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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A technique for chronic cisternal cerebrospinal fluid (CSF) sampling in conscious rats was used to obtain multiple 50 microliters samples before and up to 7 days after middle cerebral artery occlusion. Neuron-specific enolase (NSE) concentrations were measured by radioimmunoassay using a readily available kit. The volume of infarction was measured by integrating the area of damage on 9 evenly spaced histological sections of the forebrain. This correlated well (r = 0.97, P less than 0.001) with the concentration of CSF neuron-specific enolase integrated over the first 5 days post occlusion, in animals with pure cortical and mixed cortical and striatal lesions. The correlation was maintained in animals given the NMDA antagonist MK-801. There was also a good correlation between the CSF NSE concentration 3 days post-MCAO and the volume of infarction (r = 0.92, P less than 0.01). It is therefore possible that CSF neuron-specific enolase may be useful as a quantitative marker of ischaemic damage in humans and provide a useful adjunct in the assessment of neuroprotective drugs in stroke.
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PMID:CSF neuron-specific enolase as a quantitative marker of neuronal damage in a rat stroke model. 160 99

The effects of a high-fat and high-cholesterol diet (HFC diet) on serum lipoproteins and apolipoproteins were studied in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Kyo: Wistar rats (WKY). In particular, the changes in serum concentrations and distributions among lipoprotein fractions of apolipoproteins A-I, A-IV and E (apo A-I, A-IV and E) were investigated in detail. These apolipoproteins are the main protein constituents of high density lipoprotein (HDL) which is considered to be an anti-atherogenic factor and accounts for a large part of the serum lipoproteins in the rat. Serum lipoprotein fractions were isolated by stepwise density-gradient ultracentrifugation. The alterations in lipoprotein fractions and apolipoproteins in lipoprotein fractions were roughly estimated by native gradient polyacrylamide gel electrophoresis and sodium dodecyl sulfate (SDS)-gradient polyacrylamide gel electrophoresis. Next, the concentrations of apo A-I, A-IV and E in serum, serum lipoprotein fractions and serum lipoprotein-free fraction were measured by rocket immunoelectrophoresis according to the method of Laurell as modified by us. Cholesterol was enzymatically determined by a commercially available kit. The results obtained were as follows: 1) A remarkable increase in the very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) fractions was observed in WKY and SHRSP. This was associated with a remarkable increase in the cholesterol and apo B contents and with a significant increase in the apo E content. These changes in the VLDL and IDL fractions were more drastic in SHRSP than in WKY, which suggests the promotive effect of hypertension in SHRSP on the production of VLDL and IDL fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-fat and high-cholesterol diet--changes in serum concentrations and distributions of apolipoproteins A-I, A-IV and E]. 250 68

99mTc-bicisate (99mTc-ECD) is a new brain perfusion imaging agent formulated from a radiochemically stable kit (Neurolite). A multicenter trial was conducted to determine the sensitivity and specificity of single photon emission computed tomography (SPECT) imaging with 99mTc-bicisate in the localization of ischemic stroke; 170 subjects were enrolled, 128 patients with stroke and 42 controls. Imaging results from 148 subjects (107 stroke patients and 41 controls) were considered evaluable. In the evaluable subjects, SPECT brain imaging with 99mTc-bicisate (21.0 +/- 2.5 mCi) was interpreted without clinical information and was compared with a final assessment using all clinical, diagnostic, and laboratory procedures except the 99mTc-bicisate SPECT results. 99mTc-bicisate was safe and well-tolerated. SPECT imaging with 99mTc-bicisate demonstrated a specificity of 98% and a sensitivity of 86% for localization of strokes (kappa, 0.75; 95% confidence interval, 0.64-0.86). Results were unchanged over time and were similar for all stroke mechanisms except for lacunar disease (sensitivity, 58%). In a secondary analysis, a normal image or small, deep (e.g., subcortical) perfusion defect was highly predictive of a lacunar mechanism. Defects involving the cortical surface were strongly associated with nonlacunar mechanisms. SPECT imaging with 99mTc-bicisate is a sensitive marker in the localization of perfusion defects associated with ischemic stroke and may assist in the determination of the underlying mechanism of a stroke.
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PMID:The role of single photon emission computed tomography brain imaging with 99mTc-bicisate in the localization and definition of mechanism of ischemic stroke. 826 77

Tumor necrosis factor-alpha (TNF) causes vasodilatation and a hyperdynamic state by activating nitric oxide (NO) synthesis. Tyrphostins, specific inhibitors of protein tyrosine kinase (PTK), block the signaling events induced by TNF and NO production. A hyperdynamic circulatory syndrome (HCS) is often observed in portal hypertension (PHT). TNF and NO seem to mediate these hemodynamic changes. The aim of this work was to study the effect of PTK inhibition on the systemic and portal hemodynamics, TNF and NO production, in cirrhotic rats with portal hypertension. Rats with liver cirrhosis induced by chronic inhalation of carbon tetrachloride were used. Animals were treated daily with tyrphostin AG 126 (alpha-cyano-(3-hydroxy-4-nitro) cinnamonitrile) or placebo for 5 d. Mean arterial pressure (MAP), heart rate (HR), and portal pressure (PP) were measured by indwelling catheters. Cardiac output (CI) and stroke volume (SV) were estimated by thermodilution, systemic vascular resistance (SVR) was calculated (MAP/CI), and portal systemic shunting (PSS) was quantitated using radioactive microspheres. Serum and mesenteric lymph node (MLN) TNF levels were measured using an immunoassay kit, and serum NOx was determined photometrically by its oxidation products. The AG 126-treated group showed a statistically significant increase in MAP and SVR, and decreases in CI, SV, MLN TNF, and serum NO oxidation products nitrite and nitrate (NOx) in comparison with the placebo-treated rats. No significant differences were noticed in HR, PP, PSS, or serum TNF. Significant correlations were observed between MAP and NOx, MAP and MLN TNF, PSS and NOx, and serum TNF and serum NOx. The HCS observed in PHT seems to be mediated, at least in part, by TNF and NO by the activation of PTKs and their signaling pathways. PTK activity inhibition ameliorates the hyperdynamic abnormalities that characterize animals with cirrhosis and PHT.
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PMID:Tyrosine kinase inhibition ameliorates the hyperdynamic state and decreases nitric oxide production in cirrhotic rats with portal hypertension and ascites. 923 14

Dominant hand dysfunction due to cerebrovascular accident or fracture makes it more difficult to self-inject insulin. This would likely lead to diminishing a patient's quality of life. We made a new device to introduce self-injection of insulin by a patient's non-dominant hand and tested it. This device was built into a 600-g block of wood 11.5 cm x 8 cm x 8 cm, to be used with the InnoLet insulin kit system (Novo Nordisk Pharmaceuticals Inc., Bagsvaerd, Denmark). It had an insulin injector clamp on the front and a needle holder on the top. The bottom and the back were covered with silicon rubber, which allows the device's own weight to affix it on a table. The insulin injector is placed upright in a holder and fastened with a bar. A needle is installed on the insulin injector with a needle cap. After this cap was removed, the patient could remove any air bubbles by pushing 2 units of insulin through the needle. After the insulin injector was unfastened from the device, the patient injected the insulin subcutaneously into his abdomen or thigh. Then, the insulin injector was removed from the device. We introduced this device in a 59-year-old man with type 2 diabetes mellitus who had suffered from ischemic cerebral infarction in the left middle cerebral artery distribution, resulting in complete right hemiparesis. Our patient mastered this procedure within a few days. At the time of discharge, he could self-inject regular human insulin in a dose of 16 units in the morning, 6 units at noon, and 8 units in the evening. Two weeks after he was admitted to our hospital, he continued independent insulin self-injection three times per day without any help. His hemoglobin A(1c) level gradually decreased until it reached 5.7%. The self-injection of insulin may be introduced with a new device by the non-dominant hand in a patient with diabetes having a disabled dominant hand.
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PMID:A new device to introduce self-injection of insulin by his non-dominant hand in a patient with hemiplegia. 1532 Oct 7

We investigated the plasma levels of D-dimer, fibrinogen, beta-thromboglobulin (BTG) and platelet factor-4 (PF-4), indices of the occurrence of platelet activation in vivo, to find out their role in pathophysiology of ischemic stroke and whether or not such a role has any effect on the disability and the prognosis of stroke patients. A total of 76 patients with AIS aged from 26 to 85 (32 men, 44 women) and 30 cases as controls with similar age (18 men, 12 women) were included in the study. The plasma levels of D-dimer, BTG and PF-4 were measured by ELISA method using a special commercial kit. The cases were allocated into two groups as non-embolic (NEI) and cardioembolic stroke (CEI). The D-dimer levels in 76% of 42 patients in NEI group (p<0.05) and 85.2% of 34 patients in CEI group (p<0.05) were outside the confidence interval (CI) defined for the control group. The levels of BTG were elevated in 81% of 42 cases with NEI (p<0.05) and in 76% of 34 cases with CEI, with reference to CI of control group. The levels of PF-4 were significantly increased in 86% of cases with NEI (p<0.05) and in 88% of cases with CEI than controls (p<0.05). It was observed that the cases with high Rankin scores had higher levels of D-dimer (p<0.005), BTG (p<0.01) and PF-4 (p<0.01) than those with lower scores. There was a correlation between hemostatic markers, platelet activation and functional disability. D-dimer levels were an important marker that determined to degree of the activation of hemostatic system, especially in CEI subtype. The platelet aggregation had an important role in pathophysiology of ischemic stroke and this condition is significant in NEI subgroup and subjects with large infarcts and high disability scores.
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PMID:Hemostatic markers and platelet aggregation factors as predictive markers for type of stroke and neurological disability following cerebral infarction. 1592 75

DJ-1 was initially identified by us as a novel oncogene and has later been found to be a causative gene for familial Parkinson's disease PARK7. DJ-1 plays role in transcriptional regulation and in oxidative stress function, and loss of its function is thought to be related to onset age, mode of progression and clinical severity of both familial and sporadic forms of Parkinson's disease (PD). DJ-1 is localized both in the cytoplasm and nucleus, and it has been reported to be secreted into the serum or plasma of patients with breast cancer, melanoma, familial amyloidotic polyneuropathy and stroke. In this study, levels of DJ-1 secreted into the serum of healthy controls and patients with sporadic PD were examined by using a DJ-1 ELISA kit, and the level of oxidative stress in the serum was also measured. The results showed that DJ-1 was secreted into the serum of both healthy controls and PD patients. There was no significant difference between the levels of secreted DJ-1 in two groups, and correlations of levels of secreted DJ-1 with age, clinical severity of PD and level of oxidative stress were not found.
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PMID:Secretion of DJ-1 into the serum of patients with Parkinson's disease. 1816 23

Stress-promoting system is known to be involved in course and outcome of acute stage of ischemic stroke. An important predictor of an unfavorable course of stroke is so-called "low T3-syndrome". Therapy with drugs increasing T3 level on the background of reduced reaction of oxidative stress is one of a perspective direction of neuroprotection. The study aimed at investigating thyroliberin influence on a clinical course and an outcome of ischemic atherothrombotic stroke as well as on thyroid hormones level in 46 patients (27 women and 19 men) aged 55-75 years admitted to the hospital at the first 24 hours of the disease. Twenty-one patients were switched to thyroliberin in dosage 500 mcg twice a day during 5 days. A control group included 25 patients. Neurological status of the patients was evaluated on days 1, 3, 7 and 21 using the Orgogozo scale and functional recovery was assessed on day 21 with the Bartel scale. Radioimmunoassay of TTH level, cT3 and free thyroxine (cT4) in blood plasma was conducted on days 1, 2, 3 and 7 using test-kit IRMA TTG CT (Belorus). Atherosclerotic changes of MAG were measured with USDG on day 1. All the patients underwent MRI of the brain on days 1, 7 and 21 using tomograph Ellips (Russia) 0.15 Tesla. The dynamics of regress of neurological disturbances in patients receiving thyroliberin appeared as the higher total score on the Orgogozo scale on days 3, 7 and 21 especially in a severe course of the diseases compared to the control group (p<0,007 on day 7). The T3 level in these patients was significantly higher (p<0,05) on days 2, 3 and 7 and the thyroxine level was increased significantly on the 3rd day of stroke (p<0,005) as compared to the control group. In patients with moderate severity of the disease, the TTH level was significantly higher on the 2nd day of stroke (p=0,0004). However, in patients with a severe course TTH and T4 concentrations did not differ in both groups. The results of the study suggest that the use of thyroliberin in an acute stage of ischemic stroke prevents development of "low T3 syndrome" that promotes more rapid and essential regress of neurological disturbances.
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PMID:[Clinical and immunobiochemical study of efficacy and stress-protective properties of thyroliberin at the acute stage of carotid ischemic stroke]. 1819 36

A stroke can be a catastrophic experience. Patients are confronted with alarming symptoms and then a devastating diagnosis, after which they are expected to make an "informed decision" regarding intervention. Informed decision-making is a term that, unlike informed consent, implies that the decision is made by the physician, the patient and the family based on available evidence and information. The 3-hour treatment window for thrombolysis in ischemic stroke imparts very little time for a clinician to sit down with a patient and present information in an unbiased, useful manner. The purpose of this paper is to offer a tool that may assist the physician, the patient and the family in making an informed decision in a time-sensitive manner for thrombolytic intervention in stroke. This tool visually displays outcomes and the role of chance in an intuitive "spin the wheel" type fashion. Until at least May 2011, an interactive version of this clinical tool kit will be available for download at www.sem-bc.com/cvatoolkit.
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PMID:The outcome wheel: a potential tool for shared decision-making in ischemic stroke thrombolysis. 1900 Mar 51

DL-3-n-butylphthalide (NBP) has been used for stroke treatment in China for years. Recently, we found that NBP can reduce the incidence of stroke and have protective action on cerebral microvessels, suggesting a direct action of NBP on endothelial cells. However, it is difficult to evaluate the direct action of NBP on endothelial cells in vivo because of the interactions of endothelial cells with other types of neuronal cells. Therefore, we investigated whether NBP protects against oxygen glucose deprivation (OGD)-induced cell injury in an immortalized human umbilical vein endothelial cells (HUVEC) in vitro. Cells were exposed to OGD, leading to endothelial damage. Endothelial injury was assessed by measuring MTT and the changes in chromatin morphology. Mitochondrial superoxide, mitochondrial membrane potential and mitochondrial morphology were assessed using MitoSOX Red. Rhodamine 123 and MitoTracker, respectively. Nitrosative stress was assessed by measuring the production of peroxynitrite. The activity of superoxide dismutase (SOD) is evaluated using SOD assay kit-WST. The expression of hypoxia inducible factor-1 alpha (HIF-1alpha) was assessed at the protein level by immunofluorescence and Western blotting. NBP at doses between 0.01 and 100 micromol/L dose-dependently protected against OGD-induced cell death. In addition, NBP attenuated OGD-induced mitochondria superoxide, cellular formation of peroxynitrite, and decrease in SOD activity, mitochondria fragmentation and loss of mitochondrial membrane potential. In parallel, NBP enhanced OGD-induced HIF-1alpha expression. This study demonstrates that NBP can protect HUVEC against OGD-induced oxidative/nitrosative stress, mitochondrial damage and subsequent cell death. This protective effect is, at least in part, associated with its enhancement on OGD-induced HIF-1alpha expression.
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PMID:DL-3-n-butylphthalide protects endothelial cells against oxidative/nitrosative stress, mitochondrial damage and subsequent cell death after oxygen glucose deprivation in vitro. 1961 17


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