Neuron-specific Enolase Concentrations Research Articles

Altered Expression of Glucocorticoid Receptor and Neuron-Specific Enolase mRNA in Peripheral Blood in First-Episode Schizophrenia and Chronic Schizophrenia.

IntroductionIt is well-known that altered hypothalamus–pituitary–adrenal (HPA) axis process has an important role in the neurodegenerative process in schizophrenia (SZ). However, this neurodegenerative mechanism has not been clarified in SZ. Therefore, the main purpose of this study was to determine HPA axis damage in the first-episode, unmedicated schizophrenia (FES) patients and chronic schizophrenia (CSZ) patients in comparison with healthy controls (HC) by means of quantitative analysis of the peripheral blood mRNA expression of glucocorticoid receptor (GR), GR transcripts containing exons 1B (GR-1B), and neuron specific enolase (NSE) genes and serum cortisol and NSE, a specific serum marker for neuronal damage.MethodsIn the present study, 43 FES patients, 39 CSZ, and 47 HC were included. The peripheral blood mRNA expressions for GR, GR-1B, and NSE genes were determined by real-time quantitative polymerase chain reaction (RT-qPCR). Serum cortisol and NSE were analyzed by electrochemiluminescence immunoassay technique.ResultsLevels of GR mRNA were significantly lower in FES and CSZ than that in HC. The expression of GR-1B mRNA was significantly decreased in CSZ when compared with that in FES. Levels of NSE mRNA were significantly lower in CSZ than that in FES patients or HC patients. CSZ patients showed significantly lower cortisol concentrations than FES and HC patients. FES patients showed significantly higher NSE concentrations than CSZ and HC.ConclusionOur findings support that there is disrupted HPA axis system in the SZ and suggest that CSZ patients suffer a greater HPA axis damage than FES patients. Our research implicated underlying GR mRNA dysregulation in SZ and the potential importance of the functional GR-1B transcription in CSZ.

Serum Concentrations of Neuron-Specific Enolase in Dogs Following Traumatic Brain Injury

The ability to make an accurate prognosis, which is a prerequisite for treatment decisions, is very limited in dogs with traumatic brain injury (TBI). To determine whether serum concentrations of neuron-specific enolase (NSE) have prognostic value in dogs following TBI, we conducted a prospective, observational, controlled clinical study in an intensive care unit of a university teaching hospital. The study population comprised 24 dogs admitted to the hospital within 72h of a known event of TBI between January 2010 and January 2015, as well as 25 control healthy shelter dogs admitted for elective neutering. Seventeen injured dogs (70%) survived to discharge, four were euthanized and three died within 48h. Serum samples were obtained from all dogs (in injured dogs, within 72h of TBI) and NSE concentrations were measured using enzyme-linked immonosorbent assay. Associations between NSE levels and outcome, Modified Glasgow Coma Scale, time to sampling, age or haemolysis scale were determined. Mean serum NSE concentrations were decreased in dogs with TBI compared with healthy controls (19.4±4.14ng/ml vs. 24.9±4.6ng/ml, P<0.001). No association was found between serum NSE concentrations and either survival or severity of neurological impairment. A negative correlation was found between serum NSE concentrations and time from trauma to blood collection (r=-0.50, P=0.022). These results indicate that serum NSE concentration in dogs following TBI is not an effective marker for severity or outcome. Further studies are warranted to standardize serum NSE measurements in dogs and to determine the peak and half-life levels of this potential biomarker.

Hypoxic-Ischemic Encephalopathy Evaluated by Brain Autopsy and Neuroprognostication After Cardiac Arrest

Neuroprognostication studies are potentially susceptible to a self-fulfilling prophecy as investigated prognostic parameters may affect withdrawal of life-sustaining therapy. To compare the results of prognostic parameters after cardiac arrest (CA) with the histopathologically determined severity of hypoxic-ischemic encephalopathy (HIE) obtained from autopsy results. In a retrospective, 3-center cohort study of all patients who died following cardiac arrest during their intensive care unit stay and underwent autopsy between 2003 and 2015, postmortem brain histopathologic findings were compared with post-CA brain computed tomographic imaging, electroencephalographic (EEG) findings, somatosensory-evoked potentials, and serum neuron-specific enolase levels obtained during the intensive care unit stay. Data analysis was conducted from 2015 to 2020. The severity of HIE was evaluated according to the selective eosinophilic neuronal death (SEND) classification and patients were dichotomized into categories of histopathologically severe and no/mild HIE. Of 187 included patients, 117 were men (63%) and median age was 65 (interquartile range, 58-74) years. Severe HIE was found in 114 patients (61%) and no/mild HIE was identified in 73 patients (39%). Severe HIE was found in all 21 patients with bilaterally absent somatosensory-evoked potentials, all 15 patients with gray-white matter ratio less than 1.10 on brain computed tomographic imaging, all 9 patients with suppressed EEG, 15 of 16 patients with burst-suppression EEG, and all 29 patients with neuron-specific enolase levels greater than 67 μg/L more than 48 hours after CA without confounders. Three of 7 patients with generalized periodic discharges on suppressed background and 1 patient with burst-suppression EEG had a SEND 1 score (<30% dead neurons) in the cerebral cortex, but higher SEND scores (>30% dead neurons) in other oxygen-sensitive brain regions. In this study, histopathologic findings suggested severe HIE after cardiac arrest in patients with bilaterally absent cortical somatosensory-evoked potentials, gray-white matter ratio less than 1.10, highly malignant EEG, and serum neuron-specific enolase concentration greater than 67 μg/L.

S100B protein and neuron-specific enolase as predictors of postoperative cognitive dysfunction in aged dogs: a case-control study

ObjectivePostoperative cognitive dysfunction (POCD) may be related to brain injury. S100B protein and neuron-specific enolase (NSE) have been investigated as potential biochemical markers of neural cell injury in animals and humans. This study aimed to investigate the association between POCD, brain injury and serum concentrations of S100B and NSE after periodontal surgery in aged dogs. Study designProspective observational animal study. AnimalsA total of 24 male and female dogs undergoing periodontal surgery. MethodsDogs were separated into two groups based on age: control group, 10 dogs ≤ 8 years and aged group, 14 dogs > 8 years. Cognitive function was measured preoperatively and on the seventh postoperative day using the Canine Cognitive Dysfunction Rating scale and the Age-Related Cognitive and Affective Disorders scale. S100B protein and NSE serum concentrations were measured before and immediately after the surgery. ResultsPOCD was not observed after surgery in the present study. Serum concentrations of S100B and NSE were increased postoperatively in the control group but not in the aged group (p = 0.04 and 0.03, respectively). Preoperative S100B serum concentrations were significantly higher in the aged group (p = 0.01). ConclusionsThere was no association between POCD and high concentrations of S100B and NSE in dogs. However, increased postoperative serum concentrations of S100B and NSE were found in the control group after surgery, an effect that may indicate neural damage. Clinical relevanceThe results suggest that anesthesia and oral surgery are associated with higher postoperative serum concentrations of S100B and NSE in dogs ≤ 8 years old, which may indicate neural damage. Serum concentrations of S100B were elevated in aged dogs before anesthesia, a finding that might be related to chronic preoperative brain damage.

Correction of the NSE concentration in hemolyzed serum samples improves its diagnostic accuracy in small-cell lung cancer.

Neuron-specific enolase (NSE) is a well-known biomarker for the diagnosis, prognosis and treatment monitoring of small-cell lung cancer (SCLC). Nevertheless, its clinical applicability is limited since serum NSE levels are influenced by hemolysis, leading to falsely elevated results. Therefore, this study aimed to develop a hemolysis correction equation and evaluate its role in SCLC diagnostics.Two serum pools were spiked with increasing amounts of hemolysate obtained from multiple individuals. A hemolysis correction equation was obtained by analyzing the relationship between the measured NSE concentration and the degree of hemolysis. The equation was validated using intentionally hemolyzed serum samples, which showed that the correction was accurate for samples with an H-index up to 30 μmol/L. Correction of the measured NSE concentration in patients suspected of lung cancer caused an increase in AUC and a significantly lower cut-off value for SCLC detection when compared to uncorrected results.Therefore, a hemolysis correction equation should be used to correct falsely elevated NSE concentrations. Results of samples with an H-index above 30 μmol/L should not be reported to clinicians. Application of the equation illustrates the importance of hemolysis correction in SCLC diagnostics and questions the correctness of the currently used diagnostic cut-off value.

Influence of Prenatal Hypoxia on the Content of Neuron Specific Enolase in the Structures of the Brain and Blood Serum of Rats in Early Ontogeny

Abstract—We studied the dynamics of changes in the content of neuron specific enolase (NSE, EC 4.2.1.11) in the hippocampus, cortex, cerebellum and blood serum of rats at 5th, 10th, and 30th days of postnatal development. It was shown that during the first month of life the content of NSE increases several-fold in all the structures studied, both after hypoxia and in the animals not exposed to hypoxia. It was established that prenatal hypoxia on the 14th day of embryonic development leads to significant changes in the NSE content in all the brain structures studied. In the blood serum, the content of this enzyme is higher in comparison with the control group on the 5th, 10th, and 30th postnatal days in experimental animals. Thus, the lack of oxygen affects the content of this enzyme in both the brain structures and in blood serum of rats, which makes it possible to judge the survival of neurons under conditions of prenatal hypoxia, and also suggests that this index may be used as a marker of fetal CNS disturbance after hypoxia during prenatal development.

Sodium valproate combined with levetiracetam in pediatric epilepsy and its influence on NSE, IL-6, hs-CRP and electroencephalogram improvement.

Efficacy of sodium valproate combined with levetiracetam (LEV) in pediatric epilepsy and its influence on neuron-specific enolase (NSE), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) as well as electroencephalogram (EEG) improvement were studied. Patients (n=100) with pediatric epilepsy admitted to and treated in Xiantao First People's Hospital Affiliated to Yangtze University from December 2015 to 2018 were enrolled in this study and randomly divided into observation group (n=50) and control group (n=50). Sodium valproate was administered in the control group, and the treatment with LEV was combined with sodium valproate in the observation group. After 12 weeks the cognitive function of patients was assessed using the Mini-Mental State Examination (MMSE) scale, Montreal cognitive assessment (MoCA) scale and Wechsler Memory Scale-Revised in China (WMS-RC). The quality of life (QOL) of patients was evaluated with the QOL in epilepsy-31 inventory (QOLIE-31) scale and Barthel Index, and blood was drawn from the patients to detect the neurological function indicators [NSE and glial fibrillary acidic protein (GFAP)] and inflammatory indicators (IL-6, IL-2 and hs-CRP). After treatment, the incidence rates of adverse reactions notably declined in the observation group (P<0.05), and the improvement in the cognitive function in the observation group were both superior to those in the control group (P<0.05). Observation group had lowered content of NSE, GFAP, IL-6, hs-CRP and IL-2 (P<0.05), and α wave was markedly decreased, but θ and δ waves were notably increased in the observation group (P<0.05). In the treatment of pediatric epilepsy, sodium valproate combined with LEV produces better efficacy, fewer adverse reactions, significantly improves patients' QOL and notably lowers the content of NSE, IL-6 and hs-CRP with notable EEG improvement, so it is a safe and reliable treatment that is worth popularization.

Clinical significance and diagnostic value of serum NSE, CEA, CA19-9, CA125 and CA242 levels in colorectal cancer.

The present study investigated the value of combinations of five specific tumor biomarkers for the diagnosis of colorectal cancer (CRC): Neuron-specific enolase (NSE), carcinoembryonic antigen (CEA), cancer antigen (CA)19-9, CA125 and CA242. Associations between these markers and clinicopathological characteristics (including the Tumor-Node-Metastasis stage) were also assessed. Serum levels of the 5 markers were compared between 358 patients with CRC and 298 healthy individuals (CRC and control group, respectively). The NSE concentration of the CRC group was significantly higher compared with the control. Furthermore, patients at clinical stage III+IV exhibited significantly higher NSE levels compared with those at stage I+II. The serum NSE level of N+ patients was significantly higher compared with the N− group, and the NSE level of M1 patients was significantly compared with the M0 group. NSE level was also significantly associated with tumor stage, lymph node metastasis, distant metastasis and hematochezia. The area under the receiver operating characteristic curve (AUC) for NSE in CRC was 0.766, which was significantly higher than that of the other four markers, which ranged from 0.560–0.682. The AUC of NSE, CEA, CA19-9, CA125, CA242 combined was significantly higher compared with any of the markers individually (range, 0.796–0.858). Therefore, serum NSE may be a good clinical tool for the auxiliary diagnosis of colorectal cancer. Besides, the combination of NSE, CEA, CA19-9, CA125 and CA242 was significantly more sensitive compared with NSE alone. Thus, the combined detection of the 5 tumor markers may be more useful for the diagnosis of CRC.

Neonatal neuron specific enolase, a sensitive biochemical marker of neuronal damage, is increased in preeclampsia: A retrospective cohort study

BackgroundPreeclampsia leads to chronic intrauterine hypoxia by interfering with placental blood supply. We aimed to investigate whether preeclampsia exposure has an influence on central nervous system of infants, as evaluated by analyzing neonatal serum neuron specific enolase (NSE). MethodsThis was a retrospective study including infants born in Nanfang hospital between Jan 2018 and Feb 2019 without asphyxia. They were divided into normotensive control group and preeclampsia group to compare the NSE levels. Furthermore, PE group was divided into five subgroups by lipstick of urine protein from 0 to 4+ to examine the relationship between urine protein and neonatal NSE. ResultsOf the 86 selected neonates, there were 40 in control group and 46 in preeclampsia group. The NSE levels were significantly higher in infants with preeclampsia exposure compared to those infants in control group (45.504 ± 17.926 vs 30.690 ± 4.475, P < 0.0001). Multiple regression analyses revealed that the preeclampsia (β coef = 0.394, p = 0.041), 4+ proteinuria (β coef = 0.558, p < 0.0001) and 3+ proteinuria (β coef = 0.356, p = 0.005) were significant independent variables predicting elevated serum NSE concentration. ConclusionFor the first time, this research has suggested the increase of neonatal NSE in preeclampsia, and the quantity of maternal proteinuria may be able to predict neonatal NSE elevation. Long-term neurodevelopmental follow-up and targeted preventive strategies are advised for this underrecognized high-risk population.

Neuron-specific enolase as a diagnostic marker of chronic gastroduodenitis in children

Objective: to assess the nature of changes in the level of neuron-specific enolase (NSE) in children suffering from chronic gastroduodenitis, depending on the severity of the disease, gender and physical development indicators.Materials and methods. The study group included 154 children aged 8–15 years with chronic gastroduodenitis. The main group includes children with superficial gastroduodenitis (group I) and erosive gastroduodenitis (group II). The control group consisted of 56 healthy children. All children underwent an assessment of physical development. The serum NSE level was determined by enzyme-linked immunosorbent assay. It was revealed that the main parameters of the physical development of children from the control group exceeded the values of similar parameters of children of the main group. High NSE values were established in children with chronic gastroduodenitis in comparison with the control (p≤0.01). The NSE level in boys exceeded the value of the indicator in girls in the main group and in the control group. The level of NSE in girls of the main group exceeded the value of NSE in healthy girls (p≤0.05). Studying the level of NSE taking into account gender and the severity of the pathological process revealed higher rates in boys with erosive gastroduodenitis compared with the control group (p≤0.05). In the group of children with erosive gastroduodenitis, higher NSE rates were found in boys compared with girls (p&lt;0.05).Conclusions: A high level of NSE in children with erosive gastroduodenitis and revealed gender differences in NSE concentrations in blood serum indicate the possible role of this indicator in the development of severe forms of the disease and do not exclude the possible association of the effects of this enzyme with the function of sex hormones. The quantitative values of NSE for predicting the development of chronic gastroduodenitis in children are established.

Histological conversion from adenocarcinoma to small cell carcinoma of the lung after treatment with an immune checkpoint inhibitor: a case report

The transformation of adenocarcinoma to small cell lung cancer has been reported as acquisition of resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors. We here report a patient who presented histologically confirmed transformation of adenocarcinoma to small cell lung cancer after treatment with immune checkpoint inhibitor. A 65-year-old man was treated with pembrolizumab as first-line therapy and achieved temporarily a stable disease with progression after six cycles of this agent. At that stage, a transbronchial biopsy showed small cell lung cancer, and he was found to have high serum concentrations of neuron-specific enolase despite concentrations of numerous tumor markers, including neuron-specific enolase, having been within normal limits at the time of presentation. The patient thereafter was treated as a small cell carcinoma patient using cisplatin plus irinotecan and amrubicin.

Measurement of Serum Neuron-Specific Enolase in Neuroblastoma: Is There a Clinical Role?

The measurement of neuron-specific enolase (NSE) in serum is frequently requested for diagnosis, risk stratification, and treatment monitoring of neuroblastoma (NB) in the pediatric population. However, authoritative clinical practice guidelines advise about the poor diagnostic performance of NSE. We critically appraised the available literature evaluating the diagnostic and prognostic value of NSE in the management of NB, paying special attention to the definition of appropriate threshold levels. In addition, we discuss the interfering conditions causing artifactual increases of NSE concentrations in serum and potentially influencing the clinical evaluation of patients with suspected NB. No definitive evidence supports the use of serum NSE for diagnosis and monitoring of NB. The risk of obtaining false-positive NSE results associated with confounders (e.g., sample hemolysis) and other pathophysiologic conditions (e.g., inflammation) is remarkable and hampers the diagnostic value of this test. NSE may be helpful to define the risk of death of patients with NB, mainly in the advanced stages of disease. However, further studies validating currently marketed immunoassays and defining threshold values useful for this scope are warranted.

Combining serum calcitonin, carcinoembryonic antigen, and neuron-specific enolase to predict lateral lymph node metastasis in medullary thyroid carcinoma.

BackgroundThis study aimed to investigate the clinical application of combined detection of serum calcitonin (Ctn), carcinoembryonic antigen (CEA), and neuron‐specific enolase (NSE) in predicting lateral lymph node metastasis (LLNM) in medullary thyroid carcinoma (MTC).MethodsSeventy‐four consecutive patients with MTC were enrolled. The relationship between serum Ctn, CEA, and NSE and LLNM was retrospectively analyzed by univariate analysis and logistic regression analysis. Furthermore, the clinical application of serum Ctn, CEA, and NSE combined detection in prediction of LLNM in MTC was also evaluated.ResultsThe rate of LLNM in this study was 48.64% (36/74).The expression levels of serum Ctn, CEA, and NSE in MTC with LLNM were significantly higher than those without LLNM (all P < .01). The area under the curve (AUC) predicted by serum Ctn, CEA, and NSE for LLNM in MTC patients was 0.867, 0.831, and 0.726, respectively, and the AUC of serum Ctn, CEA, and NSE combined detection was up to 0.890, higher than using a single biomarker. The sensitivity and specificity of serum Ctn, CEA, and NSE combined detection in prediction of LLNM were 88.89% and 81.57%, respectively.ConclusionsThe concentrations of serum Ctn, CEA, and NSE are closely related to LLNM in MTC, and the combined detection of all three biomarkers has a higher clinical value in the evaluation of MTC patients with LLNM. With more perspective study in the future, it would be an indicator of influencing personalized surgical strategy for different MTC patients.

Influence of butyphthalide combined with urinary kallikrein in ACI treatment on neuro-cytokines and vascular endothelial function and its clinical effect

Objective: To study the influence of butyphthalide combined with urinary kallikrein in acute cerebral infarction (ACI) treatment on neuro-cytokines and indicators of vascular endothelial function, observe the curative effect and adverse effects, and discuss its safety and feasibility.Method: 110 ACI patients were chosen as the objects, and classified into observation group (55 cases) and control group (55 cases) according to the method of random number table. Butyphthalide injection combined with urinary kallikrein was adopted for the observation group based on conventional treatment, while cinepazide maleate injection combined with alprostadil injection was applied for the control group based on conventional treatment. The following indicators of both groups were compared before and after treatment: neurotrophic factor (NTF), nerve growth factor (NGF), neuron specific enolase (NSE); content of CXC chemotactic factor ligand 16 (CXCL16), soluble CD ligand (CD40L), Fibulin-5 and high mobility group box B1 (HMGB1); the content of indicators of vascular endothelial function including plasma endothelin −1 (ET-1) and no therapeutic effects and adverse effects were recorded.Results: NSE of both groups after treatment decreased obviously, and the content of NTF and NGF increased obviously. NSE content of observation group was lower than that of control group. NTF content and NGF content of observation group were higher than those of control group. The differences had statistical significance (p < 0.05). The levels of CXCL16, CD40L, Fibulin-5 and HMGB1 declined obviously, compared with pre-treatment, and the levels of observation groups were significantly lower than those of control grip. The differences had statistical significance (p < 0.05). ET-1 level rose significantly after treatment, and NO level declined obviously after treatment. ET-1 level of observation group was significantly higher than that of control group, and NO level of observation group was significantly lower than that of control group. The difference had statistical significance (p < 0.05). Clinical effect of observation group was significantly higher than that of control group. The difference had statistical significance (p < 0.05). The comparison difference of both groups in the occurrence rate of adverse effects had no statistical significance (p > 0.05).Conclusion: The application of butyphthalide combined with urinary kallikrein in ACI treatment can effectively inhibit secretion and release of neuro-cytokines, and improve patients’ vascular endothelial function, with significant treatment effect and high safety. Therefore, it deserves to be promoted clinically.

Ultrasensitive dual-signal ratiometric electrochemical aptasensor for neuron-specific enolase based on Au nanoparticles@Pd nanoclusters-poly(bismarck brown Y) and dendritic AuPt nanoassemblies

Neuron-specific enolase (NSE) is viewed as a tumor marker of small cell lung cancer (SCLC) with high diagnostic sensitivity and specificity, whose facile and sensitive detection is critical for clinical diagnosis. In this work, core-shell Au nanoparticles @Pd nanoclusters-poly(bismarck brown Y) (Au@Pd-P(BBY)) and hierarchically dendritic AuPt nanoassemblies (AuPt NAs) were synthesized independently by a one-pot aqueous method. A dual-signal ratiometric electrochemical aptasensor was developed for ultrasensitive determination of NSE based on ferrocene grafted Au@Pd-P(BBY) (Fc-g-Au@Pd-P(BBY)) and reduced graphene oxide/thionine decorated AuPt NAs (rGO/Thi/AuPt NAs). Under optimal conditions, the changes in the peak currents linearly correlate to the NSE concentrations in the wide range of 0.0001―50.0 ng mL–1 with ultralow detection limit (0.03 pg mL–1, S/N = 3). The aptasensor was explored in a diluted human serum sample with acceptable results, showing its great potential in clinical diagnosis and treatment.

Analysis of correlation between serum NSE, hs-CRP levels and NIHSS score in patients with cerebral infarction

Objective To investigate the correlation between the changes of serum neuron specific enolase (NSE) and hypersensitive C-reactive protein (hs-CRP) levels and the degree of neurological deficit (NIHSS) score in patients with cerebral infarction. Methods From January 2017 to January 2019, 63 patients with cerebral infarction admitted to Lishui Central Hospital were selected.According to NIHSS score, they were divided into 13 mild cases, 30 moderate cases and 20 severe cases.According to infarction area, they were divided into large area group (16 cases), small area group (27 cases) and lacunar infarction group (20 cases). Another 60 cases underwent health examination in our hospital from January 2017 to January 2019 were selected as the control group.Enzyme-linked immunosorbent assay (ELISA) was used to determine the content of NSE, and immunoturbidimetric assay was used to determine the content of hs-CRP.The changes of serum NSE and hs-CRP levels in the cerebral infarction group and control group, serum NSE, hs-CRP levels and NIHSS scores in different severity and infarction area, and the correlation between serum NSE and hs-CRP changes and NIHSS scores were compared. Results The serum levels of NSE [(21.34±3.27)ng/mL] and hs-CRP [(10.48±2.14)mg/L] in the cerebral infarction group were significantly higher than those in the control group [(6.23±1.08)ng/mL, (2.83±0.46)mg/L] (t=34.061, 27.095, all P<0.05). The serum levels of NSE [(26.98±3.64) ng/mL], hs-CRP [(15.36±2.57)mg/L] and NIHSS score[(38.49±3.25)points] in the severe group were higher than those in the moderate group and mild group, which in the moderate group [(20.98±3.21)ng/mL, (10.25±2.09)mg/L and (22.18±3.48)points] were higher than those in the mild group [(12.64±2.78)ng/mL, (5.47±1.40)mg/L and (7.38±2.56)], the differences were statistically significant (F=14.975, 9.132, 15.873, all P<0.05). The serum levels of NSE [(25.43±3.35)ng/mL], hs-CRP [(16.54±2.71)mg/L] and NIHSS score[(37.34±3.75)points] in the large area group were higher than those in the small area group and lacunar infarction group, which in the small area group [(21.67±3.12)ng/mL, (10.86±2.21)mg/L and (21.25±3.26)points] were higher than those in the lacunar infarction group [(13.45±2.97)ng/mL, (4.79±1.35)mg/L and (8.49±2.15)points], the differences were statistically significant (F=13.241, 9.893, 17.482, all P<0.05). The serum levels of NSE and hs-CRP were positively correlated with NIHSS score (r=0.829, 0.713, all P<0.05). Conclusion The levels of serum NSE and hs-CRP in patients with cerebral infarction increase with the progression of the disease, and there is a linear positive correlation between NSE and hs-CRP and NIHSS score.It is considered that NSE and hs-CRP are of great value in evaluating the degree of neurological impairment, the severity of the disease and the size of the infarct. Key words: Infarction, middle cerebral artery; Neuron-specific enolase; C-reactive protein; Neurological deficit score

The Role of Brain-Derived Neurotrophic Factor and Glial Cell Line-Derived Neurotrophic Factor in Chronic Fetal Oxygen Deprivation.

The aim of the study was to define the role of brain-derived and glial cell line-derived neurotrophic factors (BDNF and GDNF) in realization of compensative and adaptive mechanisms of a neonatal organism to hypoxia.Materials and MethodsThe experiments in vivo have been carried out on pregnant C57BL/6 mice (n=36). Chronic hypobaric hypoxia has been modeled in different pregnancy trimesters. On gestation days E19–20, concentration of BDNF and GDNF in the blood of the pregnant females was determined by enzyme immunoassay. Further, the number of neonatal mice, their weight and body length parameters have been assessed.Parturient mothers (n=88) and their newborn babies followed up at the Clinic of Obstetrics and Gynecology of Pavlov University took part in the clinical investigations. Concentration of BDNF, GDNF, neuron-specific enolase (NSE), and hypoxia-inducible factor (HIF-1β) in the fetal cord blood has been determined by ELISA. The obtained data were retrospectively compared with cardiotocography, dopplerometry, presence of meconium-stained amniotic fluid and the neonate state at birth, assessment according to the Apgar score, and the course of adaptation period.ResultsChronic hypobaric hypoxia in pregnant mice in trimester I and II resulted in the significant decrease of BDNF and GDNF level, decrease in the number of embryos, and in significant changes in weight/height characteristics of the newborn pups.According to the clinical observations, an increased expression of the neurotrophic factors BDNF, GDNF provides protection to a neonate even if hypoxia factors are present and realized. A low content of BDNF and GDNF was observed in the group of infants with a high risk of developing unfavorable hypoxic damaging effects.ConclusionThe protective role of BDNF and GDNF in the regulation of fetal homeostasis in chronic hypoxia has been established experimentally and clinically.

Towards the Development of an Integrative, Evidence-Based Suite of Indicators for the Prediction of Outcome Following Mild Traumatic Brain Injury: Results from a Pilot Study.

Background: Persisting post-concussion symptoms (PPCS) is a complex, multifaceted condition in which individuals continue to experience the symptoms of mild traumatic brain injury (mTBI; concussion) beyond the timeframe that it typically takes to recover. Currently, there is no way of knowing which individuals may develop this condition. Method: Patients presenting to a hospital emergency department (ED) within 48 h of sustaining a mTBI underwent neuropsychological assessment and demographic, injury-related information and blood samples were collected. Concentrations of blood-based biomarkers neuron specific enolase, neurofilament protein-light, and glial fibrillary acidic protein were assessed, and a subset of patients also underwent diffusion tensor–magnetic resonance imaging; both relative to healthy controls. Individuals were classified as having PPCS if they reported a score of 25 or higher on the Rivermead Postconcussion Symptoms Questionnaire at ~28 days post-injury. Univariate exact logistic regression was performed to identify measures that may be predictive of PPCS. Neuroimaging data were examined for differences in fractional anisotropy (FA) and mean diffusivity in regions of interest. Results: Of n = 36 individuals, three (8.33%) were classified as having PPCS. Increased performance on the Repeatable Battery for the Assessment of Neuropsychological Status Update Total Score (OR = 0.81, 95% CI: 0.61–0.95, p = 0.004), Immediate Memory (OR = 0.79, 95% CI: 0.56–0.94, p = 0.001), and Attention (OR = 0.86, 95% CI: 0.71–0.97, p = 0.007) indices, as well as faster completion of the Trails Making Test B (OR = 1.06, 95% CI: 1.00–1.12, p = 0.032) at ED presentation were associated with a statistically significant decreased odds of an individual being classified as having PPCS. There was no significant association between blood-based biomarkers and PPCS in this small sample, although glial fibrillary acidic protein (GFAP) was significantly increased in individuals with mTBI relative to healthy controls. Furthermore, relative to healthy age and sex-matched controls (n = 8), individuals with mTBI (n = 14) had higher levels of FA within the left inferior frontal occipital fasciculus (t (18.06) = −3.01, p = 0.008). Conclusion: Performance on neuropsychological measures may be useful for predicting PPCS, but further investigation is required to elucidate the utility of this and other potential predictors.

Effects of Foot-Strike Patterns on Biomarkers S100 Calcium-Binding Protein B/Neuron-Specific Enolase in Running-A Pilot Study.

Foot-strike patterns (FSP) in running are related to certain impact kinetics during ground contact. A rear-foot strike (RFS) has been associated with higher impact forces, whereas a forefoot strike (FFS) is assumed to minimize these impact forces. This study investigated the effects of running with RFS or FFS on impact-sensitive neuronal biomarkers S100 calcium-binding protein B (S100B), neuron-specific enolase (NSE), and lactate dehydrogenase (LDH). In this randomized crossover study, 18 healthy recreational runners (14 male, mean [SD] age 28.2 [4.7]y, body mass index 22.8 [1.9]) ran 2 separate 5-mile runs with RFS or FFS, respectively. Blood samples were taken before (pre), 30min after (post 0), and 24h after (post 24) the run. S100B, NSE, and LDH concentrations were determined and analyzed (3 × 2 data model). S100B, NSE, and LDH concentrations increased from pre to post 0 and decreased within 24 h back to the baseline level, demonstrating a significant time effect (all P < .01, all ηpart2>.3). No main effect for FSP or any significant interaction effect indicating FSP-specific differences between FFS or RFS was found (all P > .05, all ηpart2<.07), except for LDH (P < .001, ηpart2=.77). NSE, S100B, and LDH concentration increased in the short term after running and returned to normal in 24h. FSP with varying impact forces does not influence the increase of these biomarkers. LDH findings favor peripheral origins, but mixed effects are possible. Thus, further research is needed to estimate the risk of mild traumatic encephalopathy.

Serum Neuron-specific Enolase and S100 Calcium-binding Protein B in Pediatric Diabetic Ketoacidosis

Objective:Neuron-specific enolase (NSE) and S100 calcium-binding protein B (S100B) are markers of different neurological disorders. The aim was to investigate the relationship between NSE and S100B serum concentrations and the severity of diabetic ketoacidosis (DKA) in diabetic children.Methods:Eighty children with DKA, 40 with type 1 diabetes mellitus (T1DM) without DKA and 40 healthy controls were enrolled. Severity of DKA was assessed according to blood pH and bicarbonate concentration. Serum NSE and S100B were measured in all participants. In the DKA group serum NSE and S100B were measured at three time points, at admission and at 12 hours and 24 hours after starting treatment.Results:Children with DKA showed significantly higher serum levels of NSE at all time points compared to children with T1DM without DKA and controls (p<0.01), while serum S100B concentrations did not differ between the three cohorts. Children with T1DM but without DKA also had significantly higher serum levels of NSE (p<0.01) compared to healthy controls. Patients with low Glasgow Coma Scale score (GCSS) and those with moderate and severe DKA had significantly higher levels of NSE at all time points (p<0.01 for each) compared to patients with normal GCSS and those with mild DKA. No significant differences were found in serum S100B levels according to the severity of DKA and GCS (p>0.05). Younger age, lower GCSS, higher glucose and HbA1c, lower pH and lower serum bicarbonate were the risk factors associated with elevated NSE.Conclusion:Serum NSE is elevated in all patients with type 1 DM and, in patients with DKA, correlates with severity of DKA. However, serum S100B concentration did not differ between T1DM with or without DKA and healthy controls.