Correlation Study on the Prognostic Value of miR-21 and S-100B Protein Levels in Neonatal Hypoxic-Ischemic Encephalopathy Undergoing Hypothermia Therapy.

OBJECTIVE: To evaluate the variations in serum levels of microRNA-21 (miR-21) and S-100B protein in neonates with hypoxic-ischemic encephalopathy (HIE) after receiving hypothermia therapy and explore the correlation of these biomarkers with the neurodevelopmental prognosis of the infants. METHODS: This retrospective analysis included 90 neonatal HIE patients diagnosed and treated between January 2019 and December 2022. Real-time quantitative PCR and enzyme-linked immunosorbent assay (ELISA) methods were used to measure miR-21 and S-100B protein levels. Neurodevelopmental assessments were conducted at one year, and follow-up was performed using the Bayley Scales of Infant and Toddler Development third edition. Statistical analysis was carried out using SPSS software, with t-tests for continuous variables, chi-square tests for categorical data, Pearson correlation coefficient for correlation analysis, and multivariate regression analysis to adjust for confounding factors. RESULTS: After hypothermia therapy, the observation group showed a significant decrease in miR-21 and S-100B protein levels (P < 0.001), and neurodevelopmental scores were significantly higher than the control group (P < 0.05). Correlation analysis indicated a negative correlation between miR-21 and neurodevelopmental scores (r=-0.62, P < 0.001), as well as a negative correlation between S-100B protein levels (r=-0.76, P < 0.001). Multivariate regression analysis demonstrated that miR-21 levels and S-100B protein levels maintained independent negative correlations with neurodevelopmental scores (P < 0.001). CONCLUSION: Hypothermia therapy significantly reduces serum levels of miR-21 and S-100B protein in neonatal HIE patients and may be associated with better prognosis. miR-21 and S-100B serve as prognostic biomarkers, aiding in predicting and improving the treatment outcomes and long-term prognosis of neonatal HIE.

The Multifaceted S100B Protein: A Role in Obesity and Diabetes?

The S100B protein is abundant in the nervous system, mainly in astrocytes, and is also present in other districts. Among these, the adipose tissue is a site of concentration for the protein. In the light of consistent research showing some associations between S100B and adipose tissue in the context of obesity, metabolic disorders, and diabetes, this review tunes the possible role of S100B in the pathogenic processes of these disorders, which are known to involve the adipose tissue. The reported data suggest a role for adipose S100B in obesity/diabetes processes, thus putatively re-proposing the role played by astrocytic S100B in neuroinflammatory/neurodegenerative processes.

Significance of S100B Protein as a Rapid Diagnostic Tool in Emergency Departments for Traumatic Brain Injury Patients.

Traumatic brain injuries (TBIs) are not only the leading cause of death among people below 44 years of age, but also one of the biggest diagnostic challenges in the emergency set up. We believe that the use of serum biomarkers in diagnosis can help to improve patient care in TBI. One of them is the S100B protein, which is currently proposed as a promising diagnostic tool for TBI and its consequences. In our study, we analyzed serum biomarker S100B in 136 patients admitted to the Emergency Department of the Regional Specialist Hospital in Olsztyn. Participants were divided into three groups: patients with head trauma and alcohol intoxication, patients with head trauma with no alcohol intoxication and a control group of patients with no trauma or with injury in locations other than the head. In our study, as compared to the control group, patients with TBI had a significantly higher S100B level (both with and without intoxication). Moreover, in both groups, the mean S100B protein level was significantly higher in patients with pathological changes in CT. According to our study results, the S100B protein is a promising diagnostic tool, and we propose including its evaluation in routine regimens in patients with TBI.

Lack of association between four biomarkers and persistent post-concussion symptoms after a mild traumatic brain injury.

Approximately 15 % of individuals who sustained a mild Traumatic Brain Injury (TBI) develop persistent post-concussion symptoms (PPCS). We hypothesized that blood biomarkers drawn in the Emergency Department (ED) could help predict PPCS. The main objective of this project was to measure the association between four biomarkers and PPCS at 90 days post mild TBI. We conducted a prospective cohort study in seven Canadian EDs. Patients aged ≥ 14 years presenting to the ED within 24 h of a mild TBI who were discharged were eligible. Clinical data and blood samples were collected in the ED, and a standardized questionnaire was administered 90 days later to assess the presence of symptoms. The following biomarkers were analyzed: S100B protein, Neuron Specific Enolase (NSE), cleaved-Tau (c-Tau) and Glial Fibrillary Acidic Protein (GFAP). The primary outcome measure was the presence of PPCS at 90 days after trauma. Relative risks and Areas Under the Curve (AUC) were computed. A total of 595 patients were included, and 13.8 % suffered from PPCS at 90 days. The relative risk of PPCS was 0.9 (95 % CI: 0.5-1.8) for S100B ≥ 20 pg/mL, 1.0 (95 % CI: 0.6-1.5) for NSE ≥ 200 pg/mL, 3.4 (95 % CI: 0.5-23.4) for GFAP ≥ 100 pg/mL, and 1.0 (95 % CI: 0.6-1.8) for C-Tau ≥ 1500 pg/mL. AUC were 0.50, 0.50, 0.51 and 0.54, respectively. Among mild TBI patients, S100B protein, NSE, c-Tau or GFAP do not seem to predict PPCS. Future research testing of other biomarkers is needed to determine their usefulness in predicting PPCS.

Peripheral S100B Protein Levels in Five Major Psychiatric Disorders: A Systematic Review.

Five major psychiatric disorders: schizophrenia, major depressive disorder, bipolar disorder, autistic spectrum disorder, and attention-deficit/hyperactivity disorder, show a shared genetic background and probably share common pathobiological mechanisms. S100B is a calcium-binding protein widely studied in psychiatric disorders as a potential biomarker. Our systematic review aimed to compare studies on peripheral S100B levels in five major psychiatric disorders with shared genetic backgrounds to reveal whether S100B alterations are disease-specific. EMBASE, Web of Science, and PubMed databases were searched for relevant studies published until the end of July 2023. This study was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-analysis Protocols (PRISMA) guidelines. Overall, 1215 publications were identified, of which 111 full-text articles were included in the systematic review. Study designs are very heterogeneous, performed mostly on small groups of participants at different stages of the disease (first-episode or chronic, drug-free or medicated, in the exacerbation of symptoms or in remission), and various clinical variables are analyzed. Published results are inconsistent; most reported elevated S100B levels across disorders included in the review. Alterations in S100B peripheral levels do not seem to be disease-specific.

Serum Levels of S100B Protein and Myelin Basic Protein as a Potential Biomarkers of Recurrent Depressive Disorders.

Nowadays, nervous tissue damage proteins in serum are considered promising drug targets and biomarkers of Mood Disorders. In a cross-sectional naturalistic study, the S100B, MBP and GFAP levels in the blood serum were compared between two diagnostic groups (patients with Depressive Episode (DE, n = 28) and patients with Recurrent Depressive Disorder (RDD, n = 21)), and healthy controls (n = 25). The diagnostic value of serum markers was assessed by ROC analysis. In the DE group, we did not find changed levels of S100B, MBP and GFAP compared with controls. In the RDD group, we found decreased S100B level (p = 0.011) and increased MBP level (p = 0.015) in comparison to those in healthy controls. Provided ROC analysis indicates that MBP contributes to the development of a DE (AUC = 0.676; 95%Cl 0.525-0.826; p = 0.028), and S100B and MBP have a significant effect on the development of RDD (AUC = 0.732; 95%Cl 0.560-0.903; p = 0.013 and AUC = 0.712; 95%Cl 0.557-0.867; p = 0.015, correspondingly). The study of serum markers of nervous tissue damage in patients with a current DE indicates signs of disintegration of structural and functional relationships, dysfunction of gliotransmission, and impaired secretion of neurospecific proteins. Modified functions of astrocytes and oligodendrocytes are implicated in the pathophysiology of RDD.

Septic encephalopathy in the elderly - biomarkers of potential clinical utility.

Next to acute sickness behavior, septic encephalopathy is the most frequent involvement of the brain during infection. It is characterized by a cross-talk of pro-inflammatory cells across the blood-brain barrier, by microglial activation and leukocyte migration, but not by the entry of infecting organisms into the brain tissue. Septic encephalopathy is very frequent in older persons because of their limited cognitive reserve. The predominant clinical manifestation is delirium, whereas focal neurological signs and symptoms are absent. Electroencephalography is a very sensitive method to detect functional abnormalities, but these abnormalities are not specific for septic encephalopathy and of limited prognostic value. Routine cerebral imaging by computer tomography usually fails to visualize the subtle abnormalities produced by septic involvement of the brain. Magnetic resonance imaging is by far more sensitive to detect vasogenic edema, diffuse axonal injury or small ischemic lesions. Routine laboratory parameters most suitable to monitor sepsis, but not specific for septic encephalopathy, are C-reactive protein and procalcitonin. The additional measurement of interleukin (IL)-6, IL-8, IL-10 and tumor necrosis factor-α increases the accuracy to predict delirium and an unfavorable outcome. The most promising laboratory parameters to quantify neuronal and axonal injury caused by septic encephalopathy are neurofilament light chains (NfL) and S100B protein. Neuron-specific enolase (NSE) plasma concentrations are strongly influenced by hemolysis. We propose to determine NSE only in non-hemolytic plasma or serum samples for the estimation of outcome in septic encephalopathy.

S100B protein as a biomarker and predictor in traumatic brain injury.

OBJECTIVES: To determine the prognostic potential of S100B protein in patients with craniocerebral injury, correlation between S100B protein and time, selected internal diseases, body habitus, polytrauma, and season. METHODS: We examined the levels of S100B protein in 124 patients with traumatic brain injury (TBI). RESULTS: The S100B protein level 72 h after injury and changes over 72 h afterwards are statistically significant for prediction of a good clinical condition 1 month after injury. The highest sensitivity (81.4%) and specificity (83.3%) for the S100B protein value after 72 h was obtained for a cut-off value of 0.114. For the change after 72 h, that is a decrease in S100B value, the optimal cut-off is 0.730, where the sum of specificity (76.3%) and sensitivity (54.2%) is the highest, or a decrease by 0.526 at the cut-off value, where sensitivity (62.5%) and specificity (62.9%) are more balanced. The S100B values were the highest at baseline; S100B value taken 72 h after trauma negatively correlated with GCS upon discharge or transfer (r=-0.517, P<0.0001). We found no relationship between S100B protein and hypertension, diabetes mellitus, BMI, or season when the trauma occurred. Changes in values and a higher level of S100B protein were demonstrated in polytraumas with a median of 1.070 (0.042; 8.780) µg/L compared to isolated TBI with a median of 0.421 (0.042; 11.230) µg/L. CONCLUSION: S100B protein level with specimen collection 72 h after trauma can be used as a complementary marker of patient prognosis.

The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker.

S100B is a calcium-binding protein mainly concentrated in astrocytes in the nervous system. Its levels in biological fluids are recognized as a reliable biomarker of active neural distress, and more recently, mounting evidence points to S100B as a Damage-Associated Molecular Pattern molecule, which, at high concentration, triggers tissue reactions to damage. S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease. In addition, in experimental models of diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, multiple sclerosis, traumatic and vascular acute neural injury, epilepsy, and inflammatory bowel disease, alteration of S100B levels correlates with the occurrence of clinical and/or toxic parameters. In general, overexpression/administration of S100B worsens the clinical presentation, whereas deletion/inactivation of the protein contributes to the amelioration of the symptoms. Thus, the S100B protein may be proposed as a common pathogenic factor in different disorders, sharing different symptoms and etiologies but appearing to share some common pathogenic processes reasonably attributable to neuroinflammation.

5-HT and S100ß values in evaluating severity of cognitive impairment after traumatic brain injury.

INTRODUCTION: The aim of the study was to investigate the relationship between serum serotonin (5-HT) and central nervous system specific protein S100b application value in evaluating the severity of cognitive impairment after traumatic brain injury (TBI). MATERIAL AND METHODS: 102 patients with TBI treated in Jilin Neuropsychiatric Hospital from June 2018 to October 2020 were selected. According to Montreal Cognitive Assessment (MoCA) scale, patients were tested for cognitive function from multiple levels, such as attention, executive function, memory, and language. Patients with cognitive impairment were included into study group ( n = 64), and those without cognitive impairment were assigned to control group ( n = 58). Serum 5-HT and S100b were compared between the two groups with b level. Serum 5-HT and S100b were analyzed by receiver operating characteristic curve (ROC), b application value judging cognitive impairment. RESULTS: Serum 5-HT and S100b levels in the study group were significantly higher than those in the control group ( p < 0.05). In serum 5-HT and S100b, there was a significant negative correlation with a MoCA score ( r = -0.527, r = -0.436; p < 0.05, p < 0.05). Combined detection of serum 5-HT and S100b's area under ROC curve (AUC) was 0.810 (95% CI: 0.742-0.936, p < 0.05), sensitivity was 0.842, and specificity was 0.813. CONCLUSIONS: Serum 5-HT and S100b levels are closely related to the cognitive function of TBI patients. Combined detection is helpful to improve the accuracy of predicting cognitive impairment.

S100B serum level: A relevant biomarker for the management of non-traumatic headaches in emergency care?

BACKGROUND: The diagnostic of primary or secondary headaches in emergency units is mostly based on brain imaging, which is expensive and sometimes hardly accessible. An increase in serum S100B protein has already been found in several neurological conditions inducing brain damage. The objective of this study was to assess the diagnostic performance of S100B serum assay to distinguish primary and secondary headaches among patients with non-traumatic headaches in the emergency department. METHODS: This was a phase 2, prospective, monocentric diagnostic study. Eighty-one adult patients with non-traumatic headaches in the emergency department were included. In addition to the usual management, a blood assay of the S100B protein was performed in the emergency department, as well as a brain MRI between 48 and 96 h if not performed during the initial management. The primary or secondary headache diagnosis was made at one month by an expert committee, blindly of the results of the S100B assay. The primary outcome was the blood assay of the S100B protein. RESULTS: There was 63 patients for analysis in the primary headache group and 17 in the secondary headache group. The S100B protein assay was significantly higher in secondary headaches than primary headaches, with an AUC of the ROC curve of 0.67. The optimal threshold of 0.06 µg.L-1 allowed to obtain those diagnostic characteristics: sensitivity 75% [48; 93], specificity 62% [48; 74], PPV 35% [20; 54] and NPV 90% [76; 97]. The association between the S100B protein level and the onset of pain was significantly higher for patients with headaches <3 h. CONCLUSION: The assay of the S100B protein could be useful in the management of this pathology in emergencies. Future studies taking into account dosing time and etiologies could be conducted in order to refine its use in practice.

[Effect of transcranial direct current stimulation on neurological injury markers and prognosis in patients with acute and severe carbon monoxide poisoning].

Objective: To observe the effects of transcranial direct current stimulation (tDCS) on nerve injury markers and prognosis in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: In May 2021, 103 ASCOP patients were treated in the emergency department of Harrison International Peace Hospital of Hebei Medical University from November 2020 to January 2021. The patients were divided into two groups according to whether they received tDCS treatment. The control group (50 cases) were given oxygen therapy (hyperbaric oxygen and oxygen inhalation) , reducing cranial pressure, improving brain circulation and cell metabolism, removing oxygen free radicals and symptomatic support, and the observation group (53 cases) was treated with 2 weeks of tDCS intensive treatment on the basis of conventional treatment. All patients underwent at least 24 h bispectral index (BIS) monitoring, BIS value was recorded at the hour and the 24 h mean value was calculated. Neuron-specific enolase (NSE) and serum S100B calcium-binding protein (S100B) were detected after admission, 3 d, 7 d and discharge. Follow-up for 60 days, the incidence and time of onset of delayed encephalopathy (DEACMP) with acute carbon monoxide poisoning in the two groups were recorded. Results: The NSE and S100B proteins of ASCOP patients were significantly increased at admission, but there was no significant difference between the two groups (P=0.711, 0.326) . The NSE and S100B proteins were further increased at 3 and 7 days after admission. The increase in the observation group was slower than that in the control group, and the difference was statistically significant (P(3 d)=0.045, 0.032, P(7 d)=0.021, 0.000) ; After 14 days, it gradually decreased, but the observation group decreased rapidly compared with the control group, with a statistically significant difference (P=0.009, 0.025) . The 60 day follow-up results showed that the incidence of DEACMP in the observation group was 18.87% (10/53) , compared with 38.00% (19/50) in the control group (P=0.048) ; The time of DEACMP in the observation group[ (16.79±5.28) d] was later than that in the control group[ (22.30±5.42) d], and the difference was statistically significant (P=0.013) . Conclusion: The early administration of tDCS in ASCOP patients can prevent the production of NSE and S100B proteins, which are markers of nerve damage. and can improve the incidence and time of DEACMP.

Correlation Between Cognitive Impairment and Homocysteine and S100B Protein in Patients with Progressive Ischemic Stroke.

Purpose: This study aimed to investigate the relationship between cognitive impairment and homocysteine (Hcy) and S100B protein in patients with progressive ischemic stroke (PIS). Patients and Methods: A total of 158 patients with PIS hospitalized in the Department of Neurology in Taixing People's Hospital from January 2020 to March 2022 were enrolled in the study. After 90 days of follow-up, the patients were divided into two groups according to the MoCA score-99 cases with cognitive impairment group (observation group) and 59 cases with cognitive normal group (control group). Causal diagram was drawn to assess the association between risk factors and PIS with observation group. The risk factors indicators of cognitive impairment in patients with PIS were screened. The related predictive indicators were screened by multivariate logistic regression analysis, and Pearson correlation analysis. The predictive value was analyzed by Receiver Operating Characteristic (ROC) curve. Results: Multivariate logistic regression analysis showed that age, hypertension, lesion position, Hcy and S100B protein were related risk factors for cognitive impairment in patients with PIS. Pearson correlation analysis was conducted between Hcy and S100 B protein and MoCA score, and revealed that Hcy and S100 B protein were negatively correlated with MoCA score. ROC curve analysis showed that the Area Under the Curve (AUC) of S100 B protein and Hcy in identifying cognitive impairment after PIS was 0.709 and 0.673, respectively, and the combined AUC of Hcy and S100B protein in predicting cognitive impairment after PIS was 0.739. Conclusion: Hcy and S100B protein are related risk factors for cognitive impairment in patients with PIS, and may be used as in a prediction model to predict cognitive impairment after PIS in the future.

Serum s100b protein levels as a neuroinflammatory biomarker of acutely relapsed paranoid schizophrenia patients.

OBJECTIVE: The s100b inflammatory protein is involved in schizophrenia pathophysiology. We aim at studying the evolution of the s100b serum levels in acutely relapsed paranoid schizophrenia patients at three different time points (admission, discharge and 3 months after hospital discharge 3MAHD). METHODS: Twenty-three paranoid schizophrenia inpatients meeting DSM-IV criteria participated in the research. Twenty-three healthy subjects matched by age, gender and season acted as the control group. Psychopathology was measured with the Positive and Negative Syndrome Scale (PANSS). Serum s100b levels were determined at 12:00 and 24:00 h with an enzyme-linked immunoassay kit. RESULTS: Patients had significant higher serum s100b levels at admission and discharge (12:00 h) than the group of healthy subjects. At admission and discharge, s100b serum levels at 24 h had decreased compared to the 24:00 h s100b levels of the healthy subjects. At 3MAHD patients and healthy subjects had similar levels of serum s100b protein. Positive and negative PANSS scores decreased significantly between admission and discharge. Positive and negative PANSS scores decreased between discharge and 3MAHD, but these changes had no statistical significance. CONCLUSIONS: Our study confirms that the acute inflammatory response produced in acutely relapsed patients is reversed after 3 month of hospital discharge. The variations of serum s100b concentrations when the patients suffer from an acute relapse may be a useful predictor of disease evolution.

Post-dialysis fatigue and serum S100B protein in patients on chronic hemodialysis. A pilot study.

BACKGROUND: Aim of the present study was to assess whether post-dialysis fatigue (PDF) may be related to pre- or post-dialysis levels of serum S100B protein. Hemodialysis patients (HD) who answered to be fatigued after their hemodialysis sessions when asked: "Do you feel worse after dialysis? if they answered yes" were considered to suffer from PDF. Serum Interleukins (IL-1ß, IL-6, IL-10), TNF-α and S100B were assessed by ELISA kit. RESULTS: Thirty HD patients were studied: 22 (73.4%) reported to suffer from PDF. Serum S100B post-dialysis levels (median [IQR] = 17.4 µg [7.1 to 30.9]) were significantly higher than serum S100B pre-dialysis levels (median [IQR] = 5 µg [1.4 to 22.1]; p = 0.0001). S100B post-dialysis was significantly higher than S100B pre-dialysis either in patients with PDF or without PDF. CONCLUSIONS: Pre- and post-dialysis values of serum S100B and its delta did not differ significantly between patients with and without PDF and were not associated with the length of the TIRD in patients on chronic hemodialysis.

Effect of transcranial direct current stimulation on neurological injury markers and prognosis in patients with acute and severe carbon monoxide poisoning / 中华劳动卫生职业病杂志

Objective: To observe the effects of transcranial direct current stimulation (tDCS) on nerve injury markers and prognosis in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: In May 2021, 103 ASCOP patients were treated in the emergency department of Harrison International Peace Hospital of Hebei Medical University from November 2020 to January 2021. The patients were divided into two groups according to whether they received tDCS treatment. The control group (50 cases) were given oxygen therapy (hyperbaric oxygen and oxygen inhalation) , reducing cranial pressure, improving brain circulation and cell metabolism, removing oxygen free radicals and symptomatic support, and the observation group (53 cases) was treated with 2 weeks of tDCS intensive treatment on the basis of conventional treatment. All patients underwent at least 24 h bispectral index (BIS) monitoring, BIS value was recorded at the hour and the 24 h mean value was calculated. Neuron-specific enolase (NSE) and serum S100B calcium-binding protein (S100B) were detected after admission, 3 d, 7 d and discharge. Follow-up for 60 days, the incidence and time of onset of delayed encephalopathy (DEACMP) with acute carbon monoxide poisoning in the two groups were recorded. Results: The NSE and S100B proteins of ASCOP patients were significantly increased at admission, but there was no significant difference between the two groups (P=0.711, 0.326) . The NSE and S100B proteins were further increased at 3 and 7 days after admission. The increase in the observation group was slower than that in the control group, and the difference was statistically significant (P(3 d)=0.045, 0.032, P(7 d)=0.021, 0.000) ; After 14 days, it gradually decreased, but the observation group decreased rapidly compared with the control group, with a statistically significant difference (P=0.009, 0.025) . The 60 day follow-up results showed that the incidence of DEACMP in the observation group was 18.87% (10/53) , compared with 38.00% (19/50) in the control group (P=0.048) ; The time of DEACMP in the observation group[ (16.79±5.28) d] was later than that in the control group[ (22.30±5.42) d], and the difference was statistically significant (P=0.013) . Conclusion: The early administration of tDCS in ASCOP patients can prevent the production of NSE and S100B proteins, which are markers of nerve damage. and can improve the incidence and time of DEACMP.

Longterm Increased S100B Enhances Hippocampal Progenitor Cell Proliferation in a Transgenic Mouse Model.

(1) The neurotrophic protein S100B is a marker of brain injury and has been associated with neuroregeneration. In S100Btg mice rendering 12 copies of the murine S100B gene we evaluated whether S100B may serve as a treatment option. (2) In juvenile, adult, and one-year-old S100Btg mice (female and male; n = 8 per group), progenitor cell proliferation was quantified in the subgranular zone (SGZ) and the granular cell layer (GCL) of the dentate gyrus with the proliferative marker Ki67 and BrdU (50 mg/kg). Concomitant signaling was quantified utilizing glial fibrillary acidic protein (GFAP), apolipoprotein E (ApoE), brain-derived neurotrophic factor (BDNF), and the receptor for advanced glycation end products (RAGE) immunohistochemistry. (3) Progenitor cell proliferation in the SGZ and migration to the GCL was enhanced. Hippocampal GFAP was reduced in one-year-old S100Btg mice. ApoE in the hippocampus and frontal cortex of male and BDNF in the frontal cortex of female S100Btg mice was reduced. RAGE was not affected. (4) Enhanced hippocampal neurogenesis in S100Btg mice was not accompanied by reactive astrogliosis. Sex- and brain region-specific variations of ApoE and BDNF require further elucidations. Our data reinforce the importance of this S100Btg model in evaluating the role of S100B in neuroregenerative medicine.

Prognostic properties of the association between the S-100B protein levels and the mean cerebral blood flow velocity in patients diagnosed with severe traumatic brain injury.

Craniocerebral injury (CBI) is tissue damage caused by a sudden mechanical force. CBI can result in neurological, neuropsychological and psychiatric dysfunctions. Currently, the severity of CBI is assessed using the Glasgow Coma Scale, brain perfusion pressure measurements, transcranial Doppler tests and biochemical markers. This study aimed to determine the applicability of the S-100B protein levels and the time-averaged mean maximum cerebral blood flow velocity (Vmean) as a means of predicting the treatment outcomes of CBI in the first 4 days of hospitalization. The results validated the standard reference ranges previously proposed for the concentration of S-100B (0.05-0.23 µg/l) and the mean of cerebral blood flow velocity (30.9 to 74.1 cm/sec). The following stratification scheme was used to predict the success of treatment: Patients with a Glasgow Outcome Scale (GOS) score ≥4 or GOS <4 were stratified into 'favorable' and 'unfavorable' groups, respectively. The favorable group showed relatively constant levels of the S-100B protein close to the normal range and exhibited an increase in Vmean, but this was still within the normal range. The unfavorable group exhibited a high level of S-100B protein and increased Vmean outside of the normal ranges. The changes in the levels of S-100B in the unfavorable and favorable groups were -0.03 and -0.006 mg/l/h, respectively. Furthermore, the rate of decrease in the Vmean value in the unfavorable and favorable groups were -0.26 and -0.18 cm/sec/h, respectively. This study showed that constant levels of S-100B protein, even slightly above the normal range, associated with an increase in Vmean was indicative of a positive therapeutic outcome. However, additional research is required to obtain the appropriate statistical strength required for clinical practice.

Neuron-Specific Enolase and S100B: The Earliest Predictors of Poor Outcome in Cardiac Arrest.

Background: Proper prognostication is critical in clinical decision-making following out-of-hospital cardiac arrest (OHCA). However, only a few prognostic tools with reliable accuracy are available within the first 24 h after admission. Aim: To test the value of neuron-specific enolase (NSE) and S100B protein measurements at admission as early biomarkers of poor prognosis after OHCA. Methods: We enrolled 82 consecutive patients with OHCA who were unconscious when admitted. NSE and S100B levels were measured at admission, and routine blood tests were performed. Death and poor neurological status at discharge were considered as poor clinical outcomes. We evaluated the optimal cut-off levels for NSE and S100B using logistic regression and receiver operating characteristic (ROC) analyses. Results: High concentrations of both biomarkers at admission were significantly associated with an increased risk of poor clinical outcome (NSE: odds ratio [OR] 1.042 per 1 ng/dL, [1.007−1.079; p = 0.004]; S100B: OR 1.046 per 50 pg/mL [1.004−1.090; p < 0.001]). The dual-marker approach with cut-off values of ≥27.6 ng/mL and ≥696 ng/mL for NSE and S100B, respectively, identified patients with poor clinical outcomes with 100% specificity. Conclusions: The NSE and S100B-based dual-marker approach allowed for early discrimination of patients with poor clinical outcomes with 100% specificity. The proposed algorithm may shorten the time required to establish a poor prognosis and limit the volume of futile procedures performed.

Oxidative Stress and Indicators of Brain Damage Following Pediatric Heart Surgery.

Pediatric cardiac surgery induces an increased oxidative stress (OS) response. Increased OS is associated with poor neurologic outcomes in neonatal populations with similar patterns of brain injury. We investigated OS and brain injury in infants undergoing heart surgery. Patients 6 months or younger, undergoing cardiac surgery with or without cardiopulmonary bypass (CPB), were included in this prospective, observational study. Patients were divided into infant (30 days−6 months) and neonatal (<30 days) groups for analysis. Urine OS biomarker 8-iso-prostaglandin F2α (8-iso-PGF2α) was quantified pre-surgery and at 0 and 24 h post-surgery. A serum brain damage biomarker S100B protein was also measured pre-surgery and at 0 and 72 h post-surgery. Amplitude-integrated electroencephalography during surgery was analyzed. Neuropsychological evaluation using the Bayley III or Vineland test was performed in all patients at 24 months of age. Sixty-two patients were included, 44 of whom underwent follow-up neurologic evaluation. 8-iso-PGF2α and S100B levels were increased after surgery. Postoperative levels of S100B were positively correlated with 8-iso-PGF2α levels 24 h after surgery (rho = 0.5224; p = 0.0261). There was also a correlation between immediate post-surgery levels of 8-iso-PGF2α and intra-surgery seizure burden (rho = 0.4285, p = 0.0205). Patients with an abnormal neurological evaluation had increased levels of S100B 72 h after surgery (p = 0.048). 8-iso-PGF2α levels 24 h after surgery were also related to abnormal neurologic outcomes. Levels of 8-iso-PGF2α following pediatric cardiac surgery are associated with several indicators of brain injury including brain damage biomarkers, intra-operative seizures, and abnormal neurological evaluation at follow-up, suggesting the importance of oxidative stress response in the origin of brain damage in this population.