Fetal electrocardiographic monitoring during labor in relation to cord blood levels of the brain-injury marker protein S-100

2008 ◽  
Vol 36 (2) ◽  
Author(s):  
Andrea Stuart ◽  
Linda Edvinsson ◽  
Karin Källen ◽  
Per Olofsson ◽  
Charlotte Hellsten ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cord Blood ◽  
Protein S ◽  
Blood Levels ◽  
Marker Protein ◽  
Electrocardiographic Monitoring ◽  
S 100 ◽  
The Brain

scholarly journals Maternal Allopurinol During Fetal Hypoxia Lowers Cord Blood Levels of the Brain Injury Marker S-100B

2009 ◽  
Vol 64 (11) ◽  
pp. 705-706 ◽  
Author(s):  
Helen L. Torrance ◽  
Manon J. Benders ◽  
Jan B. Derks ◽  
Carin M. A. Rademaker ◽  
Arie F. Bos ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cord Blood ◽  
Blood Levels ◽  
Fetal Hypoxia ◽  
The Brain

scholarly journals Identification of biomarkers for the detection of subtle brain injury after cannabis and/or tramadol administration

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Omar M. E. Abdel-Salam ◽  
Amany A. Sleem ◽  
Eman R. Youness ◽  
Enayat A. Omara
Keyword(s):  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Neuronal Damage ◽  
Neuronal Cell ◽  
Protein S ◽  
Serum Levels ◽  
Neuronal Cell Body ◽  
Combined Use ◽  
S 100 ◽  
The Brain

Abstract Background There is a need to identify biomarkers which could indicate the occurrence of brain injury in drug abuse. Objectives We aimed to investigate ubiquitin-C-terminal hydrolase-1 (UCH-L1), a neuronal cell body injury marker, the glial protein S-100 beta (S100β), and the glial fibrillary acidic protein (GFAP) as putative markers for neuronal injury due to cannabis, tramadol, or their combined use. Materials and methods Rats were treated with cannabis and/or tramadol subcutaneously daily for 6 weeks and UCH-L1, S100β, and GFAP were immunoassayed in the brain and serum. Results The results are as follows: (i) either cannabis or tramadol increased UCH-L1 and GFAP in the brain, (ii) serum UCH-L1 and GFAP increased by the highest dose of cannabis or tramadol, (iii) there was no additive effect for cannabis and tramadol on UCH-L1 or GFAP level in the brain or serum, (iv) S100β decreased in the brain by 5–20 mg/kg of cannabis and in the serum following 20 mg/kg of cannabis, and (v) S100β levels increased in the brain after 20 mg/kg of tramadol but decreased the brain and serum after both cannabis and tramadol. Cytoplasmic vacuolations, apoptotic cells, and gliosis were observed in the brain tissue of cannabis and/or tramadol-treated rats. Conclusions These results suggest that changes in UCH-L1, GFAP, or S100β are likely to reflect neurotoxicity and serum levels could be used to detect neuronal damage in chronic users.

scholarly journals Maternal Allopurinol During Fetal Hypoxia Lowers Cord Blood Levels of the Brain Injury Marker S-100B

PEDIATRICS ◽  
2009 ◽  
Vol 124 (1) ◽  
pp. 350-357 ◽  
Author(s):  
H. L. Torrance ◽  
M. J. Benders ◽  
J. B. Derks ◽  
C. M. A. Rademaker ◽  
A. F. Bos ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cord Blood ◽  
Blood Levels ◽  
Fetal Hypoxia ◽  
The Brain

scholarly journals Free radicals induced lipid peroxidation following reperfusion in infants cardiac surgery: relationship to the release of the brain marker protein S-100 into the serum

Critical Care ◽  
10.1186/cc322 ◽  
1999 ◽  
Vol 3 (S2) ◽  
Author(s):  
H Abdul- Khaliq ◽  
LE Blasig ◽  
MO Baur ◽  
M Hohlfeld ◽  
V Alexi-Meskheshvili ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cardiac Surgery ◽  
Free Radicals ◽  
Protein S ◽  
Marker Protein ◽  
S 100 ◽  
The Brain

Protein S-100 and neuropsychological functioning following severe traumatic brain injury

Brain Injury ◽  
2006 ◽  
Vol 20 (10) ◽  
pp. 1007-1017 ◽  
Author(s):  
Sharon E. Watt ◽  
E. Arthur Shores ◽  
Ian J. Baguley ◽  
Nicholas Dorsch ◽  
Michael R. Fearnside
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Neuropsychological Functioning ◽  
Protein S ◽  
S 100

scholarly journals NEURODESTRUCTION OF HYPOTHALAMIC NUCLEI IN BRAIN INJURY. EFFECT OF CARBACETAM

2018 ◽  
Vol 13 (3-4) ◽  
pp. 3-9
Author(s):  
S.V. Ziablitsev ◽  
T.I. Panova ◽  
O.O. Starodubska
Keyword(s):  
Brain Injury ◽  
Nervous Tissue ◽  
Free Fall ◽  
Benzodiazepine Receptor ◽  
Expression Level ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
The Brain ◽  
Supraoptic Nuclei

Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline. Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI. Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP. Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam. Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.

scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

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