bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of low-to-high doses of aspirin on platelet aggregability and metabolites of thromboxane A2 and prostacyclin.
Authors: Tohgi H , Konno S , Tamura K , Kimura B , Kawano K 
Published: June 2011

The purpose of this study was to compare the effects of low-to-high doses of aspirin on platelet aggregability determined by different methods and on the metabolism of thromboxane A2 and prostacyclin.
We administered increasing doses (40, 320, and 1,280 mg/day) of aspirin to 19 poststroke patients and studied the differences in 1) the changes in platelet aggregability depending on the methods of evaluation and 2) the concentrations of prostaglandin metabolites in the blood and urine.
Aggregation of platelet-rich plasma induced by a strong stimulus (10 microM ADP) was significantly reduced after 40 mg/day aspirin (p less than 0.005), and this reduction was similar to that after higher aspirin doses. In contrast, aggregation of platelet-rich plasma induced by weaker stimuli (1 and 5 microM ADP) decreased less significantly after 40 mg/day aspirin compared with that after higher aspirin doses. The serum thromboxane B2 generated after ex vivo incubation was reduced significantly (by 85%) after 40 mg/day aspirin and decreased further after 320 mg/day (by 96%) and 1,280 mg/day (by greater than 99%) of aspirin. The urinary 11-dehydro-thromboxane B2 concentration decreased less significantly after 40 mg/day aspirin (by 42%) compared with that after 320 mg/day (by 78%) and 1,280 mg/day (by 91%) aspirin doses. The urinary concentration of 2,3-dinor-6-keto-prostaglandin F1 alpha did not decrease after 40 mg/day aspirin but decreased significantly after higher doses of aspirin.
These findings suggest that different doses of aspirin may be necessary to prevent thrombogenesis induced by different triggers of different strengths and that 40 mg/day aspirin is able to inhibit a large proportion of maximum thromboxane A2 release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.
Endothelium-derived relaxing factor in brain blood vessels is not nitric oxide.
Authors: Rosenblum W I 
Published: June 2011

The endothelium-derived relaxing factor that mediates the actions of acetylcholine is now most frequently identified as nitric oxide. Nitric oxide is believed to have numerous important regulating actions in neurons, blood vessels, and several other biological systems.
The literature concerning tissue other than cerebral blood vessels supports the conclusion that the endothelium-derived relaxing factor for acetylcholine is either nitric oxide or a compound formed from and containing nitric oxide (for example, a nitrosothiol). However, papers can be found indicating that this endothelium-derived mediator is not nitric oxide. In brain blood vessels the evidence is strongly against the conclusion that nitric oxide is the endothelium-derived mediator for acetylcholine. If this mediator is formed from nitric oxide, either in brain vessels or in other vessels, no data are available delineating how this synthesis is regulated or whether and where nitric oxide leaves the nitroso compound to initiate dilation. Indeed, cerebrovascular data now cast doubt on the commonly held belief that nitrosovasodilators regulate vascular tone by giving off nitric oxide to vascular smooth muscle.
In brain blood vessels the chemical identity of the endothelium-derived relaxing factor mediating the action of acetylcholine is unknown, but this relaxing factor does not appear to be nitric oxide. If the mediator contains nitric oxide, as is probably the case, the means by which it activates vascular guanylate cyclase and/or produces dilation is unknown. Since this relaxing factor inhibits platelet adhesion/aggregation in cerebral vessels as well as relaxing these vessels, the chemical identification of this relaxing factor and the elucidation of its mode of action are extremely important to our understanding and control of cerebrovascular phenomena in health and disease.
Lipoprotein and apolipoprotein profile in men with ischemic stroke. Role of lipoprotein(a), triglyceride-rich lipoproteins, and apolipoprotein E polymorphism.
Authors: Pedro-Botet J , Sentí M , Nogués X , Rubiés-Prat J , Roquer J , D'Olhaberriague L , Olivé J 
Published: June 2011

The role of lipoprotein abnormalities in the development of ischemic cerebrovascular disease has not been sufficiently clarified. The aim of this study was to identify the lipoprotein profile in ischemic cerebrovascular disease and the possible role of apolipoprotein E polymorphism.
The relation between the concentrations of lipoprotein(a), intermediate density lipoproteins, apolipoprotein A-I, apolipoprotein B, apolipoprotein E, and other lipoproteins was studied in 100 men with ischemic cerebrovascular disease (48 atherothrombotic, 28 lacunar, and 24 of unknown type) and in 100 healthy age-matched men as a control group.
Patients with ischemic cerebrovascular disease had significantly higher levels of lipoprotein(a), lipids carried by intermediate density lipoproteins, and low density lipoprotein cholesterol and lower levels of high density lipoproteins than control subjects. Patients with atherothrombotic infarction had higher total serum cholesterol and low density lipoprotein cholesterol concentrations than patients with lacunar infarction. To assess lipoprotein abnormalities in normolipidemic subjects, a subgroup of 38 patients with ischemic cerebrovascular disease and 53 control subjects, both with serum cholesterol levels < 5.2 mmol/l (200 mg/dl) and triglycerides < 2.3 mmol/l (200 mg/dl), was analyzed. Serum lipoprotein(a), lipids carried by very low density lipoproteins and intermediate density lipoproteins, and low density lipoprotein triglycerides were significantly higher in normolipidemic patients compared with normolipidemic control subjects, whereas high density lipoprotein cholesterol levels were lower. Apolipoprotein E polymorphism in our ischemic cerebrovascular patients differed from that of the control group, with the epsilon 4 allele being more prevalent.
Increased serum lipoprotein(a) levels and intermediate density lipoprotein abnormalities together with decreased high density lipoprotein levels are major risk factors for ischemic cerebrovascular disease, even in normocholesterolemic and normotriglyceridemic subjects. Finally, the epsilon 4 allele could probably be a predisposing genetic marker for ischemic cerebrovascular disease.
Cerebral cysticercosis as a risk factor for stroke in young and middle-aged people.
Authors: Alarcón F , Vanormelingen K , Moncayo J , Viñán I 
Published: June 2011

A probable association between cerebral cysticercosis and susceptibility to stroke, especially among young and middle-aged patients, has been reported. We examined the association between cerebral cysticercosis and stroke and the possible factors causing this association.
In 169 stroke patients (75 males and 94 females) under 65 years of age admitted to our neurology department, we evaluated the following possible risk factors: arterial hypertension, diabetes, cardiac disease, hyperlipidemia, smoking, alcohol abuse, and cerebral cysticercosis. In 169 control patients under 65 years of age matched by sex and age, we evaluated the same possible risk factors for stroke.
In the univariate matched analyses, the frequencies of cerebral cysticercosis (p < 0.001), arterial hypertension (p < 0.001), cardiac disease (p < 0.001), hyperlipidemia (p < 0.05), and alcohol abuse (p = 0.05) were higher in the stroke patients than in the control patients. After controlling for possible confounding factors, we found that arterial hypertension (p < 0.001), cardiac disease (p < 0.001), and cerebral cysticercosis (p < 0.001) were independent risk factors for stroke.
Cerebral cysticercosis should be considered a risk factor for stroke in young and middle-aged individuals.
Prediction of cerebral ischemia by ophthalmoscopy after carotid occlusion in gerbils.
Authors: Oostveen J A , Timby K , Williams L R 
Published: June 2011

The Mongolian gerbil provides a unique model of unilateral focal cerebral ischemia because of the lack of posterior communicating arteries in all gerbils as well as an absence of an anterior communicating artery in approximately 20% of the gerbil population. It is unclear how to identify unequivocably the subpopulation of animals that would suffer a severe focal cerebral ischemia after unilateral carotid occlusion.
Ninety-three male gerbils were exposed to unilateral occlusion of the right common carotid artery. The severity of neuronal loss was evaluated histologically in gerbils selected as having significant focal ischemia based on either behavioral criteria (i.e., the demonstration of stereotypical behavior within 1 hour after occlusion) or ophthalmoscopic criteria (i.e., interruption of the retinal arterial perfusion within 10 minutes of carotid ligation as assessed with an ophthalmoscope). After 3 hours of unilateral carotid occlusion, cerebral blood flow was reinstated for 24 hours before fixation for histological analysis. The viability of the CA1 region of the hippocampus, lateral cortex, and medial cortex was scored on a scale of 0-4 based on the percentage of apparent neuronal loss (e.g., 0, no damage; 4, > 75% damage (the Viability Index).
Twenty-eight percent of the gerbils met the behavioral selection criteria, and 17% met the ophthalmoscopic criteria. In the specimens selected by behavioral criteria (n = 7), 30% demonstrated no evidence of postischemic neuronal loss; the mean +/- SEM Viability Index scores for CA1, lateral cortex, and medial cortex were 1.6 +/- 0.6, 1.0 +/- 0.3, and 0.3 +/- 0.2, respectively. Of the animals selected by ophthalmoscopic criteria (n = 12), 100% had severe ischemic tissue damage to the ipsilateral hemisphere; the Viability Index scores for CA1, lateral cortex, and medial cortex were 3.5 +/- 0.1, 3.1 +/- 0.2, and 1.2 +/- 0.2, respectively; all scores were significantly larger than those observed in the behaviorally selected group.
Selection of animals by ophthalmoscopic criteria provides a reliable, consistent method to predict animals with severe focal cerebral ischemia.
Effects of nicardipine on tube formation of bovine vascular endothelial cells in vitro.
Authors: Kaneko T , Nagata I , Miyamoto S , Kubo H , Kikuchi H , Fujisato T , Ikada Y 
Published: June 2011

The purpose of this study was to assess the effect of nicardipine, a Ca2+ channel blocker, on angiogenesis in vitro.
Bovine carotid artery endothelial cells were cultured between type I collagen gel layers with 10(-9) to 10(-5) M nicardipine. The morphological changes were monitored by phase-contrast microscopy and photographed. The total length of tubular structures was measured with an image analyzer system. Endothelial proliferation and migration assays were also performed with the same doses of nicardipine.
Cultured endothelial cells form tubular structures between collagen gel layers. Tube formation of endothelial cells was suppressed by culture with 10(-9) to 10(-5) M nicardipine in a dose-dependent manner. Migration of endothelial cells was also suppressed by the same doses of nicardipine. However, proliferation of endothelial cells was not enhanced.
Nicardipine acts as an inhibitor of angiogenesis in vitro by inhibiting the migration of endothelial cells. This result suggests that nicardipine may have therapeutic potential in angiogenic disorders such as tumor growth, atherogenesis, and diabetic retinopathy.
Prevalence and determinants of carotid atherosclerosis in a general population.
Authors: Prati P , Vanuzzo D , Casaroli M , Di Chiara A , De Biasi F , Feruglio G A , Touboul P J 
Published: June 2011

The aim of this study was to assess the prevalence of asymptomatic carotid atherosclerotic lesions and their relation to principal risk factors. The importance of the relation between asymptomatic carotid atherosclerotic lesions, stroke, and coronary atherosclerosis has been widely discussed, but there are few transversal and longitudinal studies on a general population.
A noninvasive examination was carried out using high-resolution B-mode ultrasonography, which has been shown to be a reliable tool for epidemiological studies. We examined 630 men and 718 women aged 18-99 years (participation rate, 74.9%).
The global prevalence of carotid atherosclerosis was 25.4% in men and 26.4% in women. Intimal-medial thickening was found in 9.4% of men and 11.7% of women. Plaque prevalence was 13.3% in men and 13.4% in women; prevalence of stenotic plaques was 2.7% and 1.5%, respectively. Subjects aged < or = 39 years showed a very low prevalence of any asymptomatic carotid atherosclerotic lesions. In the multiple logistic regression, the analysis of subjects aged > or = 40 years showed a positive significant association between the severity of carotid atherosclerotic lesions (plaques and stenosis) and age (p < 0.001), systolic blood pressure (p < 0.01), cigarette smoking (p < 0.0001), and the protective effect of high density lipoprotein cholesterol (p < 0.037). This analysis did not provide evidence of a clear-cut association between risk factors and intimal-medial thickening.
This population study shows the high prevalence of asymptomatic carotid atherosclerotic lesions in a general population (approximately 25% of adults) and its relation with the classic risk factors. It emphasizes the value of ultrasonography in the detection of early atherosclerotic lesions.
Insulin-induced normoglycemia improves ischemic outcome in hyperglycemic rats.
Authors: Warner D S , Gionet T X , Todd M M , McAllister A M 
Published: June 2011

Hyperglycemia is known to aggravate ischemic brain damage. This study sought to determine if preischemic insulin-induced normoglycemia would improve outcome in hyperglycemic rats.
Normal rats and rats with 5-7 days of streptozotocin-induced diabetes were studied. Normal rats served as either fasted normoglycemic controls or dextrose-infused (hyperglycemic) controls. In the acutely diabetic rats either no insulin was given or insulin was given at 30 or 90 minutes before ischemia so as to induce preischemic normoglycemia. All rats underwent 10 minutes of forebrain ischemia. After 5 days of recovery, motor function and histological outcome were assessed.
Untreated diabetic rats and dextrose-infused control rats had greater hippocampal CA1 damage than normoglycemic control rats. In contrast, insulin-treated diabetic rats had less hippocampal CA1 damage than either untreated diabetic rats or dextrose-infused control rats. Injury in the two insulin-treated groups was not significantly different from that in the normoglycemic control group (all three groups had plasma glucose values of 120-150 mg/dl immediately prior to ischemia). Despite similar plasma glucose values (300-400 mg/dl), fewer postischemic seizures (0% versus 67%) were observed in the untreated diabetic group than in the dextrose-infused control group (p < 0.001).
Hyperglycemia caused by either dextrose infusion or streptozotocin-induced diabetes resulted in exacerbated ischemic brain damage. Insulin therapy to rapidly induce preischemic normoglycemia improved outcome from forebrain ischemia in the acutely diabetic rats. Glucose-infused hyperglycemic rats frequently exhibited postischemic generalized seizures while acutely diabetic rats did not. The latter results implicate some adaptive/protective mechanism associated with acute streptozotocin-induced diabetes that results in a decreased sensitivity to hyperglycemia-augmented ischemic brain damage.
Course of carotid artery occlusions with impaired cerebrovascular reactivity.
Authors: Kleiser B , Widder B 
Published: June 2011

Retrospective studies have found a close correlation between an impaired cerebrovascular reserve capacity and the incidence of hemodynamic stroke. The present study evaluates this relation prospectively.
We measured the CO2 reactivity in 85 patients with internal carotid artery occlusions by transcranial Doppler sonography (Doppler CO2 test). All patients were prospectively followed for 38 +/- 15 (mean +/- SD) months.
In the group with sufficient CO2 reactivity, four of 48 (8%) developed ipsilateral transient symptoms, none a stroke. In cases with diminished or exhausted cerebrovascular reserve capacity, 12 of 37 (32%) suffered an ipsilateral event (four transient ischemic attacks, eight strokes) (p less than 0.01).
The Doppler CO2 test seems to be a valuable method of estimating the risk of stroke in patients with carotid artery occlusions.
Markers of a hypercoagulable state following acute ischemic stroke.
Authors: Takano K , Yamaguchi T , Uchida K 
Published: June 2011

The nature of hematologic disorders in different stroke subtypes remains uncertain. The purpose of this study was to clarify the differences in the coagulation and fibrinolytic activities among ischemic stroke subtypes.
We performed sequential measurements of hematologic parameters in 21 patients with acute cardioembolic stroke, 10 patients with atherothrombotic stroke, 23 patients with lacunar stroke, and 20 age-matched controls.
A marked elevation of plasma concentrations of the thrombin-antithrombin III complex and crosslinked D-dimer was observed only in cardioembolic stroke within 48 hours of onset (p less than 0.01), persisting for one month with a gradual decline. In atherothrombotic stroke, however, the level of crosslinked D-dimer was not elevated at the onset, but increased seven days after onset (p less than 0.01). No significant changes in these marker levels were observed in lacunar stroke.
Our findings suggest that the nature of altered coagulation and fibrinolysis are different in various subtypes of ischemic stroke, and that an assessment of these hematologic parameters may be useful for the early classification of these subtypes.
Effect of flunarizine on electroencephalogram recovery and brain temperature in gerbils after brain ischemia.
Authors: Cohan S L , Redmond D , Chen M 
Published: June 2011

This study was designed to determine whether flunarizine enhances the rate of brain recovery as measured by electroencephalography after cerebral ischemia and whether these effects are attributable to changes in brain temperature.
Male gerbils (n = 81) were treated with either 10 mg/kg flunarizine or its vehicle, beta-cyclodextrin, intraperitoneally, 60 minutes before bilateral carotid occlusion of either 4 or 6 minutes' duration. The electroencephalogram was continuously recorded in the preischemic, ischemic, and postischemic stages of the experiment and rated for the time necessary for the return of 4-6, 7-10, and 11-15 Hz activity. In a second set of experiments, intracerebral temperature was monitored for 60 minutes before ischemia, during 10 minutes of carotid occlusion, and for 60 minutes after ischemia.
Flunarizine pretreatment resulted in significantly more rapid return of electroencephalographic activity in each of the three frequency categories monitored when compared with those animals pretreated with vehicle alone (p less than 0.001). Flunarizine had no effect on brain temperature before, during, or up to 60 minutes after termination of ischemia.
Flunarizine, which has been of efficacy in reducing neuronal death, mortality, and functional impairment when administered after ischemic insults, may have prophylactic value in accelerating brain recovery from ischemia, but does not have this effect as a result of altered brain temperature.
Comparison of magnetic resonance angiography, conventional angiography, and duplex scanning.
Authors: Riles T S , Eidelman E M , Litt A W , Pinto R S , Oldford F , Schwartzenberg G W 
Published: June 2011

To determine the accuracy of magnetic resonance angiography in assessing patients with cerebrovascular disease, we performed a study comparing the results of conventional cerebral angiography, duplex scanning, and magnetic resonance angiography.
From 42 patients, a total of 25 carotid arteries were evaluated by all three techniques. The studies were independently read and sorted into five categories according to the degree of stenosis: 0-15%, normal; 16-49%, mild; 50-79%, moderate; 80-99%, severe; and totally occluded.
Magnetic resonance angiography correlated exactly with conventional angiography in 39 arteries (52%); duplex scanning correlated with conventional angiography in 49 cases (65%). Compared with conventional angiography, both magnetic resonance angiography and duplex scanning tended to overread the degree of stenosis. The most critical errors associated with magnetic resonance angiography were three readings of total occlusion in vessels found to be patent on conventional angiograms.
Although magnetic resonance angiography offers great hope of providing high-quality imaging of the carotid artery with no risk and at less cost, data from this study suggest that misreading the degree of stenosis, or misinterpreting a stenosis for an occlusion, could lead to errors in clinical decisions. Guidelines for use of magnetic resonance angiography in a clinical setting are offered.
Stroke registry in Malmö, Sweden.
Authors: Jerntorp P , Berglund G 
Published: June 2011

A stroke registry covering the city of Malmö, Sweden (population 232,000) was started in January of 1989 to prospectively follow up stroke incidence, recurrence, and fatality rates.
Patients with presumed stroke were interviewed within 1 week after admission to the hospital, and their medical records were examined. Continuous validation against hospital diagnosis showed well over 90% of all stroke cases in Malmö to have been included.
Incidence rates per 100,000 residents were 300 for all stroke events and 225 for first-ever stroke, lower than those reported from other studies. The distribution of stroke diagnostic categories was 3% subarachnoid hemorrhage, 10% intracerebral hemorrhage, 50% cerebral infarction, and 38% unspecified stroke. The diagnosis was based on computed tomography in 51% of first-ever stroke cases. Median age was 73.1 years for men and 79.7 years for women. Incidence rates for all stroke diagnostic categories except subarachnoid hemorrhage increased with age. Prior stroke, hypertension, smoking, atrial fibrillation, and diabetes mellitus were major risk factors for all stroke events. The presenting symptoms were hemiparesis in 74%, speech disorder in 49%, and clouded consciousness in 19% of the patients. The overall case-fatality rate at 30 days was 15%; the rate for intracerebral hemorrhage was 37% and that for cerebral infarction was 10%.
Our findings confirm the value of a stroke registry for stroke epidemiology purposes and as a tool for specific stroke research.