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Background: Neuron-specific enolase (NSE) is released into serum when nerve cells are damaged, and the levels thereof are used to determine neurological prognosis in patients who have suffered cardiac arrest or stroke. Delayed neuropsychiatric sequelae (DNS), a major complication of carbon monoxide poisoning (COP), can be caused by inflammatory response which is a mechanism of neuronal injury in cardiac arrest and stroke. NSE is known as a predictor of neurological prognosis in ischemic brain injury after cardiac arrest, and it is also reported as a predictor of DNS in acute COP. When serum NSE is measured serially in cardiac arrest patients, the best time to predict neurological prognosis is known at 48-72 h, but there are no studies analyzing serial serum NSE in acute COP. Thus, we explored whether serum NSE levels measured three times at 24 h intervals after COP predicted the development of DNS., Methods: This prospective observational study was conducted on patients treated for COP from May 2018 to April 2020 in a tertiary care hospital in Korea. Neuron-specific enolase levels were assessed 24, 48, and 72 h after presentation at hospital. We used logistic regression to explore the association between NSE levels and DNS development., Results: The NSE level was highest at 48 h, and the difference between the DNS group and the non-DNS group was greatest on the same time point. On multivariable logistic regression analysis, the NSE level at 48 h of >20.98 ng/mL (odds ratio [OR], 3.570; 95% confidence interval [CI], 1.412-9.026; P = .007) and the initial Glasgow Coma Scale (GCS) score of <9 (OR, 4.559; 95% CI, 1.658-0.12.540; P = .003) was statistically significant for DNS development., Conclusion: Early identification of those who will experience DNS in acute COP patients is clinically important for deciding treatment. In this study, we revealed that NSE level of >20.98 ng/mL at 48 h time point can be used as an independent predictor of DNS (OR, 3.570; 95% CI, 1.412-9.026; P = .007; AUC, 0.648).

Fluoroacetic acid (FAcOH) was once a highly toxic rodenticide widely used in the world. In the past, studies on the toxicity of FAcOH have focused on animal experiments. The toxicity of FAcOH to humans and the changes of FAcOH in plasma have not been studied. Therefore, the present study aimed to describe the changes of plasma FAcOH concentrations, hematological, and biochemical characteristics in patients with FAcOH intoxication. According to clinical symptoms, 68 patients from the emergency department were divided into different groups: convulsion group, unconsciousness group, death group, and control groups. Plasma FAcOH concentrations, hematological, and biochemical parameters were investigated. Results demonstrated that patients in the convulsion group and the unconsciousness group had a significant increase ( p < 0.01) in the level of neuron-specific enolase (NSE), creatine kinase MB (CKMB), glucose (GLU), and white blood cell count (WBC) and a significant decrease ( p < 0.01) in serum potassium compared with the control group, respectively. Moreover, patients in the death group had a significant increase ( p < 0.01) in the level of NSE, CKMB, N -terminal pro-brain natriuretic peptide, GLU, and WBC and a significant decrease ( p < 0.01) in serum potassium and total calcium compared with the survival group. The concentrations of FAcOH in plasma in the convulsion group, the unconsciousness group, and the death group were 72.31 ± 42.29, 118.33 ± 55.41, and 163.78 ± 43.32 μg/mL, respectively. These changes and the plasma FAcOH concentrations may increase our understanding of the toxicity of FAcOH to humans and may help doctors to judge the clinical prognosis of patients with FAcOH intoxication.

Introduction: The accuracy of serum neuron-specific enolase (NSE) measurements is critical, particularly in neurologic diseases and cancer. NSE measurements are compromised by slight, even invisible, hemolysis, which can produce apparently higher NSE levels, leading to inappropriate clinical decisions. In this article, we describe this issue and propose a solution for avoiding incorrect results., Methods: Twenty blood samples from donors with NSE values that were within the reference interval were considered. Experimental hemolysis was induced in vitro to examine the relationship between the degree of hemolysis and the increase in serum NSE. The data were then subjected to statistical analysis., Results: There was excellent correlation ( r 2 0.953) between the degree of hemolysis and the rise in NSE concentration. Each hemolysis unit (equal to 1 mg/dL of free hemoglobin) corresponded to a mean value of 0.29 ± 0.09 ng/mL NSE that was released from red blood cells., Conclusion: The hemolysis index must be measured in every sample with no evident hemolysis before assaying it for NSE. Moreover, if the degree of hemolysis is between 5 and 30 units, the increase in NSE (from 1.5 to 9.0 ng/mL) must be calculated, and the laboratory results should be appended with comments that suggest the approximate rise in NSE.

Background: Delirium is very common among patients with polytrauma, although no suitable means exist to feasibly reduce the incidence and duration of delirium in these patients. Recent reports have suggested that continuous intravenous (IV) infusions of dexmedetomidine, rather than benzodiazepine, be administered for sedation to reduce the duration of delirium in this population. However, serum neuron-specific enolase (NSE), S100 calcium binding protein B (S100B), and brain-derived neurotrophic factor (BDNF) levels have not yet been investigated in polytrauma patients who received sedation with dexmedetomidine rather than other conventional sedatives. The aim of this study was to assess the association of blood BDNF, NSE, and S100B with the occurrence of delirium among polytrauma patients who had been sedated with dexmedetomidine., Materials and Methods: Consecutive patients were randomly assigned to 1 of 2 treatment study groups, namely the "dexmedetomidine group" or the "common group." This case-control study included 18 patients with delirium and 34 matched controls in a 63-bed general intensive care unit (ICU). Blood samples were collected from all patients upon ICU admission, on the day when delirium was diagnosed, and on days 3 and 5 following diagnosis. The serum levels of S100B, BDNF, and NSE were determined by enzyme-linked immunosorbent assay. The sedation levels and delirium were assessed using the Richmond Agitation and Sedation Scale and the Confusion Assessment Method for the ICU., Results: The median BDNF, NSE, and S100B concentrations were significantly lower in the dexmedetomidine group than in the common group on the day when delirium was diagnosed and on the third day after delirium was diagnosed. The rate of delirium was significantly lower in the dexmedetomidine group than in the common group. There were clear differences in the BDNF, NSE, and S100B levels between the 2 groups on the fifth day after delirium was diagnosed., Conclusions: Our randomized controlled study suggests that the sedation of polytrauma patients with dexmedetomidine could help reduce the serum BDNF, S100B, and NSE levels, which appear to be associated with the occurrence of delirium in the dexmedetomidine group.

Objective: Anti-α-enolase antibody (Ab) combined with β2 microglobulin (β2-MG) were investigated to predict the incidence of nephritis in systemic lupus erythematosus (SLE) patients., Methods: Levels of serum anti-α-enolase Ab and urinary β2-MG were detected in 115 SLE patients, 29 SLE patients with nephritis and 70 healthy controls by ELISA and immunoturbidimetry, respectively. Furthermore, the correlation between anti-α-enolase Ab combined with β2-MG and the incidence of nephritis in SLE patients was evaluated by correlation analysis., Results: The optical density value of serum anti-α-enolase Ab in SLE patients with nephritis (0.84) was greatly increased compared with SLE patients (0.76) or healthy controls (0.54). Moreover, the levels of urinary β2-MG in SLE patients with nephritis (6.75 mg/L) were increased compared with SLE patients (3.45 mg/L) or healthy controls (1.48 mg/L). There was a positive correlation between the level of anti-α-enolase Ab and β2-MG ( r = 0.754). Furthermore, anti-α-enolase Ab combined with β2-MG for evaluating the incidence of nephritis in SLE patients had the best assessment of the effectiveness (area under the receiver operating characteristic curve (AUC): 92.7%) compared with only anti-α-enolase Ab (AUC: 80.9%) or β2-MG (AUC: 84.5%)., Conclusion: These data suggested that anti-α-enolase Ab may be a potential indicator for the prediction of nephritis in SLE patients.

Objective: To investigate the relationship between pretreatment plasma D-dimer levels and survival in Chinese patients with small cell lung cancer (SCLC)., Methods: This retrospective study enrolled 82 patients with SCLC treated at Beijing Chaoyang Hospital, Capital Medical University, from January 2012 to January 2015. All patients were followed up. Associations between pretreatment plasma D-dimer levels measured by immunoturbidimetric assay and clinical outcomes were analyzed by Kaplan-Meier and multivariate analyses, using a cut-off level of 0.55 mg/L fibrinogen equivalent units (FEU)., Results: Median progression-free survival (PFS) and overall survival (OS) were significantly higher in patients with low D-dimer levels (≤0.55 mg/L FEU; 8.0 and 17.0 months, respectively) compared with patients with high levels (>0.55 mg/L FEU; 5.0 and 9.0 months, respectively). Plasma D-dimer levels, Karnofsky performance status, N stage, TNM stage, treatment, and neuron-specific enolase (NSE) levels were significantly associated with PFS, while D-dimer levels, N stage, TNM stage, and treatment were significantly associated with OS. Multivariate analysis revealed that TNM stage, treatment, and NSE levels were independently associated with PFS, while D-dimer levels and treatment were independently associated with OS., Conclusions: Pretreatment plasma D-dimer levels were independently associated with OS in patients with SCLC.

Objective: Catheter ablation of atrial fibrillation (AF) can lead to thromboembolic complications, especially stroke. We measured the periprocedural serum neuron-specific enolase (NSE) level, which is a biomarker of neuronal injury, after ablation of AF., Methods: Forty-three patients with paroxysmal AF were prospectively enrolled before radiofrequency ablation. A neurological examination was performed before and after the procedure. The serum NSE level was determined before and at the end of the procedure and at 2, 24, and 48 h after the procedure., Results: No patients developed new neurological deficits. However, the median (interquartile range) NSE level increased after ablation from 6.7 (3.87) ng/mL at baseline to 11.48 (5.3) ng/mL at 24 h postoperatively. The NSE level exceed the upper reference limit of normal (17 ng/mL) in 14 patients (33%), and these patients were found to have a larger left atrium., Conclusions: Serum NSE increased in most of the patients undergoing ablation for AF, and it exceeded the normal limit in one-third of the patients. Although NSE is a biomarker of neuronal injury, the clinical importance of this increase after AF ablation and its relationship with the left atrial diameter should be evaluated in a longitudinal study.

Objective This study was performed to investigate the correlation among decreased regional cerebral oxygen saturation (rSO 2 ), blood levels of brain injury biomarkers, and postoperative cognitive disorder (POCD) after cardiac surgery with cardiopulmonary bypass (CPB). Methods This prospective observational study included 59 patients undergoing coronary artery bypass graft surgery with CPB. All patients underwent neuropsychological tests (Mini Mental State Evaluation, Rey Auditory Verbal Learning Test, digit span test, digit symbol substitution test, and Schulte table) the day before and 10 days after the surgery. The blood levels of two brain injury biomarkers, neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP), were measured before and 1 day after the surgery. Results The rSO 2 decreased during surgery in 21 (35%) patients. POCD was detected in 22 (37%) patients. After the surgery, no significant changes in the GFAP blood level occurred in any patients. No significant correlations were found among the decreased rSO 2 , increased NSE blood level, and rate of POCD. Conclusion These results suggest that a decrease in rSO 2 during cardiac surgery is not necessarily related to the development of POCD or an increased blood level of the brain injury biomarker NSE.

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.

The aim of this study is to evaluate the incidence and predictors of silent neuronal injury (SNI) after coronary angiography (CAG) and intervention by serial measurement of serum neuron-specific enolase (NSE) in patients presented with acute coronary syndrome (ACS). Ninety-eight consecutive patients presented with ACS and underwent CAG and intervention were included in the study. The NSE levels significantly increased after CAG and intervention compared to baseline levels (22.03 ± 27.70 and 10.08 ± 3.15 consecutively). Left ventricular ejection fraction in the SNI+ group was significantly lower than that in the SNI- group (43.71% ± 12.51%, 50.84% ± 9.34%, P = .002). Maximal creatinine kinase myocardial band, troponin I, and SYNTAX score of the SNI+ group were significantly higher than those of the SNI- group (103.83 ± 99.22, 51.92 ± 78.33, P = .006; 50.04 ± 66.18, 19.18 ± 30.50, P = .002; 103.83 ± 99.22, 51.92 ± 78.33, P = .006; and 50.04 ± 66.18, 19.18 ± 30.50, P = .002 successively). SYNTAX score and performing percutaneous coronary intervention were the independent predictors of SNI (P = .009, odds ratio [OR] = 1.06, 95% confidence interval [CI] = 1.014-1.107, P = .036, OR = 4.262, 95% CI = 1.097-16.56). Percutaneous coronary intervention and coronary artery lesion complexity may increase the risk of SNI in patients with ACS., (© The Author(s) 2014.)

Background: Olfactory dysfunction is a diagnostic criterion for chronic rhinosinusitis (CRS). During chronic inflammation and olfactory neuronal damage in CRS, it is likely that neuron-specific enolase (NSE) can leak into nasal secretions (NS) and serum. Therefore, we postulated that NSE levels in NS and in circulation may be indicative of olfactory dysfunction in CRS., Objective: To evaluate the relationship between the NS and serum concentrations of NSE with olfactory dysfunction in subjects with CRS., Methods: The patients with CRS were classified into two groups, depending on the presence of polyps: CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). A group of age- and sex-matched healthy volunteers served as controls. Olfactory function assessment was performed by using Sniffin' Sticks. NSE concentrations in serum and NS were analyzed by using the enzyme immunometric assay kit specific for the γ subunit., Results: The study included 46 patients with CRSsNP, 25 women (54.3%) and 21 men (45.7%), mean (standard deviation [SD]) age, 34.1 ± 12.3 years; and 54 patients with CRSwNP, 24 women (44.4%) and 30 men (55.6%), mean (SD) age, 37.9 ± 17.5 years. A group of 40 healthy volunteers who were matched for age and sex served as controls. Significantly higher serum and NS levels of NSE were measured in patients with CRS compared with healthy controls (p < 0.001). In the CRSwNP group, both mean (SD) serum (83.5 ± 37.6 ng/mL) and mean (SD) NS (6.1 ± 2.3 ng/mL) levels of NSE were significantly higher than in the CRSsNP group (46.4 ± 7.3 ng/mL [p < 0.001] and 1.7 ± 0.5 ng/mL [p < 0.001], respectively). In both the CRSsNP and CRSwNP groups (but not in the healthy controls), significant negative correlations between NS NSE levels and TDI scores (r = -0.63, p < 0.001 for the CRSwNP group, and r = -0.51, p < 0.001 for CRSsNP group) were observed, which meant that higher NSE was associated with worse olfactory function., Conclusions: The study demonstrated a contribution of CRS to NSE and olfactory dysfunction.

Objective: Neuropsychiatric (NP) lupus, a common manifestation of systemic lupus erythematosus (SLE), is still insufficiently understood, in part, because of the lack of specific biomarkers. Neuron specific enolase (NSE), an important neuronal glycolytic enzyme, shows increased serum levels following acute brain injury, and decreased serum levels in several chronic disorders of the nervous system, including multi infarct dementia, multiple sclerosis and depression. The aim of the study was to evaluate serum NSE levels in SLE patients with and without nervous system involvement, and in healthy controls, and to assess the correlation of NSE serum levels of patients with neuropsychiatric systemic lupus erythematosus (NPSLE) with clinical parameters., Methods: The study comprised 47 SLE patients and 28 controls. SLE activity was assessed using the Systemic Lupus Activity Measure (SLAM). A neurologist and a psychiatrist examined all patients. NP involvement was diagnosed according to strict NPSLE criteria proposed by Ainiala and coworkers, as modification to American College of Rheumatology (ACR) nomenclature and case definitions. NSE serum levels were determined by use of an immunoassay., Results: Mean NSE serum concentrations in patients with NPSLE were significantly lower than in non-NPSLE patients (6.3 ± 2.6 µg/L vs. 9.7 ± 3.3 µg/L, p < 0.01) and in controls (8.8 ± 3.3 µg/L, p < 0.05). There were significant negative correlations between NSE serum levels and SLE activity (r = -0.42, p < 0.05) and the number of NPSLE manifestations diagnosed (-0.37; p = 0.001)., Conclusion: Decreased serum concentrations of NSE may reflect chronic neuronal damage with declined metabolism of the nervous tissue in patients with NPSLE., (© The Author(s) 2015.)

Background: Cerebral neurochemicals are markers of traumatic brain injury (TBI)., Objectives: The aim of the study was to determine whether kicks to the head (KTH) in full contact karate significantly increased serum concentrations of protein S-100B, and neurone specific enolase (NSE). Kicks to the body (KTB) were also quantified to asses muscle tissue injury. Muscle damage was assessed by analysis of serum total creatine kinase (CK)., Methods: Twenty-four full contact karate practitioners were observed and filmed during actual competition and divided into two main groups post event: (1) Kicks to the head and body group (KTH): n = 12; mean ± SD; age, 30.4 ± 6.7 years; height, 1.74 ± 0.1 m; weight, 79.1 ± 2.1 kg; and (2): Kicks to the body group (KTB): n = 12; mean ± SD; age, 28.2 ± 6.5 years; height, 1.75 ± 0.1 m; weight, 79.2 ± 1.7 kg. The KTH group received direct kicks to the head, while group KTB received kicks and punches to the body. Blood samples were taken before and immediately post-combat for analysis of serum S-100B, NSE, CK and cardiac troponin., Results: Significant increases in serum concentrations of S-100B (0.12 ± 0.17 vs. 0.37 ± 0.26, µg.L(-1)) and NSE (11.8 ± 4.1 vs. 20.2 ± 9.1 ng.mL(-1)) were encountered after combat in the KTH group and CK (123 ± 53 vs. 184 ± 103 U.L(-1)) in the KTB group (all P <0.05)., Conclusions: Head kicks in full contact karate cause elevation of neurochemical markers associated with damaged brain tissue. The severity of injury is related to the early post-traumatic release of protein S-100B and NSE. The early kinetics and appearance post injury can reflect intracranial pathology, and suggest S-100B and NSE are extremely sensitive prognostic markers of TBI., (© The Author(s) 2015.)

The main purpose of this study was to assess the role of S100B protein, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP) in the evaluation of hypoxic brain injury in acute carbon monoxide (CO)-poisoned patients. This cross-sectional study was conducted among the patients with acute CO poisoning who referred to the emergency department in a 1-year period. Serum levels of S100B protein, NSE, and GFAP were determined on admission. A total of 55 CO-poisoned patients (mean age ± standard deviation, 45 ± 20.3 years; 60% women) were included in the study. The control group consisted of 25 healthy adults. The patients were divided into two groups according to whether they were conscious or unconscious. The serum levels of S100B, NSE, and GFAP were higher in patients than that in the control group. There was no significant difference between unconscious and conscious patients with respect to these markers. There was a statistically significant difference between the conscious and unconscious patients and the control group in terms of S100B and NSE levels. There was also a statistically significant difference between the unconscious patients and the control group in terms of GFAP levels. Increased serum S100B, NSE, and GFAP levels are associated with acute CO poisoning. These biomarkers can be useful in assessing the clinical status of patients with CO poisoning., (© The Author(s) 2014.)

Chronic kidney disease (CKD) has reached epidemic levels. It is a multisystem disease associated with elevated systemic inflammatory and hypercoagulable states. Most concerning are the cardiovascular risks associated with all stages of kidney disease. It is difficult to assess kidney disease stage progression and cardiovascular risk with current indicators such as estimated glomerular filtration rate and conventional cardiovascular risk factors. However, the use of biomarkers to assess the underlying pathological disease state may bridge the gap. This study evaluated biomarkers of inflammation including C-reactive protein, d-dimer, neuron-specific enolase, neutrophil gelatinase-associated lipocalin, tumor necrosis factor receptor I, and thrombomodulin in 3 groups of patients: CKD stages 2-4, end-stage renal disease (ESRD), and age-matched controls. The study demonstrated a statistically significant progressive upregulation in mean concentration of all markers when comparing controls to CKD and ESRD. Therefore, biomarkers may be able to evaluate the inflammatory state in kidney disease and potentially predict the cardiovascular risk.

Background: The high sensitivities and specificities reported for blood biomarkers as a supportive test in the diagnosis of acute stroke do not correspond with their performance for decision-making in emergency situations., Methods: Seventy-two patients with suspected stroke were recruited: 44 with ischaemic stroke, 17 with haemorrhagic stroke and 11 stroke mimics, as well as a high-risk control group of 79 individuals. Serum neuron-specific enolase (NSE) and S100 calcium binding protein B (S100B) biomarker levels were determined on admission, using immunoassay kits. The sensitivities and specificities of NSE and S100B for distinguishing acute stroke from stroke mimics and high-risk controls were calculated., Results: For cut-off values (NSE ≤ 14 micrograms per litre and S100B ≤130 nanograms per litre) the sensitivity was 53% and 55% respectively. Specificity was 64 for both versus the stroke mimic group. Specificity was higher (79% and 86% respectively) when calculated on the basis of the control group., Conclusions: This study supports the evidence indicating that serum levels of NSE and S100B do not improve the diagnosis of acute stroke.

Systemic vascular changes contribute to both the pathogenesis and thrombotic comorbidities of end-stage renal disease (ESRD). This study aims to profile various biomarkers and better understand their role in the pathogenesis of ESRD. Plasma samples from 49 patients with ESRD and 56 control individuals were analyzed for markers for inflammation, specifically C-reactive protein (CRP), tumor necrosis factor receptor 1 (TNFR1), neutrophil gelatinase-associated lipocalin (NGAL); thrombomodulin (TM); neuron-specific enolase (NSE), and thrombosis-D-dimer (DD). Compared to controls, all markers studied showed a statistically significant upregulation in patients with ESRD. These results indicate a polypathologic process in patients with ESRD, leading to cardiovascular and cerebrovascular events. However, the clinical significance of previously untested markers, such as TNFR1, NGAL, and NSE, still needs to be further explored. This study further validates the role of endothelial damage and endogenous thrombotic processes in ESRD as evidenced by the increased levels of TM and DD.

Serum levels of S-100B and neurone-specific enolase (NSE) reflect cerebral injury in a variety of neurological conditions such as stroke, traumatic brain injury, and cardiac arrest. There are limited data on the release of S-100B and NSE following carotid artery stenting (CAS). In 22 patients undergoing CAS, serial blood samples for S-100B and NSE were collected before and 2, 4, and 6 to 8 hours after the procedure. A group of 20 patients with significant CAS undergoing purely diagnostic angiography served as controls. A significant increase in S-100B levels was observed 2 hours after the procedure in patients with CAS (P = .001) with a gradual decline over the next hours. In contrast, patients who underwent purely diagnostic angiography did not show significant changes in S-100B levels up to 8 hours after the procedure. Neither patients with CAS nor those undergoing diagnostic angiography displayed any significant changes in serial NSE levels.

Boxing exposes participants to the physiological response to high intensity exercise and also to direct body and brain trauma. Amateur boxing is increasing and females have also been included in the Olympics. The aim of this study is to assess the stress response and possible brain injury incurred during a match by measuring serum biomarkers associated with stress and cellular brain injury before and after combat. Sixteen male amateur boxers were studied retrospectively. The study population was divided into two groups: (a) a group that received predominantly punches to the head (PTH) and (b) a group that received predominantly punches to the body (PTB). Blood samples were taken before and five minutes after each contest. They were analysed for S-100B, neuron-specific enolase (NSE), creatine kinase (CK) and cortisol. The PTH group received direct contacts to the head (not blocked, parried or avoided) and to the body (n=8, age: 17.6 ± 5.3, years; height: 1.68 ± 0.13, meters; mass: 65.4 ± 20.3, kg). The PTB group received punches to the body including blocked and parried punches, but received no direct punches to the head, (n=8, mean ± SD, age: 19.1 ± 3.2 years; height: 1.70 ± 0.75, meters; mass: 68.5 ± 15 kg). Significant increases (P<0.05) were observed between pre- and post-combat serum concentrations in serum concentrations in PTH of S-100B (0.35 ± 0.61 vs. 0.54 ± 0.73, μg.L-1) NSE (19.7 ± 14 vs.31.1 ± 26.6, ng.ml-1) and cortisol (373 ± 202 vs. 756 ± 93, nmol.L-1). Significant increases (P<0.05) of creatine kinase were recorded in both groups. This study demonstrates significant elevations in neurochemical biomarkers in boxers who received direct blows to the head. However, further work is required to quantify this volumetric brain damage and long term clinical sequelae.

This study evaluated serum neuron-specific enolase (NSE), cytokine and high-sensitivity C-reactive-protein (hs-CRP) levels, along with the Glasgow Coma Scale (GCS) and Revised Trauma Score (RTS), as predictors of mortality in the early posttraumatic period, in 100 Turkish patients with blunt head trauma. Overall patient mortality was 27%. There was a significant association between age and mortality, and mortality was negatively correlated with GCS and RTS. Head injury severity (GCS) was significantly related to NSE, hs-CRP, interleukin (IL)-6, IL-8 and tumour necrosis factor (TNF)-alpha levels. Mortality correlated positively with IL-6, IL-8, TNF-alpha and hs-CRP levels. NSE, hs-CRP, IL-6, IL-8 and TNF-alpha levels were significantly higher in non-survivors compared with survivors. GCS score < or =8, younger age and NSE levels were significant independent predictors of mortality. During the early post-traumatic period, NSE may be an objective alternative criterion to the GCS, in the management of patients with blunt head trauma.

Pulmonary and digestive neuroendocrine tumors (NETs) are a group of neoplasms whose incidence and prevalence has been constantly increasing over the last years thanks to the significant improvements in instrumental diagnostic techniques. Because NETs are extremely heterogeneous a correct histopathological diagnosis is essential for appropriate treatment. More specifically, the histopathological diagnosis of NETs can be regarded as a multistep: identification of the neuroendocrine nature of the neoplasm, determination of tumor grading; identification of unknown primary. Laboratory biomarkers for the study of gastroenteropancreatic neuroendocrine tumors include both specific markers and non-specific or general markers. At the moment, chromogranin A is the best available and most frequently used biomarker for the diagnosis of NETs, offering the highest overall sensitivity. CgA has also demonstrated some utility in the assessment of response to treatment and as indicator of tumor recurrence.

The study was designed to compare patients after laparoscopic and conventional colectomy with regard to early postoperative mood, cognitive function, and neurocognitive variables S100beta and neuron-specific enolase (NSE). Forty-five laparoscopic and 25 open colectomies were enrolled into the prospective study. Outcome measurements were positive and negative postoperative mood (BSKE), neuropsychological tests (Trail-Making Test; word reproduction; Stroop Test), and serum biochemical parameters (S100beta; NSE). Following laparoscopic procedure, patients described significantly better positive mood (P< .05), tended to require less time in the Trail-Making Test and Stroop Test, and had lower postoperative serum concentrations of S100beta compared to conventional colectomy patients (P< .01). The current results revealed several group differences, which, in their entirety, seem to represent a more beneficial outcome after laparoscopic colonic surgery.

Improved survival for infants with congenital heart disease (CHD) has led to increased focus on the most significant morbidities that are neurodevelopmental. Neurologic injury in neurodevelopmental outcome may have many causes in children with complex CHD undergoing cardiopulmonary bypass and deep hypothermic circulatory arrest, including genetic syndromes, abnormal blood flow patterns, prenatal insults, and hemodynamic instability. Although gross neurological injury can be detected in the perinatal and postoperative period, more subtle injury may not be identified until much later. Disabilities in speech and language, motor skills, and attention deficit disorder are present by school age in up to 50% of the complex CHD population. It is imperative that the mechanisms of these injuries be identified to enable the application of neuroprotective interventions. To facilitate clinical investigation, evaluation of surrogate markers for these longer term "real" outcomes continues. Because some abnormalities may not be detected for years, the evaluation of a surrogate marker takes a long time. Thus, identification of surrogate markers is in its infancy. Serologic proteins, seizures, magnetic resonance findings, cerebral oxygenation, and the neurologic examination have all been studied. Continuing innovation in the use of magnetic resonance imaging techniques and the application of physiologic measures including near-infrared spectroscopy currently pose the greatest potential for advances. This article summarizes the state of the art and an admission about how far we have yet to travel as we strive to make the neurodevelopmental outcomes of patients with CHD comparable to their healthy peers.

Conventional and promising new markers of myocardial injury have become an important diagnostic tool and their prognostic significance is also recognized. In addition, they help identify patients who will derive the most benefit from therapeutic interventions. The literature was searched from the websites of the National Library of Medicine (http://www.ncbi.nlm.nih.gov/) and PubMed Central, the U.S. National Library of Medicine's digital archive of life sciences journal literature (http://www.pubmedcentral.nih.gov/). The data were accessed from books and journals that published relevant articles in this field. The diagnosis of acute myocardial infarction (AMI) has traditionally relied on the combination of chest pain, ECG features, and elevation in serum markers. However, chest symptoms are frequently atypical or absent and ECG changes may be nonspecific or absent. Hence, the diagnosis of acute coronary syndromes has become increasingly dependent on serum markers of cardiac injury. Among them, creatine kinase (CK) is an effective and widely used test, with the recent CKMB assay offering greater specificity and sensitivity. Cardiac troponins facilitate early and rapid diagnosis, enable effective risk stratification in patients with AMI (with or without traditional criteria for MI), and identify those who will benefit from aggressive medical or surgical intervention. Recent data suggest the potential of myoglobin and CKMB isoforms as sensitive markers in the early hours after symptom onset. Cardiac-specific troponins help in rapid diagnosis, prognostication, and treatment of AMI. Troponins also facilitate early detection of recent infarction owing to their prolonged diagnostic window and also aid in the detection of "microinfarction.'' CKMB is used to detect reinfarction or infarct extension, if levels rise again after declining. Finally, novel biochemical markers are receiving attention in ongoing trials. They may prove to be more effective in diagnosis and prognosis than their existing counterparts.

Objective: The two most commonly used heparin-coated systems for cardiopulmonary bypass (CPB) are the Carmeda Bio-Active Surface (CBAS) (Medtronic, Minneapolis, MN, USA) and the Duraflo II coating (Baxter Healthcare, Irvine, CA, USA). The two surfaces are technically unequal and previous experimental studies have demonstrated disparities in effects on the immune system and blood cells. However, little is known concerning the influence of the two surfaces on markers for brain and myocardial dysfunction., Methods: Forty patients undergoing elective, primary coronary bypass grafting with CPB were prospectively randomized to either the CBAS system or the Duraflo II circuit. During and after CPB, biological markers for brain dysfunction and myocardial injury were analysed., Results: Both markers for brain dysfunction S-100B and neuron-specific enolase (NSE) increased significantly during CPB (p = 0.01). The elevation during bypass correlated significantly with the duration of CPB (r = 0.39 and r = 0.38, respectively, both p < 0.02). NSE was somewhat more elevated in the Duraflo II group at the end of CPB (p = 0.01) and 5 h after CPB (p = 0.02); for S-100B, there were no intergroup differences. Also, the markers related to myocardial injury, myoglobin and creatine kinase (CK-MB) mass increased during CPB (p = 0.01), while elevation of troponin-I occurred 5 h after CPB (p = 0.01). There were no statistically significant intergroup differences. No significant correlation was seen between the release of cardiac markers and the duration of CPB. The clinical course was similar in both groups., Conclusions: Except for a slightly higher elevation of NSE at the end of CPB and 5 h after CPB in the Duraflo II group, there were no significant differences between the CBAS group and the Duraflo II group concerning markers for brain and myocardial dysfunction.

Neurone-specific enolase (NSE) and Sangtec 100 (S-100) (Sangtec Medical, Sweden) assays are designed for clotted samples, but when studying cerebral damage following cardiac surgery, perioperative samples will contain heparin and/or protamine. The lipid emulsion propofol is also frequently used during cardiac surgery and could affect the assays. We, therefore, studied the effects of heparin, protamine and propofol on the accuracy of NSE and S-100 assays in five healthy patients. Blood samples were taken and divided into four groups: normal saline was added to group A; heparin to group B; heparin followed by protamine to group C; and propofol to group D. NSE and S-100 concentrations were measured for all samples. Neither heparin, protamine nor propofol affected the accuracy of S-100 and NSE assays; therefore, samples can be taken throughout operations involving cardiopulmonary bypass without influencing the results.

Neurone-specific enolase (NSE) and Sangtec 100 (S-100) are useful for detecting cerebral damage during cardiopulmonary bypass (CPB). However, red cells contain NSE, and the haemolysis frequently caused by CPB could produce a false rise in NSE; S-100 is not found in red cells and should not be affected. We, therefore, compared the effects of haemolysis on NSE and S-100 to see if correction was necessary and possible. From seven patients, serial dilutions of haemolysed red cells were added to plasma (1/64-1/2048), measured for absorption at 540 nm and assayed for NSE and S-100. S-100 concentrations showed no change with haemolysis. Measured NSE increased significantly with haemolysis > 1/512 (an increase of 6.6 micrograms/ml): a correction formula is presented. In 39/48 patients after CPB, mean haemolysis was < 1/256 and would not need any correction. NSE and S-100 assay can, therefore, be used throughout CPB, which allows both glial and neuronal damage to be studied.

Sangtec 100 (S-100) (Sangtec Medical, Sweden) and neurone-specific enolase (NSE) assays are showing promise in the assessment of cerebral damage following cardiopulmonary bypass (CBP). The manufacturer's instructions state, however, that samples must be spun and frozen within 30 min, which is inconvenient for serial studies. We, therefore, investigated whether strong blood samples at room temperature (RT) or 4 degrees C for up to 48 h affected the measured levels. Blood samples were taken before and after CBP in six patients and stored for 15 min, 4, 8, 24 or 48 h at RT or 4 degrees C. S-100 and NSE levels did not alter in either 'before surgery' or CPB samples when stored for up to 48 h at 4 degrees C. There was a small, nonsignificant rise when stored at RT. Samples may, therefore, be collected throughout long operations or stored overnight without affecting NSE or S-100 plasma levels.

Aims and Background: The somatostatin analog octreotide has an antiproliferative effect on small cell lung cancer lines in vitro and in experimental xenograft transplantation systems in vivo. Thus it is worth investigating octreotide activity in the clinical setting., Methods: We studied the effect of octreotide (200 micrograms three times a day subcutaneously for seven days) on serum levels of the tumor marker neuroenolase in 13 patients with small cell lung cancer., Results: A decrease in neuroenolase levels was observed at day 7 during octreotide treatment, with a mean +/- SD of 32.6 +/- 42.0 ng/ml compared to basal values of 44.4 +/- 57.7 ng/ml and to washout values of 50.3 +/- 65.7 ng/ml (P < 0.03)., Conclusions: Our results indicate that octreotide is effective in reducing neuroenolase levels in small cell lung cancer patients. These data suggest a possible role for octreotide in the treatment of this kind of tumor.