Serum S100B Levels Research Articles

Study of serum level of S100B as a biomarker of vitiligo activity

BackgroundVitiligo is a common acquired depigmenting skin disorder. Current pathophysiologic insights promote the theory that melanocytes are destroyed by the immune system, leaving persistent areas of depigmentation, other theories have been suggested regarding the causes for depigmentation, including deficient adhesion proteins, an increased presence of oxidative stress, and neurogenic factors.ObjectiveThe study aims to evaluate the serum level of S100B in vitiligo patients and its correlation with disease activity in comparison with healthy controls.Patients and methodsThis is a case–control study that included 60 patients with vitiligo who were diagnosed with clinical evaluation and 30 healthy individuals as a control group. All patients were assessed for activity by Vitiligo Disease Activity Score (VIDA score) last year and the authors used Vitiligo Extent Score (VES), which is estimated body mass index % and measured serum level of S100B by the enzyme-linked immunosorbent assay system.ResultsThere was a significant increase in the serum level of S100Bng/l in the patient group compared with the control (P value < 0.001) and a significant positive correlation between serum level of S100Bng/l and VIDA in the patient group.ConclusionSerum levels of S100B in vitiligo were used as a biomarker for activity.

Neuroprotective effect of memantine on serum S100-B levels after on-pump coronary artery bypass graft surgery: A randomized clinical trial.

Background:Brain injury is one of the complications of open heart surgery. Glutamate plays a key role in this process. In this study, we evaluated the neuroprotective effect of memantine as NMDAR inhibitor in patients undergoing on-pump coronary artery bypass graft surgery (CABG).Methods:From July 2019 to May 2020, thirty-four consecutive patients selected for elective isolated on-pump coronary artery bypass graft surgery (CABG) enrolled in the trial. Patients were randomly assigned into two groups; memantine and the control group. For the memantine group, 10 mg of memantine twice daily was administered at least 72 h before surgery. Venous blood samples were collected before surgery (T1), at the end of cardiopulmonary bypass (CPB) (T2), 6h and 24h after CPB (T3 and T4). Serum concentration of S100-B was measured by enzyme-linked immunosorbent assay (ELISA) technique.Results:Serum S100-B increased during CPB with a peak plasma concentration at the termination of CPB. Then it gradually decreased during the first 24 hours in both groups (P=0.001). The mean S100-B levels were significantly lower in the memantine group compared to the control group at the termination of CPB (0.863±0.203 μg/l vs 1.117±0.304 μg/l), at 6 hours post-CPB (0.731±0.168 μg/l vs 0.938±0.206 μg/l), and 24 hours post-CPB (0.595±0.189 μg/l vs 0.852±0.227 μg/l), respectively (P=0.023). The mean level of serum S100-B in memantine group was about 0.19 μg/l less than the control group during the study (CI, 0.07 to 0.30; P=0.001). One (6.2%) patient in the control group had post-operative left arm paresthesiaConclusion:Administration of memantine before on-pump CABG can attenuate the post-operative concentrations of serum S100-B, which may reduce cerebral damage during surgery.

Early Effect of Radiotherapy on Serum Levels of HSP70 and S100B in Patients with Breast Cancer

Early Effect of Radiotherapy on Serum Levels of HSP70 and S100B in Patients with Breast Cancer

Evaluation of Serum S100B Levels in Male Children Younger than 6 Years Old with Autism Spectrum Disorder: A Psychiatric and Biochemical Perspective

Aim: Autism spectrum disorder is a neurodevelopmental disorder. The S100 calcium binding protein B (S100B) is among the markers of astrocyte activation as well as brain damage. Herein, it was aimed to evaluate S100B levels to determine whether there is a relation with the severity of autism spectrum disorder and establish possible causes of different results among the studies in the literature from a psychiatric and biochemical perspective. Material and Methods: Twenty-five male children with autism spectrum disorder were included as the study group along with twenty-seven male children as the control group. The childhood autism rating scale and the autism behavior checklist were applied. Serum S100B protein levels were measured by enzyme-linked immunosorbent assay (ELISA). Results: The mean serum S100B level was 1008.61±171.34 pg/mL in the study group and 1060.14±182.83 pg/mL in the control group, and no statistically significant difference was found between the groups (p=0.300). Based on the childhood autism rating scale scores, 60% (n=15) of the children with autism spectrum disorder had severe autism, whereas 40% (n=10) had mild-to-moderate autism. There was no significant difference in terms of the serum S100B levels between the groups of autism spectrum disorder severity (p=0.935) or according to the autistic regression status (p=0.667). Conclusion: For S100B to be accepted as a reliable biomarker for autism spectrum disorder, more studies considering some factors with larger samples should be performed. Moreover, to understand the effect of biochemical methodology on the results, further studies are suggested on this subject.

The genetic and epigenetic profile of serum S100β in the Lothian Birth Cohort 1936 and its relationship to Alzheimer’s disease

Background: Circulating S100 calcium-binding protein (S100β) is a marker of brain inflammation that has been associated with a range of neurological conditions. To provide insight into the molecular regulation of S100β and its potential causal associations with Alzheimer’s disease, we carried out genome- and epigenome-wide association studies (GWAS/EWAS) of serum S100β levels in older adults and performed Mendelian randomisation with Alzheimer’s disease. Methods: GWAS (N=769, mean age 72.5 years, sd = 0.7) and EWAS (N=722, mean age 72.5 years, sd = 0.7) of S100β levels were performed in participants from the Lothian Birth Cohort 1936. Conditional and joint analysis (COJO) was used to identify independent loci. Expression quantitative trait locus (eQTL) analyses were performed for lead loci that had genome-wide significant associations with S100β. Bidirectional, two-sample Mendelian randomisation was used to test for causal associations between S100β and Alzheimer’s disease. Colocalisation between S100β and Alzheimer’s disease GWAS loci was also examined. Results: We identified 154 SNPs from chromosome 21 that associated (P<5x10 -8) with S100β protein levels. The lead variant was located in the S100β gene (rs8128872, P=5.0x10 -17). We found evidence that two independent causal variants existed for both transcription of S100β and S100β protein levels in our eQTL analyses . No CpG sites were associated with S100β levels at the epigenome-wide significant level (P<3.6x10 -8); the lead probe was cg06833709 (P=5.8x10 -6), which mapped to the LGI1 gene. There was no evidence of a causal association between S100β levels and Alzheimer’s disease or vice versa and no evidence for colocalisation between S100β and Alzheimer’s disease loci. Conclusions: These data provide insight into the molecular regulators of S100β levels. This context may aid in understanding the role of S100β in brain inflammation and neurological disease.

Blood brain barrier permeability increases with age in individuals with 22q11.2 deletion syndrome

22q11.2 deletion syndrome (22q11.2DS) is characterised by high rates of psychotic disorders and immune abnormalities. Blood–brain barrier (BBB) permeability is known to be a risk factor for schizophrenia and immune aberrations. Objective To evaluate the relationship between psychosis and BBB permeability in this population. Methods We examined two biomarkers for BBB permeability, s100β and neuron-specific enolase (NSE), in 22q11.2DS individuals with/without psychosis. The first cohort of this Israeli–Belgium study was comprised of 20 22q11.2DS adults (30.58 ± 9.42 years) afflicted with a psychotic disorder, another group of 69 non-psychotic 22q11.2DS adults (23.42 ± 8.36 years), and 58 healthy controls (26.39 ± 7.77 years). A second cohort was comprised of 18 non-psychotic 22q11.2DS Israeli children (5.83 ± 1.55 years) and 14 healthy controls (5.34 ± 1.43 years). NSE and s100β serum levels were detected in all participants. Results Both factors were elevated in adults with 22q11.2DS compared to healthy controls, specifically in the non-psychotic sub-group. In contrast, there were no significant differences in their levels between the two groups of the paediatric cohort. Conclusions Increased BBB permeability seems to be a trait of 22q11.2DS that evolves sometime in early adulthood. Our findings are in line with previous reports on non-syndromic schizophrenia, and suggest potential novel neural pathways to psychosis in 22q11.2DS.

Correlation between S100B and severity of depression in MDD: A meta-analysis

Background Previous studies have demonstrated elevated levels of the S100B protein (located in glial cells) in major depressive disorder (MDD) as compared to healthy controls. However, studies reporting correlation between S100B levels and depression severity have been conflicting. Methods We investigated, through systematic review and meta-analysis, whether the correlation between S100B levels and depression severity is significant in patients with MDD. Pearson correlation coefficients reported in the individual studies were converted to Fisher’s Z scores, then pooled using the random effects model. Meta-regression was used to test modifiers of the effect size. Results Sixteen studies including 658 patients with MDD met eligibility criteria. No publication bias was observed. There was a significant and positive correlation between serum S100B level and depression severity (r = 0.204, z = 2.297, p = 0.022). A meta-regression determined that onset age of MDD and percentage of female participants are significant modifiers of this correlation. A moderate, but non-significant heterogeneity was observed in serum studies (44%). Conclusion As many studies have reported significantly increased levels of S100B in MDD compared to controls, this meta-analysis supports the assumption that the increase in S100B correlates with the severity of MDD. Additional studies investigating the precise biological connection between S100B and MDD are indicated.

Predictive Performance of Serum S100B Versus LDH in Melanoma Patients: A Systematic Review and Meta-Analysis

BackgroundCurrently, no consensus on the use of blood tests for monitoring disease recurrence in patients with resected melanoma exists. The only meta-analysis conducted in 2008 found that elevated serum S100B levels were associated with significantly worse survival in melanoma patients. Serum LDH is an established prognostic factor in patients with advanced melanoma.ObjectiveTo compare the discriminative and prognostic ability of serum S100B with that of serum LDH in patients with melanoma.MethodsThis systematic review and meta-analysis were reported in accordance with the PRISMA Statement. The study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD42019137138).ResultsA quantitative analysis of data from 6 eligible studies included 1,033 patients with cutaneous melanoma. The discriminative ability of serum S100B at identifying disease relapse [pooled Area Under the ROC (AUROC) 78.64 (95% CI 70.28; 87.01)] was significantly greater than the discriminative ability of serum LDH [AUROC 64.41 (95% CI 56.05; 7278)] (p=0.013). Ten eligible studies with 1,987 patients were included in the risk of death analysis. The prognostic performance of serum S100B [pooled estimate of adjusted hazard ratio (HR) 1.78 (95% CI 1.38; 2.29)] was independent but not superior to that of serum LDH [HR 1.60 (95% CI 1.36; 2.29)].LimitationsA relatively small number of articles were eligible and there was considerable heterogeneity across the included studies.ConclusionsSerum biomarkers may provide relevant information on melanoma patient status and should be further researched. Serum S100B is a valid marker for diagnosis of melanoma recurrence.Systematic Review RegistrationThe study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD42019137138).

Association of Changed Serum Brain Biomarkers With Perihematomal Edema and Early Clinical Outcome in Primary ICH Patients.

Perihematomal edema (PHE) following primary intracranial hemorrhages (ICHs) affects the patient outcome. Also, serum biomarkers such as S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) have been associated with ICHs outcome. We aimed to investigate the association between these biomarkers and PHE in ICH patients. In this cross-sectional study, patients with primary ICH between January 2020 and August 2020 were evaluated. All participants underwent spiral brain computed tomography scans upon admission, and 48 to 72 hours later and quantification of initial hematoma volume was performed. Serum level of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), GFAP, and S100B on admission were measured by enzyme-linked immunosorbent assays. Acute clinical outcome was assessed by the modified-Rankin scale, National Institute of Health Stroke Scale (NIHSS), and ICH score. Thirty-seven ICH patients (21 patients with a favorable outcome and 16 unfavorable) were studied. Compared with survival patients, nonsurvivor patients showed a higher serum level of MMP-9, VEGF, GFAP, and S100B ( P <0.05). Scores of absolute PHE, edema expansion distance, and PHE growth rate in the nonsurvivor group were higher than the survivors ( P <0.001). The regression model revealed that MMP-9, VEGF, ICH score, and hematoma volume were associated with the PHE growth rate. S100B and ICH score were associated with edema expansion distance. Our data showed that the serum level of molecular biomarkers was associated with higher PHE volume and PHE scores were higher in nonsurvival patients, suggesting it may have a pathogenic role in developing PHE after ICH.

Cognitive training programimprovescognitive ability and daily living ability in elderly patients with mild cognitive impairment.

Mild cognitive impairment (MCI) is a clinical syndrome of mild memory or other cognitive impairment without dementia and is a clinical transition state between normal aging and dementia. Careful and meticulous nursing intervention can improve the clinical symptoms of MCI and delay the progression of the disease. This research aimed to evaluate the efficacy of cognitive function training interventions in elderly patients with MCI. 106 patients were randomized into the intervention group or the control group. They received conventional nursing intervention and those in the intervention group received additional cognitive training program for 6weeks. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), activities of daily living (ADL) scales, and Barthel index (BI) were evaluated before and 6weeks after the intervention, as well as the serum levels of S100β and neuron-specific enolase (NSE) at two time points. After intervention, the MMSE scores and MoCA scores in both groups were significantly increased and the score in the intervention group was significantly higher. In the intervention group, the performance of conventional nursing intervention and cognitive training program significantly increased the scores of ADL and BI (p < 0.001). The serum levels of NSE and S100β in the intervention group were significantly lower. The performance of cognitive training program alleviated the brain tissue damage in elderly patients with MCI. The performance of cognitive training program in elderly patients with MCI improved their cognitive ability and daily living ability.

Protein expression of prognostic genes in primary melanoma and benign nevi

PurposeTo evaluate the protein expression characteristics of genes employed in a recently introduced prognostic gene expression assay for patients with cutaneous melanoma (CM).MethodsWe studied 37 patients with CM and 10 with benign (melanocytic) nevi (BN). Immunohistochemistry of primary tumor tissue was performed for eight proteins: COL6A6, DCD, GBP4, KLHL41, KRT9, PIP, SCGB1D2, SCGB2A2.ResultsThe protein expression of most markers investigated was relatively low (e.g., DCD, KRT9, SCGB1D2) and predominantly cytoplasmatic in melanocytes and keratinocytes. COL6A6, GBP4, and KLHL41 expression was significantly enhanced in CM when compared to BN. DCD protein expression was significantly correlated with COL6A6, GBP4, and KLHL41. GBP4 was positively correlated with KLHL41 and inversely correlated with SCGB2B2. The latter was also inversely correlated with serum S100B levels at time of initial diagnosis. The presence of SCGB1D2 expression was significantly associated with ulceration of the primary tumor. KRT9 protein expression was significantly more likely found in acral lentiginous melanoma. The presence of DCD expression was less likely associated with superficial spreading melanoma subtype but significantly associated with non-progressive disease. The absence of SCGB2A2 expression was significantly more often observed in patients who did not progress to stage III or IV.ConclusionsThe expression levels observed were relatively low but differed in part with those found in BN. Even though we detected some significant correlations between the protein expression levels and clinical parameters (e.g., CM subtype, course of disease), there was no major concordance with the protective or risk-associated functions of the corresponding genes included in a recently introduced prognostic gene expression assay.

The genetic and epigenetic profile of serumS100β in the Lothian Birth Cohort 1936 and its relationship to Alzheimer's disease.

Background: Circulating S100 calcium-binding protein (S100β) is a marker of brain inflammation that has been associated with a range of neurological conditions. To provide insight into the molecular regulation of S100β and its potential causal associations with Alzheimer's disease, we carried out genome- and epigenome-wide association studies (GWAS/EWAS) of serum S100β levels in older adults and performed Mendelian randomisation with Alzheimer's disease. Methods: GWAS (N=769, mean age 72.5 years, sd = 0.7) and EWAS (N=722, mean age 72.5 years, sd = 0.7) of S100β levels were performed in participants from the Lothian Birth Cohort 1936. Conditional and joint analysis (COJO) was used to identify independent loci. Expression quantitative trait locus (eQTL) analyses were performed for lead loci that had genome-wide significant associations with S100β. Bidirectional, two-sample Mendelian randomisation was used to test for causal associations between S100β and Alzheimer's disease. Colocalisation between S100β and Alzheimer's disease GWAS loci was also examined. Results: We identified 154 SNPs from chromosome 21 that associated (P<5x10 -8) with S100β protein levels. The lead variant was located in the S100β gene (rs8128872, P=5.0x10 -17). We found evidence that two independent causal variants existed for both transcription of S100β and S100β protein levels in our eQTL analyses . No CpG sites were associated with S100β levels at the epigenome-wide significant level (P<3.6x10 -8); the lead probe was cg06833709 (P=5.8x10 -6), which mapped to the LGI1 gene. There was no evidence of a causal association between S100β levels and Alzheimer's disease or vice versa and no evidence for colocalisation between S100β and Alzheimer's disease loci. Conclusions: These data provide insight into the molecular regulators of S100β levels. This context may aid in understanding the role of S100β in brain inflammation and neurological disease.

The clinical value of EEG monitoring and silver nanoparticles to detect the levels of serum Nesfatin-1, S100β and neuron-specific enolase in evaluating the severity and prognosis of epilepsy

This study aimed to explore the clinical value of electroencephalogram (EEG) monitoring and the use of silver nanoparticles to detect serum levels of Nesfatin-1, S100β and Neuron-specific enolase (NSE) in assessing the severity and prognosis of epilepsy. A total of 54 epilepsy patients treated at our hospital from June 2017 to June 2019 were selected as the epilepsy group, and 54 healthy subjects were selected as the control group. EEG and serum levels of Nesfatin-1, S100β, and NSE in epilepsy patients without seizure and within 1 hour of seizure were ascertained and compared. The Liverpool Seizure Severity Scale (LSSS) score was used to evaluate the severity of epilepsy in patients, and the correlation between EEG findings and serum Nesfatin-1, S100β , and NSE levels was analyzed. ROC analysis was also conducted on the levels of the three factors. The patients were followed up for 1 year, the mortality rate was calculated, and the levels of Nesfatin-1, S100β, and NSE in deceased and non-deceased patients were compared. There were 50 cases (92.6%) with EEG abnormalities in the epilepsy group and 31 cases (57.4%) with epileptic EEGs in the epileptic non-seizure group. There was a significant difference in the proportion of abnormal EEGs between the two groups of epilepsy patients (P &lt;0.05); the biomarker (Nesfatin-1, S100β, and NSE) serum levels were higher in both the non-seizure group and epileptic group than the control group, and the levels in the seizure group were higher than those in the non-seizure group (P &lt; 0.05); seizures in patients with epilepsy were positively correlated with EEG abnormalities and biomarker serum levels. There was, however, no significant correlation between EEG abnormalities and biomarker serum levels. ROC analysis of epilepsy patients and their serum levels of Nesfatin-1, S100β and NSE showed that the area under the curve corresponding to each index was 0.850, 0.881, and 0.868, respectively (P &lt; 0.05). With regards to deceased patients, the proportion with an abnormal EEG was 100% (15/15), which was higher than 41.0% (16/39) of non-deceased patients. Serum levels of biomarkers were also significantly higher than those in non-deceased patients (P &lt; 0.05). Changes in EEG and biomarker serum levels were closely related to the severity of epilepsy. The proportion of patients with abnormal EEGs during seizure periods was higher, and the expression of serum Nesfatin-1, S100β and NSE was also increased, which means they can be used as markers of epilepsy and have an impact on its prognosis

Usability of the Level of the S100B Protein, the Gosling Pulsatility Index, and the Jugular Venous Oxygen Saturation for the Prediction of Mortality and Morbidity in Patients with Severe Traumatic Brain Injury.

The high frequency of traumatic brain injury imposes severe economic stress on health and insurance services. The objective of this study was to analyze the association between the serum S100B protein, the Gosling pulsatility index (PI), and the level of oxygen saturation at the tip of the internal jugular vein (SjVO2%) in patients diagnosed with severe TBI. The severity of TBI was assessed by a GCS score ≤ 8 stratified by Glasgow outcome scale (GOS) measured on the day of discharge from the hospital. Two groups were included: GOS < 4 (unfavorable group (UG)) and GOS ≥ 4 (favorable group (UG)). S100B levels were higher in the UG than in the FG. PI levels in the UG were also substantially higher than in the FG. There were similar levels of SjVO2 in the two groups. This study confirmed that serum S100B levels were higher in patients with unfavorable outcomes than in those with favorable outcomes. Moreover, a clear demarcation in PI between unfavorable and FGs was observed. This report shows that mortality and morbidity rates in patients with traumatic brain injury can be assessed within the first 4 days of hospitalization using the S100B protein, PI values, and SjVO2.

Neuromodulatory effects of Transcranial Pulsed Current Stimulation (tPCS) in Fibromyalgia: protocol for a double-blinded, sham-controlled, randomized clinical trial

Fibromyalgia (FM) is a functional syndrome characterized by musculoskeletal, diffuse and persistent (&gt; 3 months) chronic pain, that is also characterized by sleep disturbances, fatigue, humor changes and cognitive and psychological changes. Transcranial Pulsed Current Stimulation (tPCS) is a new Transcranial Electrical Stimulation (tES) that has been studied as a treatment option for chronic pain and neurological conditions . Studies have shown that tPCS is capable of pain and cognitive modulation; however, there are not enough studies with evidence of its efficacy.Therefore, the primary aim of this study is to evaluate the effects of tPCS in pain, evaluated through Visual Analogue Scale (VAS) in FM patients; besides that, it is aimed to evaluate the effects of tPCS on quality of life, cognitive impairments, pain pressure threshold, descending inhibitory system of pain, and serum levels of Brain Derived Neurotrophic Factor (BDNF) and S100 Calcium-Binding Protein B (S100B). A randomized, double-blinded, controlled with sham clinical trial will be conducted with 70 (Critical f: 2.003; ES: 0.76; alpha: 0.05; power: 0.80) women with Fibromyalgia, from 30 to 65 years with pain on the Visual Analogue Scale (VAS) higher than 6 in the last 3 months. All patients will read and sign an Informed Consent Form (ICF). Each patient will be randomized to either 1+4 sessions of tPCS (2mA, 6-10Hz, 1-20ms, 20-25 minutes) or Sham. Patients will complete the following questionnaires/tests: Visual Analogue Scale (VAS), Pittsburgh Sleep Quality Index (PSQI), Fibromyalgia Impact Questionnaire (FIQ), Pain Catastrophizing Scale (PCS), Profile of Chronic Pain (PCP), Conditioned Pain Modulation Task (CPM-T), Pain Pressure Threshold Task (PPT-T), Rey Auditory-Verbal Learning Test (RAVLT), Controlled Oral Word Association Test (COWAT) and blood collection for serum levels of BDNF and S100B. For the main outcome, comparison between variables during time will be made through linear regression, with an adjustment for baseline levels and possible confounders.

Effect of Mild Hypothermia after Craniotomy on the Function of Related Organs in Patients with Traumatic Brain Injury.

Objective To investigate the effect of mild hypothermia after craniotomy on the function of related organs in patients with traumatic brain injury. Method A total of 240 patients with craniocerebral injury from January 2017 to December 2020 were retrospectively analyzed. Patients were randomly divided into a control group and an experimental group, with 120 cases in each group. The control group was treated with craniotomy decompression, and the experimental group was treated with early mild hypothermia based on craniotomy decompression. Patients' venous blood was collected before operation (T0), at the end of operation (T1), 24 h after operation (T2), and 2 weeks after operation (T3) to detect the serum levels of the beta-subunit of S100 protein (S100-β); soluble growth stimulation expressed gene 2 (sST2), neutrophil gelatinase-associated lipocalin (NGAL), and interleukin 6 (IL-6). The prognostic effect was evaluated after 2 weeks of treatment. Results After mild hypothermia treatment after craniotomy and decompression, the patients' serum S100-β, sST2, NGAL, and IL-6 levels at different time points were significantly lower than the control group, and the total effective rate was higher than that of the control group. Conclusion The treatment of mild hypothermia after craniotomy can reduce the related organs function damage indicators and inflammatory stress response, thus improving clinical efficacy and prognosis.

Statin therapy associated with decreased neuronal injury measured by serum S100β levels in patients with acute ischemic stroke.

Background:Acute ischemic strokes (AIS) are a common cause of morbidity, mortality, and disability. The serum biomarker S100β correlates with poor neurological outcomes in the setting of AIS. This study describes the impact of statin treatment on S100β levels following AIS.Methods:This was a prospective case–control study of AIS patients compared to healthy controls. Patients were stratified into three groups: (1) AIS patients on statin therapy, (2) AIS patients not on statin therapy, and (3) healthy controls. Demographics, clinical parameters, stroke risk scores (SRS), and S100β levels were recorded for all patients.Results:Blood pressure, lipids, and SRS scores were higher in stroke versus control patients (all P < 0.05), and lower in Group I versus II (all P < 0.05). S100β levels were higher in stroke versus nonstroke patients (P = 0.001), and lower in Group I versus II (P = 0.001). Furthermore, patients on atorvastatin showed greater S100β reductions than those on rosuvastatin therapy (P = 0.01).Conclusion:In acute stroke patients, statins therapy correlated with reductions in the neuronal injury biomarker S100β, with greater reductions observed for atorvastatin than rosuvastatin therapy.

S100 Calcium-Binding Protein B and Glial Fibrillary Acidic Protein in Patients with Mild Traumatic Brain Injury.

Objective:To examine the GFAP and S100B ability in prevention unnecessary brain Computed tomography (CT) scan in mild traumatic brain injury (mTBI) and compare them with the single extremity fracture in orthopedic patients.Methods:In this prospective cohort study, two orthopedics patients’ groups and mTBI patients were studied to assess the biomarkers’ ability in prevention unnecessary brain CT scan at the emergency setting. There were 40 orthopedics’ patients with single extremity fracture and 41 mTBI patients. Brain CT scans were done for all mTBI patients. Results:Brain CT scans showed no intracranial traumatic lesions. The median levels for S100B in the mTBI group was 14.8 (4.4-335.9) ng/L, and in orthopedic patients’ group was 13.3 (5-353.10) ng/L. Statistically significant differences were observed between both groups in S100B levels (p=0.006). The median Glial Fibrillary Acidic Protein (GFAP) levels in the mTBI patients’ group were 600 (400-16300) and in the orthopedic patients’ groups was 60 ng/L (300-14900). Statistically significant differences were observed between groups in GFAP (p=0.041).Conclusion:Our results showed that S100B and GFAP serum levels were significantly higher in patients with mTBI than in patients with a single limb fracture.

Serum biomarkers in severe paediatric traumatic brain injury-a narrative review.

Severe traumatic brain injury continues to present complex management and prediction challenges for the clinician. While there is some evidence that better systems of care can improve outcome, multiple multi-centre randomised controlled trials of specific therapies have consistently failed to show benefit. In addition, clinicians are challenged in attempting to accurately predict which children will recover well and which children will have severe and persisting neurocognitive deficits. Traumatic brain injury is vastly heterogeneous and so it is not surprising that one therapy or approach, when applied to a mixed cohort of children in a clinical trial setting, has yielded disappointing results. Children with severe traumatic brain injury have vastly different brain injury pathologies of widely varying severity, in any number of anatomical locations at what may be disparate stages of brain development. This heterogeneity may also explain why clinicians are unable to accurately predict outcome. Biomarkers are objective molecular signatures of injury that are released following traumatic brain injury and may represent a way of unifying the heterogeneity of traumatic brain injury into a single biosignature. Biomarkers hold promise to diagnose brain injury severity, guide intervention selection for clinical trials, or provide vital prognostic information so that early intervention and rehabilitation can be planned much earlier in the course of a child’s recovery. Serum S100B and serum NSE levels show promise as a diagnostic tool with biomarker levels significantly higher in children with severe TBI including children with inflicted and non-inflicted head injury. Serum S100B and serum NSE also show promise as a predictor of neurodevelopmental outcome. The role of biomarkers in traumatic brain injury is an evolving field with the potential for clinical application within the next few years.

Effects of early-life stress and sex on blood-brain barrier permeability and integrity in juvenile and adult rats.

Early-life stress (ELS) is considered a relevant etiological factor for neurodegenerative and mental disorders. In the present study, we hypothesized that ELS may persistently and sex dependently influence blood-brain barrier (BBB) integrity and function during critical periods of brain development and consequently determine susceptibility to and sex-related prevalence of chronic diseases in adult life. We used the maternal separation (MS) procedure in rats to model ELS and evaluated BBB permeability and gene expression of selected tight junction (TJ) proteins, glucose transporter type 1 (Slc2a1) and aquaporin 4 (Aqp4) in the medial prefrontal cortex (mPFC), dorsal striatum (dSTR) and hippocampus of juvenile and adult rats. Serum concentrations of a peripheral marker of BBB function (S100β) and proinflammatory cytokines were also assessed. We observed developmental sealing of the BBB and sex differences in the permeability of the BBB and the mRNA expression of TJ proteins and Slc2a1. Adult females showed lower BBB permeability and higher levels of Cldn3, Cldn5, Ocln, and Slc2a1 in the mPFC and dSTR than males. MS temporarily increased BBB permeability in the dSTR of juvenile males and affected mRNA expression of the majority of studied proteins related to BBB function in age-, region- and sex-dependent manners. Additionally, MS sex dependently decreased serum S100β levels and did not affect proinflammatory cytokine concentrations. In general, our study did not reveal a clear or strong negative effect of MS on BBB integrity. However, the results suggest that ELS may induce adaptive/maladaptive changes or compensatory mechanisms within the BBB of unknown yet consequences.