mechanisms, were investigated using a loss-of-function approach with NSE-targeting small interfering (si)RNA. The knockdown of NSE markedly decreased the proliferation of NCI-H209 cells, as indicated by MTT assay (P<0.05). Furthermore, the silencing of NSE resulted in the formation of smaller and fewer colonies compared with that in the control group (P<0.001). Flow cytometric analysis indicated that the silencing of NSE resulted in a decreased S-phase population among NCI-H209 cells (P<0.05). Transwell assay demonstrated that the silencing of NSE suppressed the migration of NCI-H209 cells (P<0.001). NCI-H209 cells transfected with NSE siRNA-1 or negative control were collected and the protein levels of metastasis-associated genes were detected using western blot analysis. The results indicated that the knockdown of NSE led to downregulation of the pro-metastatic gene vascular endothelial growth factor (VEGF; P<0.05) and the upregulation of metastasis suppressor genes NM23 and E-cadherin (P<0.05). Taken together, the results of the present study demonstrated that the silencing of NSE suppressed the migration, proliferation and colony formation ability of SCLC cells and decreased the S-phase population. In addition, the knockdown of NSE resulted in the upregulation of E-cadherin and NM23 and the downregulation of VEGF. Collectively, these results indicated that intracellular NSE may have an important role in the progression of SCLC.

New insights into the role of neuron-specific enolase in tic disorders.

Neuron-specific enolase (NSE) has been suggested for demonstrating brain metabolism in neuropsychiatric disorders. This study assessed serum NSE levels in patients with tic disorders (TD). In this retrospective case-control study, we investigated whether NSE levels were increased in TD patients. Then, the influencing factors and correlations between NSE levels and clinical features were analyzed. Finally, we tested its diagnostic value for identifying tic severity. NSE levels were increased in TD patients, although no statistically significant difference was present between transient TD, chronic TD, and Tourette syndrome. Factors influencing NSE levels assessed by multiple linear regression were the Yale Global Tic Severity Scale (YGTSS) global severity scores and gender. There were significant correlations between NSE levels and tic severity. The optimal cut-off value to distinguish mild tics from moderate-severe tics estimated by receiver operating characteristics curve was 24.95ng/ml (AUC = 0.683). Our findings suggested that NSE may be a significant biomarker in TD but should be confirmed in further investigation.

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection.

Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells. While α-enolase is present in all neurological tissues, it can also be converted to neuron specific enolase (NSE). NSE is a glycolytic enzyme found in neuronal and neuroendocrine tissues that may play a dual role in promoting both neuroinflammation and neuroprotection in SCI and other neurodegenerative events. Elevated NSE can promote ECM degradation, inflammatory glial cell proliferation, and actin remodeling, thereby affecting migration of activated macrophages and microglia to the injury site and promoting neuronal cell death. Thus, NSE could be a reliable, quantitative, and specific marker of neuronal injury. Depending on the injury, disease, and microenvironment, NSE may also show neurotrophic function as it controls neuronal survival, differentiation, and neurite regeneration via activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways. This review discusses possible implications of NSE expression and activity in neuroinflammation, neurodegeneration, and neuroprotection in SCI and various neurodegenerative diseases for prognostic and therapeutic potential.

The role of serum neuron-specific enolase in patients with prostate cancer: a systematic review of the recent literature.

In this systematic review, we evaluated the value of serum concentrations of neuron-specific enolase (NSE) in patients with prostate cancer (PCa) in order to clarify the possible role of NSE in the diagnosis, management, treatment and monitoring of PCa. A comprehensive search of the recent literature was conducted to find relevant data on the role of NSE in PCa. Two hundred and eighty-two records were revealed, and 19 articles including 1,772 patients with PCa (either confirmed or suspected) were selected. After reviewing the articles, the major result was that elevated serum NSE appears to correlate with prognosis in advanced PCa, particularly in patients with progressive and metastatic castration-resistant PCa. Based on the existing literature, the role of serum NSE in PCa patients should be further evaluated.

The role of neuron specific enolase for endocrine ophthalmopathy and the formation of optic neuropathy

Aim . The aim of this work was to study the role of the neuron specific enolase during the endocrine ophthalmopathy and the formation of optic neuropathy. Materials and methods . The study 42 patients with EOC at the age of 41 (30; 47) years. It was 9 males (21%). The control group consisted of 15 healthy individuals matched by sex and age. The object of the study of blood serum and tear fluid. Measurement of NSE level was measured by ELISA CanAgNSEEJA. All persons included in the study was performed optical coherence tomography (OCT), ophthalmoscopes, perimetry. Statistical analysis of the data using the program Statistics 6.1. Results. An increase in the concentration of NSE in serum and lachrymal fluid of patients with endocrine ophthalmopathy, compared to healthy subjects. It should be noted that the increase in concentration of the test marker was associated with disease severity - more severe cases, accompanied by a large concentration of NSE. In severe IC-threatening loss of the highest concentration of NSE detected in blood serum and in the tear fluid. Conclusion . An increase in the concentration of NSE in patients with IC in the blood to a greater extent in the tear fluid, depending on the severity o f the IC. These studies allow the NSE to regard as an early marker of neuronal tissue damage GO, before the typical clinical and instrumental signs of optic neuropathy.

Elevated levels of cerebrospinal fluid neuron-specific enolase (NSE) in Alzheimer's disease

Neuron-specific enolase (NSE) is a neuronal glycolytic enzyme of which cerebrospinal fluid (CSF) levels are found altered following acute or prolonged neuronal damage. Investigations concerning the role of NSE in Alzheimer's disease (AD) are conflicting with both elevated and reduced levels. We measured CSF-levels of NSE in 32 patients with AD and 32 healthy subjects (HS) using an electrochemiluminescence immunoassay (ECLIA). Mean levels of adjusted NSE were significantly elevated in AD (18.12ng/mL (95% CI 15.63–20.60), HS 8.46ng/mL (95% CI 5.98–10.94), p=0.00002) and effect size for mean group differences high (1.84). NSE alone (cut-off score 15.80ng/mL, 94% sensitivity, 97% specificity) and in combination with T-tau and P-Tau had high diagnostic accuracy to differentiate AD from HS. NSE correlated significantly with T-tau (r≥0.87, p<0.000001) and P-tau (r≥0.88, p<0.000001) in both AD and HS. Our results indicate elevated CSF-NSE levels to reflect altered neuronal metabolism in AD that may be used in supporting AD diagnostics.

Cloning and expression of neuron-specific enolase in the corpus luteum of dairy goats

Neuron-specific enolase (NSE) is the key molecular marker for diffuse neuroendocrine system (DNES) cells, its expression in the pregnant corpus luteum (CL) of dairy goats was studied by the immunofluorescence method and the ultra structural characteristics of luteal cells were detected by the electron microscopy to identify the existence of DNES cells in the pregnant CL of dairy goats. Besides, the coding sequence of dairy goats NSE gene was cloned and its biological information was analyzed. Results revealed that NSE immunopositive cells exhibited widespread cytoplasmic staining throughout the whole pregnant CL. In addition, these cells showed typical characteristics of DNES cells in the electron microscopy. These results suggested that many DNES cells exist in the pregnant CL of dairy goats. Meanwhile, we identified the coding sequence of dairy goats NSE (GenBank Accession No. JN887466). Its nucleotide sequence homology was found to be 97.9%, 89.3%, 90% and 92.6%, respectively, compared with that of Bos taurus, Rattus norvegicus, Mus musculus and Homo sapiens, while the amino acid sequence homology was 99.1%, 97%, 97.2% and 98.2% respectively. These results first showed that the functional amino acids coded by the NSE gene were highly conserved in Caprine, B. taurus, R. norvegicus, M. musculus and H. sapiens. It was implied that the gene NSE in dairy goats had close homology to that of NSE of other species. Our findings demonstrated the possible existence of DNES cells in pregnant CL, providing new clue for further understanding of interactions between the neuroendocrine and reproductive systems. Characterization of gene sequence of dairy goats NSE will enable us to synthesize interference RNA for further study on the role of NSE on the formation, function and apoptosis of pregnant CL in dairy goats.

AP020 Therapeutic hypothermia after cardiac arrest: The role of neuron-specific enolase

Introduction: Impedance compensation methods and waveforms differ among manufacturers and can play an important role in defibrillation success. Aim of study is to compare efficacy of biphasic quasi-sinusoidal pulse (BQSP) with two truncated exponential pulses (BTEP) on high impedance porcine model. Methods: We evaluated the threshold of defibrillation energy (TDE) in 7 anesthetized pigs (35–62 kg). TDE was defined as the lowest delivered energy that would terminate electrically induced 20 sec VF. MSIEE experimental defibrillator delivered BQSP, BTEP-1 – defibrillator Philips HeartStart MRx and BTEP-2 – Lifepak-12. MSIEE defibrillator compensates high impedance by controlling current with fixed pulse duration (10 ms), while the 2 defibrillators from the USA by prolonging the pulse duration (from 9 to ≥18 ms). The pulses shape and duration corresponded to load resistance 100 ohms regardless of pig chest impedance (41–52 ohms). Results: TDE of BQSP (77.6±15.1 J) was significantly lower, than in BTP-1 by 25% (104.1±14.5 J) and in BTP-2 – by 29% (109.7±12.1 J), p<0.02. Conclusions: The results demonstrate that for transthoracic impedance about 100 ohms the current-based compensation method was more effective than the duration-based compensation technique. The BQSP (named the Gurvich-Venin pulse) has been employed in Russia for about 40 years (clinical efficacy 90–115 J = 80–90%). The first Russian AEDs will generate the optimizing Gurvich-Venin pulse.

Immunoreactivity of Neuron-Specific Enolase (NSE) in Human Pancreas in Health and Type 1

The role of neuron-specific enolase (glycolytic enzyme; marker of nerve fibers and Langerhans islet in human pancreas) in the development of type 1 diabetes mellitus was studied in autopsy specimens from 6 adult patients. Autopsied specimens of the pancreas from 7 subjects without carbohydrate metabolism disorders served as the control. Autopsied specimens of the pancreas from a child with the clinical diagnosis of type 1 diabetes mellitus, a child without carbohydrate metabolism disorders, and from 7 human fetuses of 15-40 weeks gestation were also studied. In control specimens, the neuron-specific enolase was detected in the pancreatic nerve fibers and Langerhans islets. Studies of pancreatic tissue specimens from adult patients with type 1 diabetes mellitus showed no immunopositive reaction to neuron-specific enolase in insulin-negative specimens. A possible mechanism of type 1 diabetes mellitus development is suggested.

Evaluation of the efficacy of nimodipine for acute cerebrovascular disease by neuron specific enolase

Objective To explore the role of neuron specific enolase (NSE) in the evaluation of the efiicacy of nimodipine for aute cerebrovascular disease. Methods 42 patients with clinically confirmed acute cerebrovascular disease were randomly assigned to receive conventional therapy (control group), or conventional therapy combined with intravenous nimodipine (15μ gkg-1 · h-1) plus 5％ glucose of 500 ml (study group) once a day for 15 days. The treatment started within 12, 48 hours, and 5 days of admission.NSE levels were detected by ELISA on admission and 48hour,days 5, 7, and 10. The data were analyzed statistically. Results After treatment with intravenous nimodipine within 48 hours, NSE level was markedly lower, as compared with that in the control group (P＜0.05).Conclusions Nimodipine has a better efficacy in the treatment of acute cerebrovascular disease. The early use of intravenous drip (within 48 hours)is more effective. Key words: Neuron specific enolase; Nimodipine; Acute cerebrovascular disease