S100B Protein Concentrations Research Articles

Stężenie białka S100B w surowicy krwi u młodzieży z omdleniami

Stężenie białka S100B w surowicy krwi u młodzieży z omdleniami

Daño cerebral postanestesia general

Background and objectiveS100B protein is a serum marker of cerebral damage. The objective was to evaluate the brain damage caused by general anaesthesia, by determining the concentration of serum S100B protein before and after of general anaesthesia. Patients and methodPatients with chronic adenotonsillar hypertrophy and indications for tonsillectomy were included. A venous blood sample was taken from the patients before general anaesthesia (basal sample). The patients were anaesthetised using the following intravenous anaesthetic drugs: midazolam, fentanyl and propofol; and inhaled sevoflurane. A second venous blood sample (postoperative sample) was taken from patients after the surgery, in the operating room. The concentration of serum S100B protein was determined in the basal sample (S100Bb) and postoperative sample (S100Bp) by immunoassay electro-chemiluminescence in MODULAR E-170 (Roche Diagnostics). ResultsSeventy-six patients were included, 46 males and 30 females, aged between 3 to 14 (median 5 years). In all the patients, serum S100B protein levels increased after general anaesthesia. The values of S100Bp (median 164.0ng/L) were significantly higher than the values of S100Bb (median 94.5ng/L). The median of the difference between S100Bp and S100Bb was 58.0ng/L. There were statistically significant differences between S100Bb and S100Bp using the Wilcoxon test (P<.0001). ConclusionsThe concentration of serum S100B protein increased significantly after general anaesthesia. This indicates that general anaesthesia may cause brain damage.

Changes in symptom severity and biochemical markers of brain injury in patients with treatment-resistant schizophrenia

One of the major problems of the methodology of translational research is to find biomarkers that serve as indicators of treatment response. The aim was to study the dynamics of biochemical markers in the process of combined antipsychotics and electroconvulsive therapy. Material and methods Present study was conducted in 34 patients with treatment-resistant schizophrenia (31.6±9.4 years old) that underwent combined ECT (10 ECTs on average) and pharmacological treatment. The assessment included PANSS and determination of NSE and S100B protein concentrations using automated immunochemical analyzer Elecsys 2010. Blood samples were obtained before the beginning of ECT, 24 hours after the third and sixth ECTs. Results Average reduction of PANSS score was 29,1%, >20% for 85% of patients. There were no significant differences in NSE and S100B concentrations at different stages of treatment. This result is consistent with data on the safety of ECT from the point of view of the integrity of cells. There were found statistically significant differences between S100B concentration in women and men (60±18 and 43±23 ng/L, respectively, P =0.029) and a trend of increase in S100 levels with the increase of disease duration ( r =0.372, P =0.062). Serum S100B concentrations at baseline negatively correlated with positive and negative symptoms severity and with PANSS composite score. No correlation between treatment efficiency and biochemical markers' levels was found. Conclusion Combined antipsychotic and electroconvulsive therapy was effective for treatment-resistant schizophrenic patients and did not induce nerve cells damage. Initial symptom severity was correlated with S100B levels.

Effect of sevoflurane preconditioning on brain injury induced by cardiopulmonary bypass in rats

Objective To evaluate the effect of sevoflurane preconditioning on brain injury induced by cardiopulmonary bypass(CPB)in rats. Methods Forty adult male Sprague-Dawley rats, aged 6-8 months, weighing 350-450 g, were randomly divided into 5 groups(n=8 each)using a random number table: sham operation group(S group), CPB group, and preconditioning with different concentrations of sevoflurane groups(SP1, SP2 and SP3 groups). In SP1, SP2 and SP3 groups, sevoflurane with the final concentrations of 1.2%, 2.4% and 3.6%, respectively, was inhaled for 1 h, and then CPB was started.After sevoflurane preconditioning and before CPB(T0), at 30 min of CPB(T1), at the end of CPB(T2), and at 1, 2 and 3 h after termination of CPB(T3-5), venous blood samples were collected from the right internal jugular vein for determination of serum S100-β protein concentrations by enzyme-linked immunosorbent assay.Rats were sacrificed at T5, and hippocampi were isolated for determination of neuronal apoptosis(by TUNEL)and NF-κB p65 expression(by immunohistochemistry). Results Compared with group S, the concentration of serum S100-β protein was significantly increased at T1-5, the number of apoptotic neurons was significantly increased, and the expression of NF-κB p65 was significantly up-regulated in CPB, SP1, SP2 and SP3 groups(P<0.05). Compared with group CPB, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in SP1, SP2 and SP3 groups(P<0.05). Compared with group SP1, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in SP2 and SP3 groups(P<0.05). Compared with group SP2, the serum S100-β protein concentration was significantly decreased at T1-5, the number of apoptotic neurons was significantly decreased, and the expression of NF-κB p65 was significantly down-regulated in group SP3(P<0.05). Conclusion Sevoflurane preconditioning can attenuate CPB-induced brain injury probably by inhibiting activation of NF-κB in hippocampal neurons of rats. Key words: Anesthetics, inhalation; Ischemic preconditioning; Cardiopulmonary bypass; Brain injuries

Effect of limb ischemic post-conditioning in combination with hypothermia on brain injury after cardiopulmonary resuscitation in swine

Objective To evaluate the effect of limb ischemic post-conditioning (LIPC) in combination with hypothermia on brain injury after cardiopulmonary resuscitation (CPR) in swine. Methods Eighteen adult male white swine, weighing 35-40 kg, were used.The swine model of brain injury was established by inducing ventricular fibrillation for 10 min followed by 5 min of CPR.The animals were randomly divided into 3 groups (n=6 each) using a random number table: cardiac arrest-CPR group (group CA-CPR), group LIPC, and LIPC combined with hypothermia group (group LIPC+ H). In LIPC and LIPC+ H groups, LIPC was performed at the onset of CPR.In addition, the body temperature was cooled down to 32-34 ℃ by using a cooling blanket after successful resuscitation, and then maintained at this level until 4 h after resuscitation, followed by 4 h of re-warming at a rate of 1 ℃/h in group LIPC+ H.At 24, 48 and 72 h after resuscitation (T1-3), neurologic deficit score (NDS) and neurologic alertness score (NAS) were evaluated.Blood samples were collected from the auricular vein for determination of the concentrations of neuron-specific enolase (NSE) and S100B protein in serum by enzyme-linked immunosorbent assay. Results Compared with group CA-CPR, the NDS was significantly decreased, and the NAS was increased at T1-3, and the concentrations of NSE and S100B protein in serum were decreased at T2, 3 in LIPC and LIPC+ H groups (P<0.05). Compared with group LIPC, the NDS was significantly decreased, and the NAS was increased at T1-3, and the concentrations of NSE and S100B protein in serum were decreased at T3 in group LIPC+ H (P<0.05). Conclusion The combination of LIPC and hypothermia provides better efficacy than either alone in reducing brain injury after CPR in swine. Key words: Hypothermia, induced; Ischemic postconditioning; Extremities; Heart arrest; Cardiopulmonary resuscitation; Reperfusion injury; Brain

Effect of sevoflurane on brain injury in pigs with hemorrhagic shock

Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS). Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22–25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham), group HS, and sevoflurane group (S group). In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured. The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated. The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40% blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury. In group S, 2% sevoflurane was inhaled for 30 min after successful establishment of the model. Immediately before establishment of the model (T0), and at 30, 60, 90, 120, 180 and 240 min after HS (T1-6), blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method). Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P<0.05). Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P<0.05). Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses. Key words: Anesthetics, inhalation; Shock, hemorrhagic; Brain injuries

Postoperative cognitive dysfunction after inhalational anesthesia in elderly patients undergoing major surgery: the influence of anesthetic technique, cerebral injury and systemic inflammation.

BackgroundElderly patients are reportedly at higher risk of postoperative cognitive dysfunction (POCD) after inhalational anesthesia with sevoflurane. We hypothesized that the incidence of POCD would be higher in elderly patients undergoing major surgery under inhalational rather than intravenous anesthesia. We also measured plasma S-100β protein concentration as a biomarker of central nervous system injury, and plasma interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations to judge the contribution of systemic inflammation to POCD.MethodsNinety patients aged 65–75 years scheduled for resection of an esophageal carcinoma were randomly assigned to one of three groups (n = 30) as follows: a group receiving sevoflurane anesthesia (Group S); a group receiving preoperative methylprednisolone before sevoflurane anesthesia (Group S + MP); and a control group maintained with intravenous propofol (Group C). The mini-mental state examination (MMSE) and Montreal cognitive assessment (MoCA) were used to measure patients’ cognitive function the day before surgery, and on the first, third and seventh postoperative days. The plasma concentrations of TNF-α, IL-6 and S-100β protein were measured 10 min before anesthesia, and on the first, third and seventh postoperative days.ResultsThere were no significant differences in the demographic or clinical characteristics, or perioperative hemodynamic status, of the three groups. The MMSE and MoCA scores were significantly lower in Group S than in the propofol control (Group C) and Group S + MP on the first, third and seventh postoperative days (P <0.05). Throughout the first postoperative week the plasma concentrations of TNF-α, IL-6, and S-100β protein were significantly elevated in Group S compared with Group C (P <0.05), but were significantly lower in Group S + MP than Group S (P <0.05).ConclusionsThe incidence of POCD was higher in elderly patients undergoing major surgery under inhalational anesthesia with sevoflurane than those maintained on intravenous propofol, and lower in elderly patients pro-treating with methylprednisolone. Furthermore, we found elevated plasma concentrations of S-100β protein, TNF-α and IL-6 in those receiving sevoflurane anesthesia.Trial registrationChiCTR-IOR-15007007 (02-09-2015).

The impact of intrauterine infection on fetal brain damage assessed by S100B protein concentrations in umbilical cord arteries

Objective: To assess the impact of intrauterine infection on fetal brain damage by measuring S100B protein concentration in umbilical cord arteries. Methods: In the intrauterine infection cases determined by pathology of 25 deliveries (Group I) and non-infection cases of 35 deliveries as control (Group C), we compared gestational age at delivery, birth weight, fetal heart rate monitoring during labor, Apgar score, umbilical cord artery pH and S100B protein concentrations in umbilical arteries measured by two-site immunoradiometric assay kit. Results: (1) There was no significant correlation between pH and concentration of S100B protein. (2) Gestational age at delivery was found to be earlier in Group I, resulting in lower birth weights, when compared with Group C. (3) There was no significant difference between two groups concerning Apgar scores, pH. (4) S100B protein concentrations in Group I was significantly higher than those of Group C (3.9 7 ± 0.66 versus 1.8 9 ± 0.56 μg/L, p < 0.05). (5) The concentration of S100B protein in severe chorioamnionitis (CAM) cases were significantly higher than those of mild CAM and control cases. Conclusion: Higher concentration of S100B protein in Group I suggests that intrauterine infection itself has a serious risk factor on fetal brain damage.

Serum S100B protein concentration in brain-dead organ donors: a pilot study.

Protein S100B is considered to be a marker of brain damage, but there is a paucity of data regarding the utility of its assessment in brain-dead organ donors. The aim of the study was to compare serum protein S100B concentrations between brain-dead organ donors and patients with a confirmed permanent neurological deficit but without signs of brain death. The concentration of serum S100B protein was measured in 12 brain-dead organ donors (including 7 males with a median age of 40 years). All measurements were taken when brain death was confirmed by the commission. Twenty-nine patients (including 13 males with a median age of 63 years) who died in the medical ICU with confirmed permanent brain injury without signs of brain death acted as controls. In these patients, S-100B protein measurements were performed upon ICU admission. In brain-dead organ donors, the median values of serum S100B protein were much higher in comparison to the control group (median and IQR, respectively: 5.04 μg L⁻¹; 1.775-6.765 vs 0.897 μg L⁻¹; 0.324-1.880, P < 0.001). S100B serum values > 1.81 μg L⁻¹ predicted brain death with the highest accuracy (AUROC = 0.83; 95% CI 0.68-0.93; P < 0.001). Concentrations of serum S100B protein in brain-dead organ donors are extremely high and may support the diagnosis of brain death. This fact may be of value when the presence of reflex movements (frequently reported despite brain death) might delay determination of brain death and result in the failure of organ donation.

The level of S100b protein in blood serum of patients with hiv/tb co-infectoin as a neurospecific biomarker of neurotoxicity

There was studied the influence of antiretroviral and antimycobacterial chemotherapy on releasing from the glia&lt;br /&gt;cell marker lesions – S100b protein in the context of possible iatrogenic. It was established that a slight increase in&lt;br /&gt;the concentration of S100b protein in blood serum of patients with co-infection of HIV /TB after starting HAART was&lt;br /&gt;not associated with the occurrence of symptoms of the central nervous system.

Early Dynamics of P-selectin and Interleukin 6 Predicts Outcomes in Ischemic Stroke

Thromboinflammatory molecules connect the prothrombotic state, endothelial dysfunction, and systemic/local inflammation in the acute phase of ischemic stroke. We prospectively investigated (1) serial changes in the levels of thromboinflammatory biomarkers in 76 patients with acute ischemic stroke (6, 24, and 72 hours after onset); (2) compared with 44 patients with asymptomatic severe (≥70%) carotid stenosis and 66 patients with Parkinson disease; and (3) we applied multiple regression methods, relating biological biomarkers combined with demographic data and comorbidities to poststroke infection, death, and functional outcome, and assessed the ability of the models to predict each outcome. Interleukin 6 (IL-6) levels and change of IL-6 concentrations by 72 hours correlated with the size of tissue damage indicated by S100B titers. Levels of IL-6 and P-selectin at 72 hours were higher in patients with large-artery versus lacunar stroke. High concentration of IL-6, monocyte chemotactic protein 1, and S100B at 6 hours were associated with poststroke infections; high concentration of IL-6, S100B, and high-sensitivity C-reactive protein (hsCRP) correlated with death. Change of P-selectin from 6 to 72 hours by 1 unit increased the incidence of poststroke infections with an odds ratio of 22.7; each 100 units of IL-6 at baseline increased the odds of death by 9‰, and at 72 hours, the odds of poststroke infections by 4‰. Each unit of baseline hsCRP elevated the odds of death by 7%. In regression models, in which biological, demographic, and comorbid factors were combined, those biological biomarkers predicted poor outcome with high accuracy, which were characterized by an increasing concentration by 72 hours. Two particular biomarkers emerged to predict outcomes besides hsCRP: early dynamic changes in the systemic levels of P-selectin and IL-6.

The Effects of Levetiracetam on Cerebrospinal Fluid and Plasma NPY and GAL, and on the Components of Stress Response System, hs-CRP, and S100B Protein in Serum of Patients with Refractory Epilepsy

Our objective is to explore the effects of levetiracetam on the levels of neuropeptides, serum activity and concentrations of oxidative stress and inflammatory response proteins, and levels of brain injury marker in patients with refractory epilepsy. Seventy-two patients with refractory epilepsy received levetiracetam treatment. Neuropeptides galanin (GAL) and neuropeptide Y (NPY) in plasma and cerebrospinal fluid (CSF) were detected using double-antibody sandwich immunoassay and radioimmunoassay, respectively. Enzyme-linked immunosorbent assay was used to detect serum activity of paraoxonase (PON1) and serum concentrations of oxidized low-density lipoprotein (ox-LDL) and S100B. Arylesterase (ARE) activity was measured by colorimetric assay, and immune scatter turbidimetry was used to detect a high-sensitivity C-reactive protein (hs-CRP). After treatment, NPY and GAL in plasma and CSF of the patients were significantly decreased as compared to concentrations before treatment (P<0.05). Levetiracetam reduced serum activities of PON1 and ARE (P<0.05) and led to markedly increased serum levels of ox-LDL (P<0.05). Serum concentrations of hs-CRP and S100B protein were significantly lower after levetiracetam administrations than before treatment (P<0.05). Levetiracetam treatment had a clear beneficial effect on the overall quality of life (QOL) scores of the patients, as indicated by significantly improved cognitive functioning, behavior problems, emotional conditioning, physical condition, social functioning, self-assessed life quality score, self-assessed health score, and the total QOL score (P<0.05). Levetiracetam can improve life quality of patients with refractory epilepsy, decrease NPY and GAL in plasma and cerebrospinal fluid, serum PON1 and ARE activities, and serum levels of ox-LDL, hs-CRP, and S100B. Levetiracetam therefore may be considered a drug of choice for treating refractory epilepsy.

Consciousness Disorders after Elective Surgery in Patients with Cerebrovascular Insufficiency

Objective: to study the impact of cerebral hypoxemia on the indicators of neuroinjury, by relying on the diagnosis of post - operative cognitive impairments, and the neuroinjury marker S100b protein and to examine the relationship of postoperative cognitive mpairments. Subjects and methods. Forty - eight non - cardiac surgical and non - neurosurgical patients with verified cerebrovascular disease, who had been operated on under total intravenous anesthesia with propofol and total myoplegia, were examined. Blood S100b protein levels were determined after cerebral hypoxemia detectable by transcranial oximetry. Postoperative delirium was diagnosed by the ICU - CAM test; postoperative cognitive dysfunction was diagnosed according to the Montreal cognitive assessment scale in the periods: 7 days, 1, 3, and 6 months, and 1 year, by using the control group, the Z scores of these indicators were standardized. Results . Cerebral desaturation led to early postoperative disorders, such as delirium and dysfunctions, in 72.7% of the cases. Cerebral saturation parameters correlated moderately, but significantly with neuropsychological indicators at 30 days of the study and 3 months after surgery and just stronger with S100b protein level. The risk of postoperative cognitive impairments in relation to the values of S100b protein was validly predicted in the models of logistic regression and ROC analysis. The rate of early and persistent cognitive dysfunction differed statistically significantly in patients with prior delirium; the logistic regression model validly predicted a relationship between this event and the neuropsychological indicators on 7 days postsurgery. Conclusion . In the patients with cerebrovascular diseases, cerebral hypoxemic episodes are dangerous. When they occur, there is an increased risk of postoperative cognitive impairments, including long - term problems. The above - threshold S100b protein concentration of 0.26 ng/mg is an early predictor of postoperative cognitive disorders.

Estetrol attenuates neonatal hypoxic–ischemic brain injury

Estetrol (E4) is a recently described natural estrogen with four hydroxyl-groups that is synthesized exclusively during pregnancy by the human fetal liver. It has important antioxidative activity. The aim of the present study was to define the importance of E4 in the attenuation of neonatal hypoxic–ischemic encephalopathy. Antioxidative effect of 650μM, 3.25mM and 6.5mM E4 on primary hippocampal cell cultures was studied before/after H202-induced oxidative stress. To examine oxidative stress and cell viability, lactate dehydrogenase activity and cell proliferation colorimetric assays were performed. To study the neuroprotective and therapeutic effects of E4 in vivo neonatal hypoxic–ischemic encephalopathy model of 7-day-old newborn rat pups was used. The neuroprotective and therapeutic effects of estetrol before/after hypoxic–ischemic insult was studied in 1mg/kg/day, 5mg/kg/day, 10mg/kg/day, 50mg/kg/day E4 pretreated/treated groups and compared with the sham and the vehicle treated groups. The body temperature of the rat pups was examined along with their body and brain weights. Brains were studied at the level of the hippocampus and cortex. Intact cell counting and expressions of microtubule-associated protein-2, doublecortin and vascular-endothelial growth factor were evaluated by histo- and immunohistochemistry. ELISAs were performed on blood samples to detect concentrations of S100B and glial fibrillary acidic protein as brain damage markers. This work reveals for the first time that E4 significantly decreases LDH activity and enhances cell proliferation in primary hippocampal neuronal cell cultures in vitro, and decreases the early gray matter loss and promotes neuro- and angiogenesis in vivo.

Effects of sevoflurane on β-amyloid-induced cognitive dysfunction and oxidative stress response of hippocampal tissues in rats

Objective To evaluate the effects of sevoflurane on β-amyloid (Aβ)-induced cognitive dysfunction and oxidative stress response of hippocampal tissues in rats.Methods Ninety-six male adlut SpragueDawley rats,weighing 250-300 g,were randomly divided into 4 groups (n =24 each) using a random number table:control group (group C) ; group Aβ ; 1.3 ％ sevoflurane group (group S1) and 2.6 ％ sevoflurane group (group S2).The animals were anesthetized with intraperitoneal.10％ chloral hydrate 350 mg/kg.Cognitive dysfunction was induced by injecting Aβ1-40 2 μ1 into the bilateral hippocampi in Aβ,S1 and S2 groups.The equal volume of normal saline was given in group C.At 22 days after injection,C and Aβ groups were exposed to 30％ oxygen for 4 h,and S1 and S2 groups inhaled 1.3 ％ and 2.6 ％ sevoflurane,respectively,for 4 h.Eight rats were chosen at days 1,3 and 7 after exposure and cognitive function was assessed by Morris water maze test.The swimming speed,escape latency and exploration time at the original platform quadrant were recorded.The rats were then sacrificed after the end of the behavioral test and blood samples were taken for determination of serum S100β protein concentration.Hippocampi were immediately isolated and the homogenate was prepared for determination of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content.Results Compared with group C,the escape latency was significantly prolonged and exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group Aβ (P ＜ 0.05).There were no significant differences in the variables mentioned above between Aβ and S1 groups (P ＞ 0.05).The escape latency was significantly prolonged and the exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group S2 as compared with Aβ and S1 groups (P ＜ 0.05).There was no significant difference in the swimining speed among the 4 groups (P ＞ 0.05).Conclusion Inhalation of 2.6 ％ sevoflurane for 4 h can aggravate the cognitive dysfunction induced by Aβ in rats and aggravation of oxidative stress response may be involved in the mechanism. Key words: Anesthetics, inhalation ; Amyloid ; Cognition disorders ; Oxidative stress

Effects of dexmedetomidine on expression of TNF-α and ICAM-1 during cerebral ischemia-reperfusion in rats

Objective To evaluate the effects of dexmedetomidine on the expression of tumor necrosis factor-α（TNF-α） and intercellular adhesion molecule-1 （ICAM-1 ） during cerebral ischemia-reperfusion （I/R ） in rats .Methods Thirty-six male Sprague-Dawley rats , aged 8-12 weeks ,weighing 280-320 g ,were randomly divided into 3 groups （ n= 12 each ）：sham operation group （group S ） , cerebral I/R group （group I/R ） and dexmedetomidine group （group D ） .The animals were anesthetized with 10% chloral hydrate 3.5 ml/kg .The focal cerebral ischemia was induced by middle cerebral artery occlusion using a nylon thread with rounded tip inserted into internal carotid artery and advanced cranially until resistance was met .In group D ,dexmedetomidine 3μg/kg was injected intravenously immediately after beginning of ischemia ,followed by infusion at 3μg·kg-1 ·h-1 for 120 min ,while the equal volume of normal saline was given in group I/R .Four rats from each group were chosen at 24 ,48 and 72 h of reperfusion , and blood samples were taken from the left ventricle to determine the concentrations of serum S100B protein .The rats were then sacrificed and the brains were removed to determine the expression of TNF-αand ICAM-1 in brain tissues .Results Compared with group S ,the concentrations of serum S100B protein were significantly increased , and the expression of TNF-α and ICAM-1 in brain tissues was up-regulated in I/R and D groups （ P〈0.05） .Compared with group I/R ,the concentrations of serum S100B protein were significantly decreased , and the expression of TNF-α and ICAM-1 in brain tissues was down-regulated in group D （ P〈0.05 ） .Conclusion The mechanism by which dexmedetomidine reduces the cerebral I/R injury is related to down-regulation of TNF-αand ICAM-1 expression in rats . Key words: Dexmedetomidine; Brain; Reperfusion injury; Tumor necrosis factor-alpha; Intercellular adhesion molecule-1

Effects of different doses of propofol on traumatic brain injury in rats

Objective To evaluate the effects of different doses of propofol on traumatic brain injury in rats .Methods Forty-eight healthy male Sprague-Dawley rats , aged 7-8 weeks , weighing 270-320 g , were randomly divided into 6 groups （ n=8 each ） using a random number table ：sham operation group （group S ） , traumatic brain injury group （group I） ,fat emulsion group （group F） and low-dose propofol group （group L） , medium-dose propofol group （group M ） ,and high-dose propofol group （group H ） .Traumatic brain injury model was established according to the method described by Feeney .In group S ,0.9% normal saline was infused into the left femoral vein at 3.49 ml·kg-1 ·h-1 .In I ,F ,L ,M and H groups ,0.9% normal saline ,20% fat emulsion 3.49 ml·kg-1 ·h-1 ,and propofol 17.46 ,34.92 and 69.84 mg·kg-1 ·h-1 were infused into the left femoral vein ,respectively .Blood samples were collected from the right common carotid artery at 15 and 60 min of infusion （T1-2 ） for determination of serum S100β protein concentrations . The rats were then sacrificed after collecting blood samples at T2 and brains were removed for microscopic examination of the pathological changes of the cerebral cortex （light microscope ） and ultrastructure of neurons in the cerebral cortex （transmission electron microscope） .Results The serum S100β protein concentrations were significantly higher at T1 ,2 in the other five groups than in group S （ P〈0.05 ） .Compared with I and F groups ,the serum S100βprotein concentrations were＆nbsp;significantly decreased at T1 ,2 in L ,M and H groups （ P〈0.05） .Compared with group L ,the serum S100βprotein concentrations were significantly decreased at T2 in M and H groups , and the serum S100β protein concentrations were increased at T1 in H group （ P〈 0.05 ） . The serum S100β protein concentrations were significantly higher at T1 ,2 in H group than in group M （ P〈0.05 ） .Light microscopic examination showed that nucleus condensation , cell necrosis , and cell edema were significantly attenuated in L ,M , and H groups as compared with group I;normal neurons could be found in group M .Transmission electron microscopic examination showed that the severity of neuronal damage was significantly attenuated in L ,M ,and H groups as compared with group I .Conclusion Different doses of propofol can reduce traumatic brain injury in rats . Key words: Propofol; Brain injuries

Impaired endothelial function after aneurysmal subarachnoid haemorrhage correlates with arginine:asymmetric dimethylarginine ratio

BackgroundEndothelial dysfunction might be involved in the development of cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH). MethodsThis prospective observational study of 48 SAH subjects and 23 control subjects examined associations between reactive hyperaemia index (RHI) measured by peripheral arterial tonometry and plasma concentrations of S-100B protein, nitrite/nitrate, arginine, and asymmetric dimethyl arginine (ADMA). Clinical variables were flow velocity in the middle cerebral artery (VMCA), angiographic vasospasm, delayed neurological deficit, and 30 day survival. Five consecutive measurements were obtained at days 0–2, 3–5, 6–8, 9–11, and 12–15. ResultsRHI was 1.67 (0.46) at days 0–2 after SAH but increased at days 3–15 to the same levels as in controls (P<0.05 compared with days 0–2). RHI was lower in subjects who died before day 30 (P=0.07), but no trends were observed in relation to angiographic vasospasm or delayed neurological deficit. Both arginine and ADMA increased after SAH compared with days 0–2 (P<0.05). S-100B was highest in non-survivors (P<0.01) and in subjects with neurological deficit (P<0.01). A positive correlation was found between RHI and arginine:ADMA ratio (r=0.43, P<0.005), but not with nitrite/nitrate, VMCA, or S-100B. ConclusionsPeripheral flow-mediated vasodilation is attenuated in the first days after SAH indicating acute systemic endothelial dysfunction. Impairment of endothelial function after SAH correlates with imbalance of the arginine/ADMA pathway.

The different pattern of blood S100B protein and GFAP concentrations in ischemic stroke

Background: S100B protein and glial fibrillary acidic protein (GFAP) released during ischemia have been associated with stroke. This study aimed to know whether there was a correlation between the concentration of these markers with the severity of neurological deficit in ischemic stroke. Methods: This was a cross-sectional study, which involved 143 ischemic stroke patients who were admitted to hospital not more than 72 hours after the onset and fulfilled the criteria. The concentration of S100B protein and GFAP was determined by ELISA method. Blood level of S100B and GFAP in patient with mild, moderate, and severe stroke were analyzed with Kruskal-Wallis test. Results: There was a significant difference between S100B protein concentration among subjects with mild (median 63.31 ng/L), moderate (median 88.93 ng/L), and severe (median 511.55 ng/L) NIHSS at admission (p < 0.05). A weak significant correlation was found between the severity of NIHSS and the S100B protein concentration. The more severe the NIHSS, the higher the S100B protein concentration (r = 0.351; p < 0.001). Subjects with moderate and severe NIHSS were more frequent to have an intermediate or high level of S100B protein than the subjects with mild NIHSS (OR = 3.9; p < 0.001). The median concentration of GFAP was significantly higher in severe NIHSS subjects (median 0.374 ng/mL) than its concentration in mild (median 0.047 ng/mL) and moderate (median 0.043 ng/mL) NIHSS subjects (p < 0.05). Conclusion: S100B protein concentration was significantly higher in linier relation with the severity of NIHSS, while the GFAP concentration was significantly higher if the NIHSS had been already severe. (Med J Indones. 2013;22:215-20. doi: 10.13181/mji.v22i4.602) Keywords: GFAP, ischemic stroke, NIHSS, S100B protein

Serum S100B Protein Is Increased and Correlates With Interleukin 6, Hypoperfusion Indices, and Outcome in Patients Admitted for Surgical Control of Hemorrhage

S100B protein, an acknowledged biomarker of brain injury, has been reported to be increased in hemorrhagic shock. Also, acute hemorrhage is associated with inflammatory response. The aim of this study was to investigate the concentrations of serum S100B and the potential relationships with interleukin 6 (IL-6), severity of tissue hypoperfusion, and prognosis in patients admitted for surgical control of severe hemorrhage. Patients undergoing elective abdominal aortic aneurysm surgery participated as control subjects. Serum samples were drawn before, at the end of surgery, and after 6 and 24 h. Sixty-four patients with severe hemorrhage (23 trauma and 41 nontrauma) and 17 control subjects were included. Increased preoperative concentrations of S100B protein (1.70 ± 2.13 and 0.81 ± 1.23 μg/L) and IL-6 (241 ± 291 and 226 ± 238 pg/mL) were found in patients with traumatic and nontraumatic reason, respectively, and remained elevated throughout 24 h. Compared with nontrauma, trauma patients exhibited higher preoperative S100B levels (P < 0.05). Overall mortality was 47%. In control subjects, preoperative S100B and IL-6 levels were within normal limits and increased at the end of surgery (P < 0.001 and P < 0.01, respectively). Preoperative S100B correlated with IL-6 (r = 0.78, P < 0.01), arterial lactate (r = 0.50, P < 0.01), pH (r = -0.45, P < 0.01), and bicarbonate (r = -0.40, P < 0.01). Multiple analysis revealed that preoperative S100B in trauma and lactate in nontrauma patients were independently associated with outcome. In predicting death, preoperative S100B yielded receiver operator characteristics curve areas of 0.75 for all patients and 0.86 for those with trauma. These results indicate that severe hemorrhage in patients without brain injury is associated with increased serum levels of S100B, which correlates with IL-6 and tissue hypoperfusion. Moreover, the predictive ability of S100B for mortality, suggests that it could be a marker of potential clinical value in identifying, among patients with severe hemorrhage, those at greater risk for adverse outcome.