bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regular light-to-moderate intake of alcohol and the risk of ischemic stroke. Is there a beneficial effect?
Authors: Palomäki H , Kaste M 
Published: June 2011

To evaluate the association between different patterns of alcohol consumption and the risk of ischemic stroke in young or middle-aged men.
One hundred fifty-six patients and 153 control subjects were included in this case-control study. The pattern and the estimated average weekly intake of alcohol were assessed using a structured questionnaire. The pattern of drinking was defined as regular (daily or almost daily) or irregular (up to three times per week), and the weekly amount of consumption was defined as nondrinking, light-to-moderate drinking (up to 150 g/wk), moderate drinking (> 150 to 300 g/wk), and heavy drinking (> 300 g/wk). Multiple stepwise logistic regression models were used, and adjustments were carried out for potential confounders.
Heavy alcohol intake associated with an increased risk of stroke (odds ratio, 4.45; 95% confidence interval, 1.09 to 18.1), whereas the risk tended to be reduced in light-to-moderate drinkers (odds ratio, 0.54; 95% confidence interval, 0.28 to 1.05). Accounting for the pattern of alcohol intake in addition to the average weekly amount in grams, regular light-to-moderate drinking showed a significant inverse association with stroke (odds ratio, 0.12; 95% confidence interval, 0.02 to 0.65), and an irregular pattern of consumption attenuated this association. Based on the same multivariate analyses, other significant independent risk factors for stroke were arterial hypertension, coronary heart disease, and history of snoring, whereas the contributions of age, diabetes mellitus, smoking, and body mass index proved to be nonsignificant.
Light-to-moderate alcohol intake appears to have an inverse association with the risk of ischemic stroke. The beneficial effect appears to be most prominent if the consumption of alcohol is regular and evenly distributed throughout the week, whereas a sporadic or an occasional pattern of drinking seems to weaken the association. This study also supports the role of heavy drinking as an independent risk factor for ischemic stroke.
The J-curve phenomenon in stroke recurrence.
Authors: Irie K , Yamaguchi T , Minematsu K , Omae T 
Published: June 2011

The relation of poststroke blood pressure to stroke recurrence remains undetermined, and the optimal control of blood pressure has not been established. We performed the present study to resolve these issues.
We analyzed 368 stroke patients with a history of hypertension (mean age, 62 years) who were admitted within 3 months after stroke onset and observed for 6 months or more. We determined stroke recurrence rate in relation to baseline (or initial) blood pressure, mean values of poststroke blood pressure, stroke subtypes, age, antihypertensive treatment, and other clinical features.
The recurrence rate had a J-curve relation to poststroke diastolic blood pressure but not to poststroke systolic blood pressure and baseline diastolic and systolic blood pressures. The stroke recurrence rate was 3.8% per patient-year in 94 patients who had a poststroke diastolic blood pressure of 80 to 84 mm Hg, significantly lower than the rates of 9.2% per patient-year (P < .05) and 11.4% per patient-year (P < .01) in those with a lower and higher poststroke diastolic blood pressure, respectively. The range of poststroke diastolic blood pressure accompanying the lowest stroke recurrence rate was higher in patients with atherothrombotic (85 to 89 mm Hg) than in those with lacunar infarction (80 to 84 mm Hg). Neither antihypertensive therapy nor patients' age affected this phenomenon.
The present study suggests that lower blood pressure does not always result in favorable effects on stroke recurrence. The effects of poststroke blood pressure and antihypertensive therapy on stroke recurrence may be complicated by the J-curve phenomenon.
Clinical analysis of incidentally discovered unruptured aneurysms.
Authors: Ujiie H , Sato K , Onda H , Oikawa A , Kagawa M , Takakura K , Kobayashi N 
Published: June 2011

We analyzed the risk factors for rupture of an intracranial aneurysm based on a retrospective angiographic study of ruptured and unruptured aneurysms.
The 44 cases of asymptomatic aneurysms were selected from 1612 patients whose lesions had been discovered fortuitously by angiography (2.7%) during the period from 1980 to 1989. All these patients were free from any sign of intracranial aneurysm. The variations in age, sex, and location of the aneurysms were analyzed compared with 638 ruptured aneurysms that had been treated in our institute during the same period. The size, shape, and arterial geometry of the unruptured aneurysms were examined angiographically.
Unruptured aneurysm was discovered fortuitously in 44 (2.7%) of 1612 patients, with greater incidence in women aged older than 60 years. Unruptured aneurysms were less likely to occur in the anterior communicating artery (12.8%) and the middle cerebral artery (6.4%). However, they were frequently found in the internal carotid artery, with an incidence of 10.6% in cavernous portion of the internal carotid artery, 19.1% in the internal carotid-ophthalmic artery, 19.1% in the internal carotid-posterior communicating artery, and 12.8% in the internal carotid-anterior choroidal artery. Seven of the nine internal carotid-posterior communicating artery aneurysms showed a hypoplastic or aplastic posterior communicating artery. The mean diameter of the unruptured aneurysms was 4.8 mm, and 80% were smaller than 6 mm.
Intracranial aneurysms are formed not only at the bifurcation of an artery but also at its branching and bending points. However, an aneurysm located at the bifurcation, such as the anterior communicating artery and the middle cerebral artery, bleeds easily in contrast with lateral aneurysms such as those found at the branching and bending points on the internal carotid artery.
Computer-assisted three-dimensional image analysis of cerebral amyloid angiopathy.
Authors: Maeda A , Yamada M , Itoh Y , Otomo E , Hayakawa M , Miyatake T 
Published: June 2011

Microaneurysms and fibrinoid necrosis of cerebral cortical arteries have been reported to be related to the pathogenesis of intracerebral hemorrhage associated with cerebral amyloid angiopathy. To elucidate the pathogenesis of such vascular lesions, we conducted the present study.
Five hundred serial sections from brain tissue of a patient with severe amyloid angiopathy and intracerebral hemorrhage were analyzed histologically and immunohistochemically. Three-dimensional reconstructions of the vascular lesions were performed using a computer-assisted image analysis system.
The microaneurysms were found to develop in small cortical arteries with diameters of about 40 to 50 microns. They were spindle-shaped dilatations, with a maximum diameter of about 200 microns, and appeared within vascular segments bearing severe amyloid deposition. In the walls of the aneurysms, the intima was thickened, and the media and adventitia showed thinning and disruption. Fibrinoid necrosis was found in the vascular walls of the most dilated, middle portions of the aneurysm. The vascular walls undergoing fibrinoid necrosis did not show any beta/A4 or cystatin C but presented with fibrinogen-like immunoreactivities, indicating invasion of plasma components.
These results suggested the following sequential events for the pathogenesis of the cerebral amyloid angiopathy-associated vascular lesions leading to hemorrhage: (1) damage of the media and adventitia due to severe amyloid deposition results in dilatation of the cortical arteries, (2) the vascular dilatation progresses and is accompanied by thickening of the intima and disruption of the media and adventitia (microaneurysm formation), (3) plasma components invade to the vascular wall (fibrinoid necrosis), and (4) finally, hemorrhage develops.
Cerebral venous thrombosis associated with pregnancy and puerperium. Review of 67 cases.
Authors: Cantú C , Barinagarrementeria F 
Published: June 2011

Cerebral venous thrombosis is characterized by its clinical pleomorphism and pathogenetic variability. We studied 67 patients with cerebral venous thrombosis associated with pregnancy and puerperium and compared them with 46 other cases unrelated to obstetric causes to disclose differences in their clinical presentation, neuroradiological findings, clinical course, and prognosis.
In this retrospective study, we analyzed the clinical, laboratory, and neuroimaging findings of 113 patients collected consecutively at our institute. The diagnosis of cerebral venous thrombosis was confirmed by angiography, magnetic resonance imaging, or neuropathological study.
Patients with cerebral venous thrombosis associated with pregnancy and puerperium were younger (average age, 26 versus 36 years), and in most, the onset of symptoms was acute (82% versus 54%; P = .003). The evolution of symptoms reached a plateau within 10 days in 70% of patients with thrombosis from obstetric causes, compared with only 45% in those from other causes (P = .01). Anemia was more frequent in the obstetric group (64% versus 26%; P = .00001). There were no differences regarding neurological and neuroradiological findings. Although the initial severity of illness was similar in both groups, the final outcome was considered good in 80% of patients with obstetric causes, compared with 58% of patients with other causes (P = .01); mortality rates were 9% and 33%, respectively (P = .002).
Cerebral venous thrombosis associated with pregnancy and puerperium has a more acute onset and a better prognosis than thrombosis due to other causes. These findings might be helpful in the diagnostic and therapeutic strategies for patients with cerebral venous thrombosis.
Correlations between morphological changes in platelet aggregates and underlying endothelial damage in cerebral microcirculation of mice.
Authors: Said S , Rosenblum W I , Povlishock J T , Nelson G H 
Published: June 2011

The aim of this study was to test the hypothesis that, once formed, platelet aggregates may injure underlying cerebrovascular endothelium. Such injury could make the same site selectively attractive to the next wave of passing emboli or activated platelets. This vicious circle could account for repetitive, stereotypic symptoms in transient ischemic attacks.
In pial arterioles, minor endothelial injury was produced by a laser/dye technique. After various periods of platelet aggregation at the damaged site, the vessels were fixed in situ for electron microscopic study. The degree of platelet activation (rounded and/or degranulated forms) was evaluated by counting these forms in the electron photomicrographs. These counts were related to the degree of endothelial damage ascertained in the micrographs. Other statistical relations were also examined.
Endothelial damage progressed in parallel with the duration of platelet aggregation and the degree of platelet degranulation at the site. Correlations were number of activated platelets versus degree of damage, r = .43, P < .03; duration of aggregation versus damage, r = .52, P < .01; and number of degranulated platelets versus the degree of endothelial damage, r = .83, P < .001. If an aggregate embolized, endothelial damage did not appear to progress. No correlation existed between the duration of exposure to the laser and the degree of injury.
The parallel between changes in platelets and endothelial damage could represent either an effect of endothelium on platelets or an effect of platelets on endothelium. Although the former alternative cannot be totally ruled out, the observations seem to fit best the hypothesis that progressive endothelial damage can result from increasing activation and degranulation of overlying platelets.
Effect of phorbol myristate acetate on cerebral blood flow in normal and neutrophil-depleted rats.
Authors: Uhl M W , Kochanek P M , Schiding J K , Nemoto E M 
Published: June 2011

Recent evidence suggests a possible role for leukocytes in ischemic brain injury. This study examined the effect of activation of endogenous circulating leukocytes on cerebral blood flow in normal and neutrophil-depleted rats.
Leukocytes were activated by rapid injection of either 50 micrograms/kg phorbol 12-myristate 13-acetate, a protein kinase C activator, or an equimolar amount of the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine, into the right carotid artery. Control rats received an equal volume of dimethyl sulfoxide in saline vehicle. H2-clearance cerebral blood flow was measured in each of the three groups and in vinblastine-treated, neutrophil-depleted rats after carotid artery injection of phorbol.
Phorbol 12-myristate 13-acetate dramatically decreased circulating leukocyte and platelet counts from 5 to 120 minutes after infusion and decreased regional cerebral blood flow in the ipsilateral parietal cortex from a baseline of 119 +/- 14 mL.min-1.100 g-1 (mean +/- SEM) to 49 +/- 5 mL.min-1.100 g-1 at 30 minutes (P < .05). Decreased flow persisted for the 2-hour study. Neither N-formyl-methionyl-leucyl-phenylalanine or vehicle had an effect on cerebral blood flow. In the neutrophil-depleted rats the initial decrease in cerebral blood flow at 30 and 60 minutes after infusion of phorbol was observed, but cerebral blood flow was restored to 70% to 80% of its baseline value (P > .05 versus baseline) by 90 to 120 minutes.
The early phorbol 12-myristate 13-acetate-induced decrease in cerebral blood flow may be due to the effects of protein kinase C activation on vascular smooth muscle or on platelet aggregation, whereas the persistent decrease in cerebral blood flow appears to be mediated in part by neutrophil activation.
Acidic foci within the ischemic penumbra of the New Zealand white rabbit.
Authors: Tomlinson F H , Anderson R E , Meyer F B 
Published: June 2011

In vivo panoramic imaging of reduced nicotinamide adenine dinucleotide (NADH), intracellular brain pH (pHi), and cortical blood flow was used to characterize the ischemic penumbra during focal ischemia. During global ischemia, hypoxia, and status epilepticus, the development of cortical acidic foci has been observed. The hypothesis tested was that during focal ischemia, acidic foci develop, which may lead to recruitment of the ischemic penumbra into infarction.
Five fasted New Zealand White rabbits underwent middle cerebral artery (MCA) occlusion under 1.5% halothane anesthesia through a retro-orbital approach, and five animals served as controls. Brain pHi and cerebral blood flow were measured with in vivo umbelliferone fluorescence.
Baseline brain pHi was 6.98 +/- 0.05, whereas cortical blood flow and NADH fluorescence measured 52.2 +/- 8.7 mL/100 g per minute and 35.5 +/- 3.7 gray-scale units, respectively. Fifteen minutes after MCA occlusion, overall brain pHi and cortical blood flow of the ischemic penumbra measured 6.61 +/- 0.06 and 31.9 +/- 9.2 mL/100 g per minute. Over 3 hours there was normalization of pHi in the majority of the penumbra due to increases in cortical blood flow. Within the ischemic penumbra acidic foci developed with an initial pHi of 6.35 +/- 0.09 and cortical blood flow of 18.0 +/- 5.7 mL/100 g per minute. These foci remained acidic with increased NADH fluorescence despite being surrounded by cortex that was recovering from ischemia. On light microscopy, these acidic foci had a mixed pattern of neuronal injury.
Within the ischemic penumbra, acidic foci develop that do not follow a vascular distribution and have microscopic evidence of ischemic neuronal injury. This suggests that there is a cortical selective vulnerability regarding pHi regulation and these acidic foci may lead to recruitment of the ischemic penumbra into infarction.
Comparative effects of angiotensin-(1-7) and angiotensin II on piglet pial arterioles.
Authors: Meng W , Busija D W 
Published: June 2011

Recent investigations indicated that degradation fragments of angiotensins could be involved in the regulation of the cerebral circulation and that their effects might be mediated by prostaglandins. The present study was designed to examine the effect of angiotensin-(1-7), a major endogenous heptapeptide fragment, on cerebral arteriolar diameter and compare it with the octapeptide angiotensin II, and further to determine whether prostaglandins mediate their effects.
Newborn, anesthetized pigs were equipped with a closed cranial window, and the diameter of one pial arteriole was measured using intravital microscopy.
Topical application of angiotensin-(1-7) (n = 9) increased the diameter by 6.8 +/- 5.3% (mean +/- SEM), 10.4 +/- 5.2%, 14.3 +/- 5.9%, and 17.5 +/- 7.7% (P < .05) at 10(-7), 10(-6), 10(-5), and 10(-4) mol/L, respectively (baseline, 94 +/- 3 microns). Topical application of angiotensin II (n = 8) increased the diameter by 9.6 +/- 7.0%, 9.6 +/- 7.6%, 11.3 +/- 8.4% (P < .05), and 5.5 +/- 7.9% at 10(-7), 10(-6), 10(-5), and 10(-4) mol/L, respectively (baseline, 94 +/- 5 microns). After administration of indomethacin (5 mg/kg IV), which did not significantly change the baseline arteriolar diameter, neither angiotensin-(1-7) at 10(-4) mol/L nor angiotensin II at 10(-5) mol/L caused significant vasodilation.
The results indicate that angiotensin-(1-7) is a modest dilator in the cerebral circulation, as is angiotensin II, and that prostaglandins may mediate responses.
Effect of cerebral blood flow generated during cardiopulmonary resuscitation in dogs on maintenance versus recovery of ATP and pH.
Authors: Eleff S M , Kim H , Shaffner D H , Traystman R J , Koehler R C 
Published: June 2011

Cardiopulmonary resuscitation with external chest compression generates low perfusion pressures that may be inadequate for restoring cerebral metabolism and may worsen intracellular pH. We tested the hypothesis that cerebral reperfusion with a low perfusion pressure after arrest restores brain adenosine triphosphate (ATP) and pH to levels attained at the same perfusion pressure without preceding complete ischemia.
Brain ATP and intracellular pH were measured by magnetic resonance spectroscopy, and cerebral blood flow was measured with microspheres in anesthetized dogs. External chest compressions were begun in group A (n = 6) immediately after the onset of arrest (ie, arrest time zero) and in group B (n = 10) after 6 minutes of arrest (ie, arrest time 6 minutes). In both groups, mean cerebral perfusion pressure was regulated at 30 mm Hg for 70 minutes by adjustment of inflation pressure of a pneumatic thoracic vest.
At 12 minutes of resuscitation, cerebral blood flow was 27 +/- 4 mL/min per 100 g in group A and 21 +/- 4 mL/min per 100 g in group B, but ATP in group B (58 +/- 10% of prearrest) was less than in group A (105 +/- 6%). With prolonged resuscitation, ATP deteriorated to near zero levels in dogs in group B, with blood flow less than 15 mL/min per 100 g. Dogs with greater blood flow never achieved complete metabolic recovery. In group B, intracellular pH was unchanged from the 6.3 value at the start of resuscitation, even in those dogs with extremely low blood flows.
Levels of cerebral perfusion pressure sufficient to maintain cerebral oxidative metabolism without complete ischemia during cardiopulmonary resuscitation are not sufficient to restore metabolism after complete ischemia during cardiopulmonary resuscitation. However, low "trickle" blood flow did not worsen intracellular acidosis.
Anatomic variation of the middle cerebral artery in the Sprague-Dawley rat.
Authors: Fox G , Gallacher D , Shevde S , Loftus J , Swayne G 
Published: June 2011

The aim of this study was to record and analyze the anatomy of the middle cerebral artery in the rat in an attempt to identify a potential source of variation of quantitative infarct measurements in commonly used models of focal cerebral ischemia.
Over a period of 22 months, as part of ongoing studies, we routinely induced focal cerebral ischemia in 263 Sprague-Dawley rats. This was achieved by permanent occlusion of a length of the right middle cerebral artery approximately 1 to 5 mm distal to the point at which it traverses the rhinal fissure combined with 60 minutes of bilateral common carotid occlusion. The branching pattern of the middle cerebral artery was recorded for each animal by drawing and photography before occlusion and at the time of death.
Six distinct branching patterns were observed. The majority (82.9%) of middle cerebral arteries studied conformed to the typical bifurcating vessel commonly referred to in the literature. However, the remaining 17.1% were far more variable with major, atypical branching, introducing, we believe, unnecessary and avoidable variation into quantitative measurements of ischemia in this and similar models.
Middle cerebral artery anatomy should be routinely recorded in models of focal cerebral ischemia in which this artery is occluded distal to the olfactory tract, thus allowing improved analysis of data.
Accelerated brain infarction in hypertension complicated by hereditary heterozygous protein C deficiency.
Authors: Kazui S , Kuriyama Y , Sakata T , Hiroki M , Miyashita K , Sawada T 
Published: June 2011

Protein C deficiency leads to reduced inhibition of coagulation and an increased likelihood of thrombosis. It is widely accepted that the most common syndromes associated with protein C deficiency are venous thrombosis and pulmonary thromboembolism, whereas arterial thrombosis is rare. Here we describe two patients with hypertension and hereditary heterozygous protein C deficiency who developed multiple lacunar infarcts.
Patient 1 was a 46-year-old man with a history of hypertension who developed a right upper quadrantanopia and gradually progressive intellectual and behavioral deterioration. Patient 2 was a 61-year-old man with history of hypertension and two episodes of right-sided motor weakness who developed left sixth and seventh cranial-nerve palsies and reduced pinprick sensation in the right extremities. In both patients, magnetic resonance imaging revealed multiple small lesions in the pons as well as the bilateral basal ganglia, thalamus, corona radiata, and other subcortical structures, which are consistent with lacunar infarcts. Protein C activity and antigen levels were reduced to approximately one half of normal in these two patients, as well as in some of their family members who had no other serological or coagulation abnormalities. A diagnosis of heterozygous protein C deficiency type 1 was thus established.
Although it remains uncertain whether protein C deficiency itself increases the risk of cerebral artery thrombosis, it may predispose a patient to develop multiple brain infarctions in association with hypertension.
Congenitally abnormal plasminogen in juvenile ischemic cerebrovascular disease.
Authors: Nagayama T , Shinohara Y , Nagayama M , Tsuda M , Yamamura M 
Published: June 2011

Congenitally abnormal plasminogen is characterized by markedly decreased fibrinolytic activity and has been reported mainly in association with venous occlusive disease.
We found three young adult patients (34, 45, and 27 years old at onset) with ischemic cerebrovascular disease, all of whom had congenital plasminogen abnormalities but no other known risk factors. Hemostatic tests of all three patients revealed plasma plasminogen activities at almost one half of the normal level despite normal plasma plasminogen antigen levels. They were found to be heterozygotes with abnormal plasminogen (normal Ala-601[GCT] to abnormal Thr-601[ACT]) by DNA sequence analysis after polymerase chain reaction.
Congenital plasminogen abnormalities could be one of the risk factors of juvenile ischemic cerebrovascular disease of the arterial as well as venous type.