S100B Protein Levels Research Articles

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.

Neurofilament Light Chain Protein Is a Predictive Biomarker for Stroke After Surgical Repair for Acute Type A Aortic Dissection.

Background: Although great progress has been made in surgery and perioperative care, stroke is still a fatal complication of acute type A aortic dissection (ATAAD). Serum biomarkers may help assess brain damage and predict patient's prognosis.Methods: From March, 2019 to January, 2020, a total of 88 patients underwent surgical treatment at the Department of Cardiovascular Surgery of Beijing Anzhen Hospital, China, and were enrolled in this study. Patients were divided into two groups according to whether they had suffered a stroke after the operation. Blood samples were collected at 8 time points within 3 days after surgery to determine the level of S100β, neuron-specific enolase (NSE) and neurofilament light chain protein (NFL). Receiver operating characteristic curves (ROC) were established to explore the biomarker predictive value in stroke. The area under the curve (AUC) was used to quantify the ROC curve.Results: The patient average age was 48.1 ± 11.0 years old and 70 (79.6%) patients were male. Fifteen (17.0%) patients suffered stroke after surgery. The NFL levels of patients in the stroke group at 12 and 24 h after surgery were significantly higher than those in the non-stroke group (all P < 0.001). However, the NSE and S100β levels did not differ significantly at any time point between the two groups. The predictive value of NFL was the highest at 12 and 24 h after surgery, and the AUC was 0.834 (95% CI, 0.723–0.951, P < 0.001) and 0.748 (95% CI, 0.603–0.894, P = 0.004), respectively. Its sensitivity and specificity at 12 h were 86.7 and 71.6%, respectively. The NFL cutoff value for the diagnosis of stroke at 12 h after surgery was 16.042 ng/ml.Conclusions: This study suggests that NFL is an early and sensitive serum marker for predicting post-operative neurological prognosis of ATAAD patients. Further studies, including large-scale prospective clinical trials, are necessary to test whether the NFL can be used as a biomarker for clinical decision-making.

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.

Correlation of serum ferritin levels with neurological function-related indices and cognitive dysfunction in patients with cerebral hemorrhage

The purpose of this study was to explore the correlation of serum ferritin (FS) levels with neurological function-related indices, such as neuron-specific enolase (NSE) and S100β protein levels, and cognitive dysfunction in patients with cerebral hemorrhage. Patients with acute non-traumatic cerebral hemorrhage (cerebrovascular disease (VD), n = 128) and healthy controls (CON, n=128) were included. FS, NSE, and S100β levels were measured using ELISA. Cognitive functions were evaluated using the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE). The receiver operating characteristic (ROC) curve was used to assess the ability of SE, NSE, and serum S100β to predict the diagnosis of cognitive dysfunction in patients with cerebral hemorrhage. Multivariate logistic regression analysis was used to assess the risk factors of cognitive impairment in patients with cerebral hemorrhage. Cognitive impairment in patients with VD was closely related to the increased levels of SE, NSE, and S100β. There was a strong correlation between MoCA and MMSE scores and the levels of FS, NSE, and S100β. The independent risk factors leading to cognitive impairment in cerebral hemorrhage mainly include family history of cerebrovascular disease, body mass index, hypertension, smoking frequency, and elevated levels of low-density lipoproteins, NSE, FS, and S100β. NSE, FS, and S100β can be used as important markers for the diagnosis of cognitive impairment in patients with cerebral hemorrhage.

Systemic inflammatory response in infants with craniostenosis sedated with propofol

AIM: This study aimed to investigate the possible effect of intravenous anesthesia (sedation) with propofol on the levels of several cytokines (interleukin [IL]-6, IL-8, IL-10, and tumor necrosis factors-) and S100B protein in the blood plasma of children aged 1 year with craniostenosis.&#x0D; MATERIALS AND METHODS: Twenty patients aged 112 months diagnosed with non-syndromic forms of craniosynostosis, who underwent magnetic resonance imaging (MRI) of the brain under propofol sedation, were classified according to ASA I-II class. Peripheral blood sampling was performed before and after the drug administration, followed by laboratory analysis.&#x0D; RESULTS: A significant increase was found in the serum level of IL-6 (p = 0.004) when intravenous sedation with propofol was used for 29 4.93 min.&#x0D; CONCLUSION: Short exposure of children aged 1 year with craniostenosis to hypnotic propofol during brain MRI significantly increased the level of the pro-inflammatory cytokine IL-6 in the blood plasma.

The Influence of Different Dexmedetomidine Doses on Cognitive Function at Early Period of Patients Undergoing Laparoscopic Extensive Total Hysterectomy.

Background This study aims to analyze the influence of different dexmedetomidine doses on cognitive function. It works on early periods of patients undergoing laparoscopic extensive total hysterectomy. Method 119 patients with gynecological cancer underwent a laparoscopic extensive total hysterectomy. The operation was performed at the Affiliated Women's and Children's Hospital of Xiamen University from January 2019 to June 2020. The score of MoCA and the level of TNF-α, IL-6, S-100β protein, NSE, and GFAP of each group were compared 1 day before and after operation and 3 and 7 days after operation. Result In four groups, remifentanil, sufentanil, and propofol were given in the following order: group A > group D > group C > group B. Group A > group D > group C in terms of time spent in the recovery room, extubation, and recovery from anesthesia. The difference between groups B and C was not significant (P > 0.05). Compared with group A, group B scored higher in MoCA at 1 day (T1), 3 days (T2), and 7 days (T3) after operation (P < 0.05). At the same scoring point, the score was group B > group C > group D > group A. The POCD of four groups all occurred at 3 days after surgery. Compared with the T0 point, the level of TNF-α and IL-6 of the four groups at T1 and T2 was significantly increased (P < 0.05). At T3, the level of TNF-α and IL-6 gradually decreased. At various periods, the levels of S-100 protein, NSE, and GFAP in groups B, C, and D were lower than those in group A (P0.05). Group B had a substantially higher rate of bradycardia than the other three groups (P0.05). The incidence of chills, respiratory depression, and restlessness in group A differed significantly from the other three groups (P < 0.05). Conclusion Using 0.5 μg/kg dexmedetomidine during the perianaesthesia can effectively reduce anesthetic drugs in patients. They had a laparoscopic extensive complete hysterectomy, which helps to reduce the adverse responses and the occurrence of POCD while also protecting brain function.

No association between children's febrile seizures and S100B protein levels: A meta-analysis

BackgroundIn recent years, studies have examined the relationship between febrile seizures in children and S100B protein with contradictory results. We systematically evaluated the relationship between children's febrile seizures and S100B protein levels. MethodsWe used Stata 11.0 software to conduct a meta-analysis of the included studies published in The China National Knowledge Infrastructure, VIP, Wanfang, Chinese Biology Medicine Disc, PubMed, Web of Science, Cochrane Library, and EMBASE databases as well as clinical trial registries in China, Europe, and the United States. ResultsSix case-control studies were finally included in the meta-analysis. The results of the meta-analysis showed that the serum S100B protein level of children with febrile seizures was 0.72 higher than the serum S100B protein level of healthy children (Z=6.85, 95% CI 0.52∼0.93, P<0.05). There was no difference in the serum S100B protein level between the children with febrile seizures and children with fever but without seizures (Z=0.70, 95% CI -0.20∼0.41, P>0.05). ConclusionThe level of serum S100B protein in children with febrile seizures was higher than that of healthy children and was statistically significant, whereas the increase in children with higher fever without seizures was not statistically significant. Because there was only a difference in serum S100B protein levels between children with febrile seizures and healthy children but not in febrile children without seizures as the strongest confounding factors for the results, febrile seizures do not elevate the level of S100B protein levels any more than fever.

Molar Sodium Lactate Attenuates the Severity of Postcardiac Arrest Syndrome: A Preclinical Study.

To determine whether continuous IV infusion of molar sodium lactate would limit cardiac arrest-induced neurologic injury and cardiovascular failure. Randomized blinded study (animal model). University animal research facility. Twenty-four adult male "New Zealand White" rabbits. Anesthetized rabbits underwent 12.5 minutes of asphyxial cardiac arrest and were randomized to receive either normal saline (control group, n = 12) or molar sodium lactate (molar sodium lactate group, n = 12) at a rate of 5 mL/kg/hr during the whole 120-minute reperfusion period. Pupillary reactivity (primary outcome), levels of S100β protein, in vitro brain mitochondria functions, cardiovascular function, and fluid balance were assessed. Molar sodium lactate reduced brain injury, with a higher proportion of animals exhibiting pupillary reactivity to light (83% vs 25% in the CTRL group, p = 0.01) and lower S100β protein levels (189 ± 42 vs 412 ± 63 pg/mL, p < 0.01) at the end of the protocol. Molar sodium lactate significantly prevented cardiac arrest-induced decrease in oxidative phosphorylation and mitochondrial calcium-retention capacity compared with controls. At 120 minutes of reperfusion, survival did not significantly differ between the groups (10/12, 83% in the molar sodium lactate group vs nine of 12, 75% in the control group; p > 0.99), but hemodynamics were significantly improved in the molar sodium lactate group compared with the control group (higher mean arterial pressure [49 ± 2 vs 29 ± 3 mm Hg; p < 0.05], higher cardiac output [108 ± 4 vs 58 ± 9 mL/min; p < 0.05], higher left ventricle surface shortening fraction [38% ± 3% vs 19% ± 3%; p < 0.05], and lower left ventricular end-diastolic pressure [3 ± 1 vs 8 ± 2 mm Hg; p < 0.01]). While fluid intake was similar in both groups, fluid balance was higher in control animals (11 ± 1 mL/kg) than that in molar sodium lactate-treated rabbits (1 ± 3 mL/kg; p < 0.01) due to lower diuresis. Molar sodium lactate was effective in limiting the severity of the postcardiac arrest syndrome. This preclinical study opens up new perspectives for the treatment of cardiac arrest.

S100β protein levels as a parameter to assess the clinical development of adult patients with mild traumatic brain injury in Dr. Moewardi Public Hospital, Surakarta.

Background: Mild traumatic brain injury (mTBI) is a health problem with an increasing incidence in many developed countries. The standard for examining mTBI is a CT scan, but it is costly, is not always available in all hospitals, and carries a risk of radiation. Meanwhile, S100β is a protein component produced by central nervous system cells. This study aims to determine the presence of changes in S100β protein in adult patients with mTBI during treatment as an alternative to examination.Methods: This research is an analytic observational quantitative study with a cross-sectional study approach to investigate changes in S100β protein levels in blood serum using the ELISA method of mTBI patients in the first 3 h posttrauma (pretest) and treatment on day 1 (27 h posttrauma/posttest). The research sample consisted of 22 people. This research was conducted in the Surgery Section, Sub-Division of Neurosurgery, Dr. Moewardi Public Hospital, during September–December 2019. The data were then analyzed using a discrimination test (comparing t-test means) and a nonparametric test (Wilcoxon).Results: There was a significant difference in mean S100β change between the pretest and posttest treatments. The S100β examination results at posttest decreased to 0.0223 + 0.0029 μg/l or decreased S100β by 21.7% after treatment. Previously, it was known that the mean of S100β at pretest was 0.0285 + 0.0137 μg/l.Conclusion: There was a significant change in S100β protein levels at each examination time. Changes in S100β levels that occurred were in the form of decreased levels from 3 h to 27 h posttrauma. Thus, S100β protein can be used as a parameter to assess the clinical development of adult patients with mTBI. Moreover, none of the patients with an S100β value >0.1 μg/l was found to be the cutoff value set by SNC in adult patients with mTBI for head CT scan.

The Effect of Biomarkers and Optic Nerve Sheath Diameter in Determining Mortality in non-Traumatic Subarachnoid Hemorrhage

AimAlthough radiological methods are sufficient for the diagnosis of spontaneous subarachnoid hemorrhage (SAH), additional biomarkers are needed to predict prognosis. The aim of this study was to investigate the effects of serum S100B protein, Glial Fibrillary Acidic Protein (GFAP) levels and, Optic Nerve Sheath Diameter (ONSD) on mortality and clinical severity in patients with spontaneous SAH. Materials and methodsFifty-six patients who were diagnosed with SAH after first evaluation in the emergency department (ED) were included in the study group; Forty-six patients who were admitted to the ED with headache of non-intracranial etiology, were included as the control group. Cerebral computed tomography (CT) images and peripheral blood samples were obtained from all patients; at the time of diagnosis and 24 h after diagnosis. Serum S100B protein and GFAP levels were measured from the blood samples and ONSD was measured on CT. ResultsSerum S100B protein and GFAP levels and, ONSDs at the time of diagnosis and 24 h after diagnosis were significantly higher in the study group (p < 0.05). Both GFAP levels and ONSD at the time of diagnosis and 24 h after the diagnosis were found to be related with increased mortality (p < 0.05). A similar association was found for serum S100B protein levels 24 h after the diagnosis, but not at the time of diagnosis (p = 0.540). ConclusionSerum S100B protein and GFAP levels and, ONSD were increased in patients with spontaneous SAH. All parameters were found to be associated with increased mortality.

Effect of acupuncture combined with rehabilitation on cognitive and motor functions in poststroke patients.

The aim of the study was to explore the effect of acupuncture combined with rehabilitation on cognitive and motor functions in poststroke patients. All patients were divided into Group A and Group B based on different interventions (Group A: acupuncture + conventional rehabilitation, Group B: conventional rehabilitation alone). Acupuncture was conducted once a day, five times a week for 8 weeks, and rehabilitation (including physical therapy and occupational therapy) was conducted for 2 hr per session, once a day, five times a week for 8 weeks. Mini-mental State Examination (MMSE) and Fugl-Meyer Assessment (FMA) were used to assess the motor and cognitive functions at baseline and the end of 8 weeks. After the intervention, FMA and MMSE scores were improved significantly in the two groups (p <.05), compared with the scores prior to intervention. After 8 weeks of intervention, a statistically significant difference in the FMA and MMSE scores was observed between the Group A and the Group B. The results suggested that the combined intervention is more effective than the conventional rehabilitation alone in improving cognitive and motor functions in poststroke patients.

Serum NSE and S100B protein levels for evaluating the impaired consciousness in patients with acute carbon monoxide poisoning.

The aim of this study was to investigate the associations between the levels of neuron-specific enolase (NSE) and S100B protein and coma duration, and evaluate the optimal cut-off values for prediction coma duration ≥ 72 hours in patients with acute carbon monoxide poisoning (ACOP).A total of 60 patients with ACOP were divided into 3 following groups according to their status of consciousness and coma duration at admission: Awake group [Glasgow Coma Scale score (GCS score) ≥ 13 points], Coma < 72 hours group (GCS score < 13 points and coma duration < 72 h), and Coma ≥ 72 hours group (GCS score < 13 points and coma duration ≥ 72 h). The levels of serum NSE and S100B protein were measured after admission.There were significant differences in GCS score, carbon monoxide (CO) exposure time, NSE, and S100B levels between the Coma ≥ 72 h group and the Awake group, and between the Coma < 72 h group and the Awake group. Significant differences in GCS score, NSE, and S100B levels were also found between Coma ≥ 72 h group and Coma < 72 h group. Correlation analysis showed that NSE and S100B were positively correlated (rs = 0.590, P < .01); NSE and S100B were negatively correlated with GCS score (rs = -0.583, rs = -0.590, respectively, both P < .01). The areas under the curve (AUCs) of NSE, S100B, and GCS score to predict the coma duration ≥ 72 hours were 0.754, 0.791, and 0.785, respectively. Pairwise comparisons did not show differences among the 3 groups (all P > .05). The sensitivity and specificity of NSE prediction with a cut-off value of 13 μg/L were 80% and 64%, respectively, and those of S100B prediction with a cut-off value of 0.43 μg/L were 70% and 88%, respectively.The NSE and S100B protein levels were significantly correlated with the degree of impaired consciousness and had the same clinical value in predicting coma duration of ≥ 72 hours in patients with ACOP.

The Impact of High Glucose or Insulin Exposure on S100B Protein Levels, Oxidative and Nitrosative Stress and DNA Damage in Neuron-Like Cells.

Alzheimer’s disease (AD) is attracting considerable interest due to its increasing number of cases as a consequence of the aging of the global population. The mainstream concept of AD neuropathology based on pathological changes of amyloid β metabolism and the formation of neurofibrillary tangles is under criticism due to the failure of Aβ-targeting drug trials. Recent findings have shown that AD is a highly complex disease involving a broad range of clinical manifestations as well as cellular and biochemical disturbances. The past decade has seen a renewed importance of metabolic disturbances in disease-relevant early pathology with challenging areas in establishing the role of local micro-fluctuations in glucose concentrations and the impact of insulin on neuronal function. The role of the S100 protein family in this interplay remains unclear and is the aim of this research. Intracellularly the S100B protein has a protective effect on neurons against the toxic effects of glutamate and stimulates neurites outgrowth and neuronal survival. At high concentrations, it can induce apoptosis. The aim of our study was to extend current knowledge of the possible impact of hyper-glycemia and -insulinemia directly on neuronal S100B secretion and comparison to oxidative stress markers such as ROS, NO and DBSs levels. In this paper, we have shown that S100B secretion decreases in neurons cultured in a high-glucose or high-insulin medium, while levels in cell lysates are increased with statistical significance. Our findings demonstrate the strong toxic impact of energetic disturbances on neuronal metabolism and the potential neuroprotective role of S100B protein.

Prognostic value of serum S100B concentration in patients with acute spontaneous supratentorial intracerebral hemorrhage

Aim of the work – to evaluate the informativeness of serum protein S100B levels in detection of short-term prognosis in patients with acute period of spontaneous supratentorial intracerebral hemorrhage (SSICH) on the background of concervative therapy. Materials and methods. Prospective cohort study of 90 patients with acute SSICH on the background of conservative therapy was done. Level of neurological deficit was evaluated using Full Outline of Unresponsiveness Scale, Glasgow Coma Scale and National Institute of Health Stroke Scale. Computed tomography was done to detect the intracerebral hemorrhage volume (ICHV), secondary intraventricular hemorrhage volume (SIVHV) and total volume of intracranial hemorrhage (TVICH). Laboratory blood samples were taken within 24 hours of hospitalization. Levels of S100B protein in serum were measured using immunoassay analysis. Unfavorable variants of course (early neurological deterioration (END) during 48 hours from hospitalization) and disease acute period outcome of ICH (modified Rankin score 4–6 on the 21st day of the disease) were considered as endpoints. Statistical processing of the obtained results included correlation analysis, logistic regression analysis and ROC-analysis. Results. Neurological deterioration during 48 hours after hospitalization was detected in 18 (20.0 %) patients, unfavorable SSICH acute period outcome was revealed in 49 (54.4 %) patients. It was detected that serum S100B protein correlates with ICHV (R = 0.34, P ˂ 0.01), SIVHV (R = 0.39, P ˂ 0.01) and TVICH (R = 0.45, P ˂ 0.01). Thus, the patients with unfavorable SSICH acute period course and outcome are characterized with the higher S100B protein levels (P ˂ 0.0001). High sensitive multipredicive logistic regression model that integrates prognostic value of serum of S100B protein concentration with informativeness of clinical, neurological parameters (National Institute of Health Stroke Scale score, SIVHV) was elaborated. It helps to detect the individual risk of unfavorable acute SSICH period outcome on the ground of conservative therapy with the accuracy 90.0 % (AUC ± SE (95 % CІ) = 0.95 ± 0.02 (0.89–0.99), P ˂ 0.0001). Conclusions. Serum S100B protein levels in patients with SSICH on the 1st day after hospitalization is the informative additional parameter in verification of short-term prognosis on the background of conservative therapy.

Effect of propofol-based total intravenous anaesthesia on postoperative cognitive function and sleep quality in elderly patients.

This study aimed to observe the effect of propofol-based total intravenous anaesthesia (TIVA) on postoperative cognitive function and sleep quality in elderly patients. From August 2019 to August 2020, 130 cases of elderly patients who underwent abdominal surgery in The Third Hospital of Hebei Medical University were enrolled in this study. All participants were randomly divided into TIVA group (n=65, receiving propofol-based TIVA) and control group (n=65, receiving inhaled of sevoflurane anaesthesia). Intra-operative indicators were recorded in both groups. The cognitive function, sleep quality, urine melatonin sulphate, free cortisol, S-100 β protein and interleukin-6 (IL-6) levels were compared at different times. On 1, 3, 7 and 15days after operation, the cognitive function of the TIVA group was better than that of the control group, with statistically significance (P<.05, respectively). On the day of surgery, the two groups had similar sleep quality. The sleep quality of the TIVA group was better than that of the control group on 1, 3 and 7days after surgery (P<.05, respectively). On the day of surgery, the levels of melatonin, cortisol, S-100β protein and IL-6 in the two groups were equivalent (P>.05). On 1, 3, 7 and 15days after surgery, cortisol and IL-6 in the TIVA group were lower than those of the control group, and melatonin was higher than that of the control group (P<.05, respectively). On 1, 3 and 7days after operation, the S-100 β protein in the TIVA group was lower than that in the control group (P<.05, respectively). Propofol-based TIVA has little effect on the cognitive function and sleep quality of elderly patients after surgery, and it is worthy of clinical application.

S100B gene polymorphisms are associated with the S100B level and Alzheimer's disease risk by altering the miRNA binding capacity.

To examine the role of S100B in genetic susceptibility to Alzheimer’s disease (AD), we conducted a case-control study to analyze four polymorphism loci (rs2839364, rs1051169, rs2300403, and rs9722) of the S100B gene and AD risk. We found an independent increased risk of AD in ApoE ε4(-) subjects carrying the rs9722 AA-genotype (OR = 2.622, 95% CI = 1.399–4.915, P = 0.003). Further investigation revealed the serum S100B levels to be lower in rs9722 GG carriers than in rs9722 AA carriers (P = 0.003). We identified three miRNAs (miR-340-3p, miR-593-3p, miR-6827-3p) in which the seed match region covered locus rs9722. Luciferase assays indicated that the rs9722 G allele has a higher binding affinity to miR-6827-3p than the rs9722 A allele, leading to a significantly decreased fluorescence intensity. Subsequent western blot analysis showed that the S100B protein level of SH-SY5Y cells, which carry the rs9722 G allele, decreased significantly following miR-6827-3p stimulation (P = 0.009). The present study suggests that the rs9722 polymorphism may upregulate the expression of S100B by altering the miRNA binding capacity and may thus increase the AD risk. This finding would be of great help for the early diagnosis of AD.

Role of S100β Glial Protein as a Serological Marker for Analysis of Acute Ischemic Stroke

Background: Stroke is a major cause of neurological disability, which can be often predicted with serological markers. Glial-derived S100β protein is a potential biomarker for cerebral ischemia and may be helpful in predicting the severity, outcome, and recovery of stroke. Aim: This study aimed to study the role of S100β glial protein as a serological marker in predicting the severity of acute ischemic stroke (AIS), outcome, and functional recovery after 1 month. Methods: A hospital-based prospective case control study included 43 consecutive patients, &gt;18 years old, who were admitted with acute middle cerebral artery (MCA) territory infarcts within 72 h of onset of neurological deficits. Control group comprised of 43 age-matched asymptomatic volunteers. Independent t-test and chi square test were used to compare the means and evaluate the association between protein level and various parameters. P ≤ .05 was statistically significant. Results: S100β protein level in AIS patients was significantly higher compared to controls ( P &lt; .05). Elevated serum S100β protein level was found to be associated with larger infarct volumes, higher National Institute Health Stroke Scale scores, and higher modified Rankin Scale scores at admission ( P &lt; .05). Patients with higher S100β protein levels at admission had poor recovery at 1 month compared to patients having normal S100β protein levels. Conclusion: S100β protein levels at admission after an acute MCA territory infarct may be used as a reliable serological tool in predicting the severity, outcome, and functional recovery in stroke.

Neuroprotective effect of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline mediated via regulation of antioxidant system and inhibition of inflammation and apoptosis in a rat model of cerebral ischemia/reperfusion

The aim of the study was the assessment of the neuroprotective potential of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline (DHQ) and its effect on inflammation, apoptosis, and transcriptional regulation of the antioxidant system in cerebral ischemia/reperfusion (CIR) in rats.The CIR rat model was constructed using the bilateral common carotid artery occlusion followed by reoxygenation. DHQ was administered at a dose of 50 mg/kg for three days. Histological staining was performed using hematoxylin and eosin. The level of S100B protein, 8-hydroxy-2-deoxyguanosine, and 8-isoprostane was assessed using an enzyme immunoassay. The intensity of apoptosis was assessed based on the activity of caspases and DNA fragmentation. The activity of enzymes was measured spectrophotometrically, the level of gene transcripts was assessed by real-time PCR.DHQ reduced the histopathological changes and normalized levels of S100B, lactate, pyruvate, and HIF-1 mRNA in the CIR rat model. In addition, DHQ decreased the oxidative stress markers in animals with a pathology. The tested compound also inhibited inflammation by decreasing the activity of myeloperoxidase, expression of interleukins and Nfkb2. DHQ-treated rats with CIR showed decreased caspase activity, DNA fragmentation, and AIF expression. DHQ changed activity of antioxidant enzymes to the control values, decreased the expression of Cat, Gsr, and Nfe2l2, which was overexpressed in CIR, and activated the expression of Sod1, Gpx1, Gsta2, and Foxo1.DHQ showed a neuroprotective effect on CIR in rats. The neuroprotective effect involve mechanisms such as the inhibition of oxidative stress, leading to a reduction in the inflammatory response and apoptosis and the modulation of the antioxidant defense components.

Targeting Mitochondrial and Brain Injury Markers in Acquired Brain Injuries: A Randomized, Double-Blind, Placebo-Controlled Study with Melatonin

Purpose: Oxidative stress-induced mitochondrial damage is the main event in acquired brain injuries (ABI). This study aimed to evaluate the effects of melatonin, a mitochondria-targeted antioxidant, on mitochondrial and brain injury markers, and the clinical outcomes of patients with ABI. Methods: In this randomized controlled trial, intensive care unit (ICU) or neurology patients with ABI (n=60) received melatonin (21 mg/day) or placebo tablets, within the first 72 hours of injury onset for five days. As a primary endpoint, serum levels of malondialdehyde (MDA), S100B and C-reactive protein (CRP) were compared at baseline, and after five days’ intervention. Secondary endpoints included assessment of Glasgow Coma Scale and Sequential Organ Failure Assessment (at the end of day 5), Rancho Los Amigos Revised Scale and modified Rankin Scale (at the end of month 3), the duration of mechanical ventilation, the lengths of ICU and hospital stays, and in-hospital and three-month mortality. Results: There were no significant effects of melatonin on the primary and secondary outcomes. However, the subgroup analysis showed a significant reduction in S100B in patients with non-traumatic brain injuries, receiving melatonin versus placebo (p: 0.016). Conclusion: This study showed that melatonin supplementation in the early phase of brain injury had no significant effects on the injury markers and clinical outcomes of patients with ABI. However, it reduced the level of S100B in the non-traumatic subgroup. Further larger-scale studies are needed to determine the effects of melatonin on the ABI and its subgroups.