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S100A1 promotes cell proliferation and migration and is associated with lymph node metastasis in ovarian cancer.
Tian, T, Li, X, Hua, Z, Ma, J, Liu, Z, Chen, H, Cui, Z
Discovery medicine. 2017;(127):235-245
Abstract
S100A1 is a calcium-binding protein belonging to the family of S100 proteins, and is highly expressed in ovarian cancer. However, its role in ovarian cancer has not yet been fully elucidated. In this study, we examined S100A1 expression in ovarian cancer tissues and normal tissue controls and analyzed the correlation between S100A1 expression and clinicopathological parameters. We found that S100A1 expression was significantly upregulated in ovarian cancer tissues compared with fallopian and normal ovarian epithelium tissues and was significantly associated with lymph node metastasis and International Federation of Gynecology and Obstetrics (FIGO) stages and tumor grades. We then investigated the biological functions of S100A1 in ovarian cancer by cell proliferation, fluorescence-activated cell sorting (FACS), and migration and invasion assays. The results indicated that S100A1 enhanced the ovarian cancer cell proliferation and migration. Together, our findings demonstrated that S100A1 plays an important role in the malignancy of ovarian cancer, and serves as a useful marker for the detection of ovarian malignancy.
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Acute sleep deprivation increases serum levels of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in healthy young men.
Benedict, C, Cedernaes, J, Giedraitis, V, Nilsson, EK, Hogenkamp, PS, Vågesjö, E, Massena, S, Pettersson, U, Christoffersson, G, Phillipson, M, et al
Sleep. 2014;(1):195-8
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Abstract
STUDY OBJECTIVES To investigate whether total sleep deprivation (TSD) affects circulating concentrations of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in humans. These factors are usually found in the cytoplasm of neurons and glia cells. Increasing concentrations of these factors in blood may be therefore indicative for either neuronal damage, impaired blood brain barrier function, or both. In addition, amyloid β (Aβ) peptides 1-42 and 1-40 were measured in plasma to calculate their ratio. A reduced plasma ratio of Aβ peptides 1-42 to 1-40 is considered an indirect measure of increased deposition of Aβ 1-42 peptide in the brain. DESIGN Subjects participated in two conditions (including either 8-h of nocturnal sleep [22:30-06:30] or TSD). Fasting blood samples were drawn before and after sleep interventions (19:30 and 07:30, respectively). SETTING Sleep laboratory. PARTICIPANTS 15 healthy young men. RESULTS TSD increased morning serum levels of NSE (P = 0.002) and S-100B (P = 0.02) by approximately 20%, compared with values obtained after a night of sleep. In contrast, the ratio of Aβ peptides 1-42 to 1-40 did not differ between the sleep interventions. CONCLUSIONS Future studies in which both serum and cerebrospinal fluid are sampled after sleep loss should elucidate whether the increase in serum neuron-specific enolase and S100 calcium binding protein B is primarily caused by neuronal damage, impaired blood brain barrier function, or is just a consequence of increased gene expression in non-neuronal cells, such as leukocytes.
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Microemboli from cardiopulmonary bypass are associated with a serum marker of brain injury.
Groom, RC, Quinn, RD, Lennon, P, Welch, J, Kramer, RS, Ross, CS, Beaulieu, PA, Brown, JR, Malenka, DJ, O'Connor, GT, et al
The journal of extra-corporeal technology. 2010;(1):40-4
Abstract
An increasing number of reports surrounding neurologic injury in the setting of cardiac surgery has focused on utilizing biomarkers as intermediate outcomes. Previous research has associated cerebral microemboli and neurobehavioral deficits with biomarkers. A leading source of cerebral microemboli is the cardiopulmonary bypass (CPB) circuit. This present study seeks to identify a relationship between microemboli leaving the CPB circuit and a biomarker of neurologic injury. We enrolled 71 patients undergoing coronary artery bypass grafting at a single institution from October 14, 2004 through December 5, 2007. Microemboli were monitored using Power-M-Mode Doppler in the inflow and outflow of the CPB circuit. Blood was sampled before and within 48 hours after surgery. Neurologic injury was measured using S100beta (microg/L). Significant differences in post-operative S100beta relative to microemboli leaving the circuit were tested with analysis of variance and Kruskal-Wallis. Most patients had increased serum levels of S100beta (mean .25 microg/L, median .15 microg/L) following surgery. Terciles of microemboli measured in the outflow (indexed to the duration of time spent on CPB) were associated with elevated levels of S100beta (p = .03). Microemboli leaving the CPB circuit were associated with increases in postoperative S100beta levels. Efforts aimed at reducing microembolic load leaving the CPB circuit should be adopted to reduce brain injury.
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Measurements of cerebrospinal fluid concentrations of S100beta protein during and after thoracic endovascular stent grafting.
Brunnekreef, GB, Heijmen, RH, Gerritsen, WB, Schepens, MA, ter Beek, HT, van Dongen, EP
European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. 2007;(2):169-72
Abstract
OBJECTIVES Thoracic endovascular aortic repair is associated with postoperative spinal cord ischemia in approximately 1 to 12.5% of all cases. S100beta is a protein that is released during acute damage of the central nervous system. This study was performed to determine the concentration of S100beta in cerebrospinal fluid during and after stenting of the thoracic aorta in patients at high risk for spinal cord ischemia. DESIGN Prospective clinical study. MATERIALS AND METHODS Eight patients who underwent elective thoracic aortic stent grafting underwent lumbar spinal fluid drainage. These patients were at high risk to develop spinal cord ischemia. METHODS CSF samples for analysis of S100beta protein were drawn after induction of anesthesia, during stenting, once every hour the following six hours and 20 hours after repair. RESULTS No significant increase in S100beta protein could be detected in CSF and no neurological deficits were detected postoperatively. CONCLUSIONS The results of this study show us that there is no significant release of S100beta protein in CSF during stenting of the thoracic aorta in this subgroup of patients at high risk for spinal cord ischemia, consistent with clinical exam that there was no significant damage to the central nervous system.
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Arterio-jugular differences in serum S-100beta proteins in patients receiving selective cerebral perfusion.
Kunihara, T, Shiiya, N, Bin, L, Yasuda, K
Surgery today. 2006;(1):6-11
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PURPOSE The early increase in serum S100beta after cardiopulmonary bypass (CPB) seems to be derived from an extracerebral source. To exclude contamination, we investigated the arterio-jugular differences in S100beta levels in patients receiving selective cerebral perfusion (SCP). We also evaluated the brain-protective effect of SCP by comparing the arterial S100beta levels with those in patients undergoing coronary artery bypass grafting (CABG). METHODS We measured arterial and jugular venous levels of S100beta in ten patients undergoing aortic arch repair with SCP for up to 12 h postoperatively (SCP group). We also measured arterial levels of S100beta in nine patients undergoing CABG (CPB group). RESULTS There was no incidence of hospital death or stroke. The arterial levels of S100beta in both groups were comparable and peaked just after the conclusion of CPB. The arterial and jugular venous levels of S100beta were almost equivalent. The arterio-jugular differences in S100beta levels were negligible, even in our SCP-group patient with postoperative delirium, who had a peak value three times higher than the other patients. CONCLUSIONS The arterio-jugular differences in S100beta did not clarify the origin of their increase. Thus, measuring the jugular venous levels of S100beta in patients without postoperative clinical neurological deterioration would be of little benefit. However, SCP seems to protect the brain against S100beta release as effectively as conventional CPB.
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Effect of stress doses of hydrocortisone on S-100B vs. interleukin-8 and polymorphonuclear elastase levels in human septic shock.
Mussack, T, Briegel, J, Schelling, G, Biberthaler, P, Jochum, M
Clinical chemistry and laboratory medicine. 2005;(3):259-68
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Abstract
Stress doses of hydrocortisone are known to have immunomodulatory effects in patients with hyperdynamic septic shock. The prognosis correlates with the presence and severity of septic encephalopathy. However, neurological evaluation is influenced by the use of analgesia sedation during artificial ventilation. The objective of this study was to demonstrate the effect of stress doses of hydrocortisone during the initial phase of human septic shock on the serum values of the neurospecific protein S-100B in comparison to the inflammation markers interleukin (IL)-8 in serum and polymorphonuclear (PMN) elastase in plasma. A total of 24 consecutive patients, who met the American College of Chest Physicians/Society of Critical Care Medicine criteria for septic shock, were enrolled in this prospective, randomized, double-blind, single-center trial. The severity of illness at recruitment was graded using the Acute Physiology and Chronic Health Evaluation II and the Simplified Acute Physiology Score II scoring systems. Multi-organ dysfunction syndrome was described by the Sepsis-related Organ Failure Assessment (SOFA) score. All patients were prospectively randomized to receive either stress doses of hydrocortisone or placebo. Hydrocortisone was started in 12 patients with a loading dose of 100 mg and followed by a continuous infusion of 0.18 mg/kg/h for 6 days. Median S-100B serum levels of the hydrocortisone group decreased from 0.32 ng/mL at study entry to 0.07 ng/mL 6 days later without significant differences compared to the placebo group. Initial IL-8 serum levels were significantly higher in the hydrocortisone group up to 12 h after study entry, and significantly decreased from 715 to 17 pg/mL at the end of the observation period. Median PMN elastase plasma levels were not affected by hydrocortisone infusion. Patients with initial S-100B serum levels > 0.50 ng/mL revealed significantly higher SOFA scores up to 30 h, IL-8 serum levels up to 12 h, and PMN elastase plasma levels up to 36 h after study entry than those patients with < or = 0.50 ng/mL. These effects were independent of the amount of fluid correction for hemodilution. Starting S-100B, IL-8 and PMN elastase values of the hydrocortisone group were within the ranges already known in patients with out-of-hospital cardiac arrest or severe traumatic brain injury. Stress doses of hydrocortisone resulted in a significant reduction in IL-8 serum, but not in S-100B serum and PMN elastase plasma concentrations in patients with hyperdynamic septic shock. For the first time, a similar extent of S-100B increase in serum of septic patients at the time of diagnosis was shown as reported for cardiac arrest or severe traumatic brain injury.
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Controversial significance of early S100B levels after cardiac surgery.
Jönsson, H, Johnsson, P, Bäckström, M, Alling, C, Dautovic-Bergh, C, Blomquist, S
BMC neurology. 2004;(1):24
Abstract
BACKGROUND The brain-derived protein S100B has been shown to be a useful marker of brain injury of different etiologies. Cognitive dysfunction after cardiac surgery using cardiopulmonary bypass has been reported to occur in up to 70% of patients. In this study we tried to evaluate S100B as a marker for cognitive dysfunction after coronary bypass surgery with cardiopulmonary bypass in a model where the inflow of S100B from shed mediastinal blood was corrected for. METHODS 56 patients scheduled for coronary artery bypass grafting underwent prospective neuropsychological testing. The test scores were standardized and an impairment index was constructed. S100B was sampled at the end of surgery, hourly for the first 6 hours, and then 8, 10, 15, 24 and 48 hours after surgery. None of the patients received autotransfusion. RESULTS In simple linear analysis, no significant relation was found between S100B levels and neuropsychological outcome. In a backwards stepwise regression analysis the three variables, S100B levels at the end of cardiopulmonary bypass, S100B levels 1 hour later and the age of the patients were found to explain part of the neuropsychological deterioration (r = 0.49, p < 0.005). CONCLUSIONS In this study we found that S100B levels 1 hour after surgery seem to be the most informative. Our attempt to control the increased levels of S100B caused by contamination from the surgical field did not yield different results. We conclude that the clinical value of S100B as a predictive measurement of postoperative cognitive dysfunction after cardiac surgery is limited.