Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay has been developed and used to measure serum neurone specific enolase (NSE) concentrations in 24 patients, following cerebral infarction. A significant correlation between cerebral infarct volume and maximum serum NSE concentration was observed (P = 0.047). Serum NSE was also assayed at times 24, 48, 72 and 96 h post ictus. At 72 h a significant correlation existed between serum NSE levels and infarct volume (P = 0.012), and levels appeared to be approaching statistical significance at 48 h (P = 0.067). No correlation existed at 24 and 96 h. In addition serum concentrations of NSE were compared to clinical outcome as determined by the Glasgow Outcome Score. Using the Mann-Whitney U test, there was no significant difference in maximum NSE level between patients graded 1-3 on the Glasgow Outcome Score and those graded 4 and 5. However, further studies are required on a larger population to more completely assess this. NSE may prove to be a useful marker of neuronal damage in the study of stroke, with particular application in the assessment of treatment.
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PMID:Serum neurone specific enolase (NSE) levels as an indicator of neuronal damage in patients with cerebral infarction. 175 89

This study relates the level of alpha and gamma enolase in cerebrospinal fluid sampled within 4 days of a stroke to the volume of the cerebral infarct measured on the CT image and to the clinical outcome of the patient. Twenty-eight patients were studied, two with transient ischaemic attacks and 26 with completed stroke due to infarction. The cerebrospinal fluid enolase was raised in the two patients with transient ischaemic attacks and 23 with completed stroke. There was a positive correlation between the volume of the infarct and the level of cerebrospinal fluid alpha and gamma enolase. A high cerebrospinal fluid enolase was always associated with a poor prognosis.
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PMID:Cerebrospinal fluid enolase in stroke. 674 47

Immunochemical studies of gamma gamma-neuron specific enolase (NSE), parvalbumin (PV), S-100 protein (S-100) and acidic fibrillary glial protein (GFAP) were studied in the cerebrospinal fluid and blood serum in 7 patients with ischemic cerebral stroke, aged 57 to 81 years. Cerebrospinal fluid and the first blood sample were taken on the first or second day of the disease. Further blood samples were taken once a week till the end of patients hospitalization, ending by patients discharge or death. Immunochemical identification of proteins under study were performed with Western-blotting technique. It was found that all proteins studied were present in both cerebrospinal fluid and blood serum on the first two days of the disease in small quantities. The blood content of both NSE and PV increased significantly during the first week of the disease. Both proteins disappeared from the blood serum between the second and fourth disease weeks. S-100 protein and GFAP contents in the blood reached significantly high level within the time interval between second and fifth disease weeks, and remained at a relatively high level till patients' death. In all cases computed tomography study and/or brain autopsy revealed extensive ischemic foci localized within areas supplied by the middle cerebral artery. No clear-cut correlation between extensiveness of the ischemic cerebral damage and the content of the proteins studied in both cerebrospinal fluid and blood serum was found. However, our data indicate that serial studies of the above proteins in patients with ischemic stroke may be useful in monitoring the progress of the disease, and occasionally in the prognosis at least in some cases.
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PMID:Immunochemical analysis of some proteins in cerebrospinal fluid and serum of patients with ischemic strokes. 798 25

Superoxide dismutase (SOD), neuron specific enolase (NSE) and lactic dehydrogenase (LDH) were measured in the serum and cerebrospinal fluid (CSF) of ischemic cerebrovascular patients, other neurological patients and in age-matched healthy controls (serum only). The levels of SOD in the CSF or serum of the ischemic patients in the first 24 hrs after stroke were similar to the control groups. However, SOD levels in the ischemic patients increased after two days, reaching their peak values after one week (2-3 fold of the initial values). NSE showed a similar kinetics while LDH showed no change. These results suggest that oxygen radicals are formed in the ischemic patients and the increased synthesis of SOD may protect the patients from the potential damage of such radicals.
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PMID:Increase in superoxide dismutase after cerebrovascular accident. 810 20

The clinical value of determination of CNS-specific proteins in peripheral blood at the acute phase of ischemic stroke is unclear. S-100 protein and neurone specific enolase were serially quantified in peripheral blood at the acute and subacute phase of ischemic stroke (hours 4, 8, 10, 24 and 72 after onset of symptoms). Whereas S-100 protein was detected in none of the matched control subjects. this protein was observed in 17/24 of the stroke patients. Patients with detectable S-100 protein had significantly larger infarctions. Cortical infarctions had already significantly increased S-100 concentrations at days 1 and 3 compared to subcortical or brainstem infarctions. Patients with volumes of brain lesion of >5 ccm exhibited significantly increased serum levels of S-100 at hours 10, 24 and 72 compared to those with lesion volumes of <5 ccm. At hours 10, 24 and 72, concentrations of S-100 correlated with scores of neurological outcome. Although kinetics of release of neurone specific enolase showed a similar pattern of release in blood, no significant association to outcome or extent of brain damage was observed. These results suggest that S-100 protein and not NSE may represent a useful serum marker of brain damage in acute stroke.
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PMID:Leakage of brain-originated proteins in peripheral blood: temporal profile and diagnostic value in early ischemic stroke. 912 96

A detrimental effect of hyperglycemia in ischemic brain has been demonstrated in laboratory experiments and it has been found that hyperglycemia in ischemic stroke is a predictor of poor outcome. We determined serum neuron specific enolase (NSE) concentrations in 41 consecutive patients with a cerebral hemispheric stroke between 12 and 24 h after stroke onset. In cortical ischemic strokes complicated by hyperglycemia (blood glucose concentration > 7 mmol/l) we found significantly higher NSE levels than in normoglycemic patients. In lacunar ischemic strokes NSE levels were not significantly different between normoglycemic and hyperglycemic patients. Our findings support the concept that hyperglycemia during acute cortical ischemic stroke is associated with enhanced neuronal cell death.
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PMID:Increased serum neuron specific enolase concentrations in patients with hyperglycemic cortical ischemic stroke. 975 8

Focal cerebral ischemia elicits an inflammatory response characterized by the infiltration and accumulation of leukocytes, as well as the secretion of inflammatory mediators (Clark et al., Brain Res. Bull., 35 (1994) 387-392; Garcia et al., Am. J. Pathol., 144 (1994) 188-199; Wang et al., J. Neurochem. 71 (1998) 1194-1204). Leukocytes eliminate microbial invaders and necrotizing tissue debris, and can also turn against surrounding healthy tissue and exacerbate tissue injury (Furie and Randolph, Am. J. Pathol., 146 (1995) 1287-1301; Kochanek and Hallenbeck, Stroke 23 (1992) 1367-1379). Inflammatory mediators are considered to play an important role in attracting and stimulating leukocytes (Weiss, N. Engl. J. Med., 320 (1989) 365-376). Monocyte chemoattractant protein-1 (MCP-1) functions as an inflammatory mediator, whose source and role in focal cerebral ischemia is worth studying. MCP-1, a potent chemoattractant factor, may play an important role in ischemia-induced inflammatory response. The aim of the present study is to determine the time course and cell type of MCP-1 protein expression after permanent focal ischemia in mice. ELISA and immunohistochemical staining were used to detect the expression of MCP-1 protein after 0 h, 2 h, 4 h, 12 h, 1 day, 2 days, 3 days, 5 days and 7 days of middle cerebral artery occlusion (n=3-5 in each group). Double-labeled fluorescent staining was used to examine the cellular localization of MCP-1. The results demonstrated that MCP-1 expression was mainly observed in the ischemic core after 12 h of middle cerebral artery occlusion, then gradually increased and extended to the ischemic perifocal area. MCP-1 expression peaked at 2 days and 3 days, and gradually decreased after 5 days of MCAO. Double-labeled immunostaining for MCP-1 and neuron specific enolase (NSE) or glial fibrillary acidic protein (GFAP) showed that MCP-1 positive neurons were observed as early as 12 h of ischemia, while MCP-1 positive astrocytes were observed after 2 days of ischemia. These results support the functional role of MCP-1 in ischemic brain injury and reveal a distinct temporal and spatial expression of MCP-1 in cells believed to be neurons and astrocytes.
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PMID:Monocyte chemoattractant protein-1 expressed in neurons and astrocytes during focal ischemia in mice. 1138 10

To identify biochemical markers for carotid stroke outcome, blood serum levels of inflammation markers (C-reactive protein, orosomucoid, soluble p-selectin) and autoantibodies (AAB) to neurospecific antigens (glial fibrillary acidic protein, neuron specific enolase, S-100 protein) were studied in 27 patients (mean age 64 +/- 6 years) with acute ischemic stroke in inner carotid artery system on day 1-2 and 21 of the disease onset. To day 21, patients with good rehabilitation of neurological functions (group 1) demonstrated a decrease of C-reactive protein and soluble p-selectin concentrations, and unfavorable disease course was associated with a significant (p<0.05) increase of concentrations of these indices. On day 1 and 7, a level of AAT to glial fibrillary acidic protein was higher (p<0.05) in group 1 than in that with minimal rehabilitation and to day 21 it decreased relatively the baseline level. At the same time, patients with minimal rehabilitation had a stable AAT level. On day 7, the AAT level correlated with expression of neurological deficit on day 21 (r=0.510; p=0.019). No stroke-course-dependent differences were found in dynamics of orosomucoid as well as of AAT to neuron specific enolase and S-100 protein levels.
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PMID:[Markers of inflammation, autoantibodies to neurospecific antigens and outcome in patients with acute ischemic stroke]. 1562 89

The rapid detection of brain injury (neuronal damage in general) is an important parameter in the management of cerebrovascular accidents, especially in hemorrhagic and/or ischemic events. Two types of 15-kDa cytoplasmic fatty acid-binding proteins (FABPs), brain-type FABP and heart-type FABP, have recently been postulated as novel markers for brain injury detection. Here we review the possible roles of these FABPs as rapid diagnostic markers for the detection of brain injury due to cerebrovascular accident, trauma or neurodegenerative diseases. The occurrence of brain- and heart-type FABPs in segments of the human brain is also described. Although only limited amounts of data are available, brain- and heart-type FABPs show higher sensitivities and specificities than protein S100 and neuron specific enolase in the rapid detection of brain injury in stroke, trauma and neurodegenerative diseases.
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PMID:Detection of brain injury by fatty acid-binding proteins. 1620 88

Hypoxia-inducible factor (HIF) prolyl 4-hydroxylases are a family of iron- and 2-oxoglutarate-dependent dioxygenases that negatively regulate the stability of several proteins that have established roles in adaptation to hypoxic or oxidative stress. These proteins include the transcriptional activators HIF-1alpha and HIF-2alpha. The ability of the inhibitors of HIF prolyl 4-hydroxylases to stabilize proteins involved in adaptation in neurons and to prevent neuronal injury remains unclear. We reported that structurally diverse low molecular weight or peptide inhibitors of the HIF prolyl 4-hydroxylases stabilize HIF-1alpha and up-regulate HIF-dependent target genes (e.g. enolase, p21(waf1/cip1), vascular endothelial growth factor, or erythropoietin) in embryonic cortical neurons in vitro or in adult rat brains in vivo. We also showed that structurally diverse HIF prolyl 4-hydroxylase inhibitors prevent oxidative death in vitro and ischemic injury in vivo. Taken together these findings identified low molecular weight and peptide HIF prolyl 4-hydroxylase inhibitors as novel neurological therapeutics for stroke as well as other diseases associated with oxidative stress.
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PMID:Hypoxia-inducible factor prolyl 4-hydroxylase inhibition. A target for neuroprotection in the central nervous system. 1622 10


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