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Neuron-specific enolase and S-100b in prolonged targeted temperature management after cardiac arrest: A randomised study.
Duez, CHV, Grejs, AM, Jeppesen, AN, Schrøder, AD, Søreide, E, Nielsen, JF, Kirkegaard, H
Resuscitation. 2018;:79-86
Abstract
BACKGROUND We aimed to investigate the impact of prolonged targeted temperature management (TTM) in cardiac arrest patients on release of serum levels of NSE and S-100b and their prognostic performances. METHODS This is a substudy of the Targeted Temperature Management for 24 vs 48h trial. NSE and S-100b levels were analysed retrospectively in serum samples collected upon admission, at 24, 48, and 72h after reaching the target temperature of 33±1°C. The primary outcome was biomarker serum concentrations and secondary outcome was the cerebral performance category score after 6 months. RESULTS 115 patients from two centres were analysed. NSE and S-100b levels did not differ between TTM groups at any single time-point. Poor outcome patients had higher biomarker levels at 24, 48, and 72h: NSE: 9.73 (7.2; 10.9) versus 20.40 (12.7; 27.2), 8.86 (6.6; 9.6) versus 17.47 (11.1; 37.3) and 6.23 (5.3; 8.5) versus 31.05 (12.8; 52.5) respectively and S-100b: 0.09 (0.07; 0.11) versus 0.23 (0.19; 0.39), 0.08 (0.07; 0.09) versus 0.18 (0.15; 0.33) and 0.07 (0.06; 0.08) versus 0.13 (0.09; 0.23). The daily changes in NSE from admission to Day 2 after the cardiac arrest (CA) were also related to the outcome (p=0.003 and p=0.02). The best prediction of outcome was found at 72h for NSE and at 24h as well as 48h for S100b. CONCLUSIONS No clinically relevant differences were found in the levels of NSE or S-100b between standard and prolonged TTM. Prognostic reliability of NSE and S-100b was unaltered by prolonged TTM.
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Interaction of an S100A9 gene variant with saturated fat and carbohydrates to modulate insulin resistance in 3 populations of different ancestries.
Blanco-Rojo, R, Delgado-Lista, J, Lee, YC, Lai, CQ, Perez-Martinez, P, Rangel-Zuñiga, O, Smith, CE, Hidalgo, B, Alcala-Diaz, JF, Gomez-Delgado, F, et al
The American journal of clinical nutrition. 2016;(2):508-17
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Abstract
BACKGROUND S100 calcium-binding protein A9 (S100A9) has previously been identified as a type 2 diabetes (T2D) gene. However, this finding requires independent validation and more in-depth analyses in other populations and ancestries. OBJECTIVES We aimed to replicate the associations between an S100A9 variant and insulin resistance and T2D and to initiate an investigation of potential interactions with the habitual diet in several independent populations. DESIGN We investigated the association of the S100A9 variant rs3014866 with insulin resistance and T2D risk and its interactions with diet in 3 diverse populations as follows: the CORDIOPREV (Coronary Diet Intervention with Olive Oil and Cardiovascular Prevention; n = 711), which consisted of Spanish white adults; the GOLDN (Genetics of Lipids Lowering Drugs and Diet Network; n = 818), which involved North American non-Hispanic white adults; and Hispanic adults who participated in the BPRHS (Boston Puerto Rican Health Study; n = 1155). RESULTS Meta-analysis indicated that T carriers presented a lower risk of T2D than CC carriers (pooled OR: 0.714; 95% CI: 0.584, 0.845; P = 0.002). In all 3 populations (CORDIOPREV, GOLDN, and BPRHS), we showed a significant interaction between the rs3014866 single nucleotide polymorphism and dietary SFA:carbohydrate ratio intake for the homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.028, P = 0.017, and P = 0.026, respectively). CC carriers had a significantly higher HOMA-IR only when SFA:carbohydrate intake was high (P = 0.045 for the CORDIOPREV, P = 0.033 for the GOLDN, and P = 0.046 for the BPRHS) but not when SFA:carbohydrate ratio intake was low. CONCLUSIONS The minor allele (T) of the S100A9 variant rs3014866 is associated with lower T2D risk in 3 populations of different ancestries. Note that individuals with the high-risk CC genotype may be more likely to benefit from a low SFA:carbohydrate ratio intake to improve insulin resistance as evaluated with the use of the HOMA-IR. These trials were registered at clinicaltrials.gov as NCT00924937 (CORDIOPREV), NCT00083369 (GOLDN), and NCT01231958 (BPRHS).
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Plasma S100A12 and soluble receptor of advanced glycation end product levels and mortality in chronic kidney disease Stage 5 patients.
Isoyama, N, Leurs, P, Qureshi, AR, Bruchfeld, A, Anderstam, B, Heimburger, O, Bárány, P, Stenvinkel, P, Lindholm, B
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 2015;(1):84-91
Abstract
BACKGROUND Alterations in the advanced glycation end-products (AGE)-receptor of AGE (RAGE) system are linked to several chronic diseases, which may result from vascular damage. A high circulating level of the pro-inflammatory RAGE-ligand S100A12, also known as EN-RAGE, is thought to promote while a high level of soluble RAGE (sRAGE) is thought to protect against development of atherosclerotic cardiovascular disease (CVD). We evaluated circulating S100A12 and sRAGE in relation to clinical characteristics, nutritional status, inflammation and mortality risk in chronic kidney disease (CKD) Stage 5 patients starting on dialysis. METHODS Plasma S100A12 and sRAGE, biomarkers of inflammation and nutritional status, and comorbidities were investigated in 200 CKD Stage 5 patients [median age of 56 years, 62% men and median glomerular filtration rate (GFR) of 6.2 mL/min/1.73 m(2)] in conjunction with initiation of dialysis therapy. Associations between mortality risk and S100A12 or sRAGE were assessed after a median follow-up period of 23 months. In addition, for comparative analyses, S100A12 and sRAGE levels were assessed also in 58 haemodialysis and 78 peritoneal dialysis patients after 1 year of dialysis, 56 CKD Stages 3-4 patients and 50 community-based control subjects. RESULTS The median level of S100A12 was 4-fold higher, median sRAGE 2.4 higher and median ratio S100A12/sRAGE 2.27 times higher in CKD 5 patients than in controls. Similar alterations were observed in CKD 3-4 patients; however, CKD 5 patients had a higher median level of sRAGE than the CKD 3-4 patients. In the CKD 5 patients, S100A12 levels were higher in those with diabetes or CVD than in those without these comorbidities. Furthermore, S100A12 correlated with high-sensitivity C-reactive protein (hsCRP) levels (ρ = 0.53; P < 0.001) and a 1-SD higher level of S100A12 associated with increased all-cause mortality risk (hazard ratio 1.32, 95% confidence interval 1.01-1.73) after adjustment for age, sex, comorbidity, nutritional status and inflammation (hsCRP). In the CKD 5 patients, sRAGE correlated negatively with GFR (ρ = -0.26; P < 0.01) but sRAGE did not associate with hsCRP, comorbidities or mortality. CONCLUSIONS Plasma concentrations of sRAGE, S100A12 and the ratio S100A12/sRAGE, are markedly elevated in CKD 5 patients starting on dialysis as well as in CKD 3-4 patients and prevalent dialysis patients suggesting that these alterations are typical for patients with moderate or severe CKD. In CKD 5 patients, an increased concentration of S100A12 are associated with inflammation, comorbidities and increased mortality risk whereas no such associations were observed for sRAGE. These results suggest that while high plasma S100A12 is an independent predictor of increased mortality risk, sRAGE does not seem to be a valid risk marker in this patient population.
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[Effects of different arterial oxygen partial pressures on serum protein S100β and neuron specific enolase during cardiopulmonary bypass in infants with cyanotic congenital heart disease].
Huang, C, Nong, SH, Chen, JM, He, SR, Chen, P, Ding, YQ, Cen, JZ, Xu, G
Zhonghua er ke za zhi = Chinese journal of pediatrics. 2012;(2):121-5
Abstract
OBJECTIVE A prospective study was conducted to probe into the relationship between arterial oxygen partial pressure (PaO2) and brain injury during cardiopulmonary bypass (CPB) in infants with cyanotic congenital heart disease (CHD). METHOD Enrolled in the study were 45 cyanotic infants, who were less than three years old and underwent corrective cardiac surgery from August 1(st), 2010 to January 31(st), 2011 at Guangdong General Hospital. All the infants had a pulse oxygen saturation (SpO2) lower than 85% and were randomly allocated into three groups by a specific computer program. In controlled group 1 (G1 group), PaO2 levels were controlled at 80 - 120 mm Hg (1 mm Hg = 0.133 kPa) during CPB; in controlled group 2 (G2 group), PaO2 levels at 120 - 200 mm Hg during CPB; while in uncontrolled group (G3 group), PaO2 levels were at 200 - 400 mm Hg during CPB. Blood samples were collected just before starting CPB, at the end of CPB, and at 3 h, 5 h, and 24 h after CPB (T1, T2, T3, T4, T5) for the determination of serum concentrations of protein S100β, neuron specific enolase (NSE), and adrenomedullin (ADM) by ELISA. RESULT Protein S100β rose significantly after starting CPB. In group G3, it reached a peak of (699 ± 139) ng/L by the end of CPB, significantly higher than those in groups G1 and G2 [(528 ± 163) ng/L and (585 ± 155) ng/L], and was positively correlated with PaO2 levels (r = 0.526, P < 0.01). NSE levels of group G1 were continuously rising after starting CPB and reached significantly high levels at 3 h or 5 h after CPB [(12.2 ± 3.4) µg/L and (12.3 ± 3.7) µg/L], while those of group G2 rose significantly during CPB [(10.9 ± 4.8) µg/L] and even higher at 3 h or 5 h after CPB [(12.6 ± 5.1) µg/L and (13.2 ± 5.4) µg/L]. NSE levels of group G3 rose significantly during CPB and maintained at a high level [(12.2 ± 5.7) µg/L] afterwards. There was no significant difference in serum ADM concentrations among different time points in each group and among these three groups. All the infants were discharged from the hospital without any obvious nervous symptom and sign. CONCLUSION High PaO2 during CPB in infants with CHD might cause an increase of serum protein S100β and NSE, indicating that brain injury might become worse with a higher PaO2 and might be positively correlated with PaO2 during CPB.
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Effects of hypothermia on NSE and S-100 protein levels in CSF in neonates following hypoxic/ischaemic brain damage.
Sun, J, Li, J, Cheng, G, Sha, B, Zhou, W
Acta paediatrica (Oslo, Norway : 1992). 2012;(8):e316-20
Abstract
AIM: The aim of the study was to evaluate the effects of hypothermia on neuron-specific enolase (NSE) and S-100 protein levels in cerebrospinal fluid (CSF) in neonates with hypoxic/ischaemic encephalopathy (HIE). METHODS Fifty-one enrolled neonates with HIE were divided into two groups: hypothermia (n = 23) and control (n = 28). NSE and S-100 protein were measured with immunoradiometric assays. Amino acid neurotransmitters were also measured by reversed-phase high-performance liquid chromatography. Neurodevelopmental assessments were performed at 3 and 12 months of age. RESULTS Neuron-specific enolase and S-100 levels were lower, and neurodevelopment outcome was better in the hypothermia group compared with the control group. Among the infants who received hypothermia, CSF NSE and S-100 were significantly higher in those who developed severe neurological impairment (mental development index or physical development index <70). There were no significant differences between the two groups in amino acid neurotransmitters. CONCLUSION These results indicated that hypothermia was associated with decreased CSF NSE and S-100 level and correlated with neurodevelopmental outcome in infants with HIE.
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Serum S100B and neuron-specific enolase levels in normothermic and hypothermic infants after perinatal asphyxia.
Roka, A, Kelen, D, Halasz, J, Beko, G, Azzopardi, D, Szabo, M
Acta paediatrica (Oslo, Norway : 1992). 2012;(3):319-23
Abstract
AIM: Serum S100B and neuron-specific enolase (NSE) levels are elevated after perinatal asphyxia, but the influence of hypothermia on these proteins has not been previously reported. The aim of this study was to evaluate the effect of systemic hypothermia on these protein levels after perinatal asphyxia, time course, and association with perinatal factors and neurodevelopmental outcome at 2 years of age. METHODS Serum S100B and NSE levels were measured at fixed time points in asphyxiated infants treated with standard intensive care on hypothermia (HT: n = 13) or normothermia (NT: n = 11). RESULTS Serum S100B and NSE levels were grossly elevated in both HT and NT groups. Compared with the values at 6 h of age, S100B values decreased over time in both groups (NT: p = 0.002, HT: p = 0.04). Serum S100B values were lower in HT infants compared with those in NT infants (p = 0.047 at 48 h). Serum S100B and NSE values were significantly higher in infants who died or developed severe neurological impairment (S100B, p < 0.05 at all time points; NSE, p = 0.036 at 24 h of age). CONCLUSION Both NSE and S100B levels are highly elevated following asphyxia. Serum S100B levels were lower in the HT group and strongly correlated with the neurodevelopmental outcome.
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Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques.
Singh, SP, Kapoor, PM, Chowdhury, U, Kiran, U
Annals of cardiac anaesthesia. 2011;(3):197-202
Abstract
Cardiac surgery with aid of cardiopulmonary bypass (CPB) is associated with neurological dysfunction. The presence of cerebrospecific protein S100β in serum is an indicator of cerebral damage. This study was designed to evaluate the influence of three different anesthesia techniques, on S100β levels, in patients undergoing coronary artery bypass grafting on CPB. A total of 180 patients were divided into three groups - each of who received sevoflurane, isoflurane and total intravenous anesthesia as part of the anesthetic technique, respectively. S100 were evaluated from venous sample at following time intervals - prior to induction of anesthesia (T1), after coming off CPB (T2); 12 h after aortic cross clamping (T3) and 24 h after aortic cross clamping (T4). In all three groups, maximal rise in S100β levels occurred after CPB which gradually declined over next 24 h, the levels at 24 h post-AOXC being significantly higher than baseline levels. Significantly low levels of S100β were noted at all postdose hours in the sevoflurane group, as compared to the total intravenous anesthesia (TIVA) group, and at 12 and 24 h postaortic cross clamp, in comparison to the isoflurane group. Comparing the isoflurane group with the TIVA group, the S100 levels were lower in the isoflurane group only at 24 h postaortic cross clamp. It was concluded that maximum rise in S100β levels occurs immediately after CPB with a gradual decline in next 24 h. The rise in S100β levels is significantly less in patients administered sevoflurane in comparison to isoflurane or TIVA. Hemodynamic parameters had no influence on the S100β levels during the first 24 h after surgery.
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The acute effect of tryptophan depletion on serum neurotrophin levels (BDNF, FGF2, and S100B) in healthy subjects.
Whale, R, Beacher, F, Golding, B, Gard, P, Critchley, H
Psychopharmacology. 2011;(2-3):651-2
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The S-100B substudy of the GLUTAMICS trial: glutamate infusion not associated with sustained elevation of plasma S-100B after coronary surgery.
Vidlund, M, Holm, J, Håkanson, E, Friberg, O, Sunnermalm, L, Vanky, F, Svedjeholm, R
Clinical nutrition (Edinburgh, Scotland). 2010;(3):358-64
Abstract
BACKGROUND & AIMS Concerns have been raised about potential neurological injury related to exogenous glutamate. In cardiac surgery glutamate has been administered as a putative cardioprotective agent by cardioplegia or intravenous infusion. In the GLUTAMICS trial, in addition to surveillance of clinical neurological injuries, a prespecified subgroup was analyzed with regard to postoperative S-100B levels to detect potential subclinical neurological injury related to glutamate infusion. METHODS Sixty-nine patients operated on for unstable coronary syndrome were randomized to intravenous infusion of glutamate (n=35) or saline (n=34) perioperatively. Plasma levels of S-100B were obtained on the third postoperative day. RESULTS S-100B in the glutamate group and the control group were 0.079+/-0.034microg/L and 0.090+/-0.042microg/L respectively (p=0.245). There were no patients with stroke or mortality. Three patients in the control group and two in the glutamate group had postoperative confusion. These patients had significantly elevated S-100B compared with those without confusion (0.132+/-0.047vs 0.081+/-0.036microg/L; p=0.003). Overall, 21 patients had S-100B above reference level (> or =0.10microg/L) and these patients had significantly more calcifications in the ascending aorta on epiaortic scanning. CONCLUSIONS Intravenous glutamate infusion during surgery for unstable coronary artery disease did not initiate a sustained elevation of plasma S-100B. Thus, no evidence for subclinical neurological injury related to glutamate infusion was found. In contrast, postoperative elevation of plasma S-100B was linked to calcification of the ascending aorta and postoperative confusion.
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Effects of remote ischemic preconditioning on biochemical markers and neurologic outcomes in patients undergoing elective cervical decompression surgery: a prospective randomized controlled trial.
Hu, S, Dong, HL, Li, YZ, Luo, ZJ, Sun, L, Yang, QZ, Yang, LF, Xiong, L
Journal of neurosurgical anesthesiology. 2010;(1):46-52
Abstract
BACKGROUND Remote ischemic preconditioning (RIPC) may protect the spinal cord from ischemic injury. This randomized clinical trial was designed to assess whether a large clinical trial testing the effect of RIPC on neurologic outcome in patients undergoing spine surgery is warranted. This trial was registered with ClinicalTrials.gov, number NCT00778323. METHODS Forty adult cervical spondylotic myelopathy patients undergoing elective decompression surgery were randomly assigned to either the RIPC group (n=20) or the control group (n=20). Limb RIPC consisted of three 5-minutes cycles of upper right limb ischemia with intervening 5-minute periods of reperfusion. Neuron-specific enolase and S-100B levels were measured in serum at set time points. Median nerve somatosensory-evoked potentials (SEPs) were also recorded. Neurologic recovery rate was evaluated using a Japanese Orthopaedic Association scale. RESULTS RIPC significantly reduced serum S-100B release at 6 hours and 1 day after surgery, and reduced neuron-specific enolase release at 6 hours, and then at 1, 3, and 5 days after surgery. No differences were observed in SEP measurements or the incidence of SEP changes during surgery between the control and RIPC groups. Recovery rate at 7 days, and at 1 and 3 months after surgery was higher in the RIPC group than in the control group (P<0.05). CONCLUSIONS Our results for markers of neuronal ischemic injury and rate of recovery suggest that a clinical trial with sufficient statistical power to detect an effect of RIPC on the incidence of neurologic complications (paresis, palsy, etc) due to spinal cord ischemia-reperfusion injury after spine surgery is warranted [corrected].