bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebral Oxygen Transport Failure?: Decreasing Hemoglobin and Hematocrit Levels After Ischemic Stroke Predict Poor Outcome and Mortality
Authors: Kellert Lars , Martin Evgenia , Sykora Marek , Bauer Harald , Gussmann Philipp , Diedler Jennifer , Herweh Christian , Ringleb Peter A. , Hacke Werner , Steiner Thorsten , Bösel Julian 
Published: August 2011

Background and Purpose—
Although conceivably relevant for penumbra oxygenation, the optimal levels of hemoglobin (Hb) and hematocrit (Hct) in patients with acute ischemic stroke are unknown.

Methods—
We identified patients from our prospective local stroke database who received intravenous thrombolysis based on multimodal magnet resonance imaging during the years 1998 to 2009. A favorable outcome at 3 months was defined as a modified Rankin Scale score ≤2 and a poor outcome as a modified Rankin Scale score ≥3. The dynamics of Hemoglobin (Hb), Hematocrit (Hct), and other relevant laboratory parameters as well as cardiovascular risk factors were retrospectively assessed and analyzed between these 2 groups.

Results—

Of 217 patients, 114 had a favorable and 103 a poor outcome. In a multivariable regression model, anemia until day 5 after admission (odds ratio [OR]=2.61; 95% CI, 1.33 to 5.11;
P
=0.005), Hb nadir (OR=0.81; 95% CI, 0.67 to 0.99;
P
=0.038), and Hct nadir (OR=0.93; 95% CI, 0.87 to 0.99;
P
=0.038) remained independent predictors for poor outcome at 3 months. Mortality after 3 months was independently associated with Hb nadir (OR=0.80; 95% CI, 0.65 to 0.98;
P
=0.028) and Hb decrease (OR=1.34; 95% CI, 1.01 to 1.76;
P
=0.04) as well as Hct decrease (OR=1.12; 95% CI, 1.01 to 1.23;
P
=0.027).

Conclusions—
Poor outcome and mortality after ischemic stroke are strongly associated with low and further decreasing Hb and Hct levels. This decrease of Hb and Hct levels after admission might be more relevant and accessible to treatment than are baseline levels.
Value of Carotid Intima-Media Thickness and Significant Carotid Stenosis as Markers of Stroke Recurrence
Authors: Roquer Jaume , Segura Tomás , Serena Joaquín , Cuadrado-Godia Elisa , Blanco Miguel , García-García Jorge , Castillo José 
Published: August 2011

Background and Purpose—
Data on the predictive value of carotid intima-media thickness (IMT) for stroke recurrence are scarce. We sought to analyze outcome differences in stroke patients with high IMT values compared with patients with significant carotid stenosis (SCS).

Methods—
The multicenter observational ARTICO study included 620 independent patients older than 60 years with a first-ever noncardioembolic stroke. Patients were followed-up for 1 year. The primary end point was a composite of cardiovascular events and death. The IMT-ARTICO substudy analyzed ultrasonographic data from 599 patients. After Doppler carotid echography, patients were classified into the SCS group (carotid stenosis ≥50%; 117 cases), high IMT group (patients with the common carotid IMT in the highest quartile ≥1.11 mm and without SCS; 110 cases), and control group (stroke patients with an IMT <1.11 mm and without SCS; 372 cases). We analyzed the impact of both conditions on the primary end point.

Results—

During follow-up, 88 patients (14.7%) had an end point event. Univariate analysis showed that male gender, diabetes, symptomatic peripheral arterial disease, ankle brachial index ≤0.9, SCS, and high IMT were related to the primary end point. Cox regression showed that peripheral arterial disease (hazard ratio [HR], 2.06; 95% confidence interval [CI], 1.18–3.59;
P
=0.011), SCS (HR, 3.02; 95% CI, 1.78–5.13;
P
=0.0001), and high IMT (HR, 1.86; 95% CI, 1.05–3.29;
P
=0.032) were related to the primary end point. If patients with scheduled revascularization procedures were excluded from the Cox regression, then ultrasonographic markers were SCS (HR, 1.84; 95% CI, 1.03–3.28;
P
<0.039) and high IMT (HR, 1.86; 95% CI, 1.06–3.27;
P
=0.030).

Conclusions—
Both SCS and high IMT have an independent impact as markers of major cardiovascular events or death after a first-ever noncardioembolic stroke.
Prevalence and Prognosis of Asymptomatic Vertebral Artery Origin Stenosis in Patients With Clinically Manifest Arterial Disease
Authors: Compter Annette , van der Worp H. Bart , Algra Ale , Kappelle L. Jaap 
Published: August 2011

Background and Purpose—
The risk of ischemic stroke in patients with asymptomatic vertebral artery stenosis is unknown. We examined the incidence of posterior circulation ischemic stroke in patients with asymptomatic stenosis of the vertebral artery origin (VAo).

Methods—
We studied a hospital-based cohort of 3717 patients (median age, 60 years; interquartile range, 52 to 68 years) with atherosclerotic arterial disease enrolled in the Second Manifestations of ARTerial disease (SMART) study. We included patients in whom duplex ultrasound of the carotid artery and vertebral artery had been performed. Patients with symptomatic VAo stenosis or planned revascularization of the carotid artery or vertebral artery were excluded. Data were analyzed with Cox regression; hazard ratios were adjusted for age and vascular risk factors.

Results—
In 282 patients (7.6%), asymptomatic VAo stenosis >50% was diagnosed with duplex ultrasound. During a mean follow-up of 4.6 years (SD, 3.0), posterior circulation ischemic stroke occurred in 5 of the 282 patients with asymptomatic VAo stenosis at baseline (annual stroke rate, 0.4%) and in 12 of the 3435 patients without VAo stenosis (annual stroke rate, <0.1%). The risk of posterior circulation ischemic stroke was higher in patients with VAo stenosis than in patients without VAo stenosis (hazard ratio, 4.2; 95% CI, 1.4 to 13.1) and was further increased in patients with both VAo and carotid artery stenosis (hazard ratio, 10.5; 95% CI, 3.0 to 37.3). In multivariable analysis, this risk remained essentially the same.

Conclusions—
Patients with atherosclerotic arterial disease and asymptomatic VAo stenosis have a higher risk of posterior circulation ischemic stroke than patients without such a stenosis, but the absolute risk remains low.
Activation of Transient Receptor Potential Vanilloid 1 by Dietary Capsaicin Delays the Onset of Stroke in Stroke-Prone Spontaneously Hypertensive Rats
Authors: Xu Xingsen , Wang Peijian , Zhao Zhigang , Cao Tingbing , He Hongbo , Luo Zhidan , Zhong Jian , Gao Feng , Zhu Zhenyu , Li Li , Yan Zhencheng , Chen Jing , Ni Yinxing , Liu Daoyan , Zhu Zhiming 
Published: August 2011

Background and Purpose—
Previous studies show that endothelial nitric oxide synthase (eNOS) plays a prominent role in maintaining cerebral blood flow and preventing stroke. Capsaicin in hot pepper can increase the phosphorylation of eNOS in endothelial cells. We test the hypothesis that chronic dietary capsaicin can prevent stroke through activation of cerebrovascular transient receptor potential vanilloid 1 (TRPV1) channels in stroke-prone spontaneously hypertensive rats (SHRsp).

Methods—
SHRsp were fed dietary capsaicin, and their onset of stroke was examined. TRPV1 knockout and transgenic mice were used for determining the function of TRPV1 channels. Expression of eNOS and cerebrovascular reactivity were examined.

Results—

Immunofluorescence showed TRPV1 channels and eNOS coexpression in cerebral arterioles. Administration of capsaicin significantly increased phosphorylated eNOS in carotid arteries from wild-type mice but not in TRPV1 knockout mice. Inhibition of eNOS using
N
G
-nitro-
l
-arginine methyl ester, removal of endothelium, or mutant TRPV1 significantly reduced capsaicin-induced endothelium-dependent relaxation of basilar arteries in mice. Chronic dietary capsaicin also remarkably increased eNOS expression in carotid arteries from SHRsp. Compared with Wistar-Kyoto rats, SHRsp had impaired endothelium-dependent relaxation of basilar arteries. Administration of capsaicin or
l
-arginine significantly improved the endothelium-dependent relaxation of basilar arteries in SHRsp. SHRsp had hypertrophy of cerebral arterioles, which was reversed by dietary capsaicin. Importantly, long-term administration of capsaicin significantly delayed the onset of stroke and increased the survival time in SHRsp.

Conclusions—
Activation of TRPV1 channels by dietary capsaicin mediated increases in phosphorylation of eNOS and could represent a novel target for dietary intervention of stroke.
Technological Advances in the Management of Unruptured Intracranial Aneurysms Fail to Improve Outcome in New York State
Authors: Zacharia Brad E. , Ducruet Andrew F. , Hickman Zachary L. , Grobelny Bartosz T. , Badjatia Neeraj , Mayer Stephan A. , Berman Mitchell F. , Solomon Robert A. , Connolly E. Sander 
Published: August 2011

Background and Purpose—
Unruptured intracranial aneurysms (UIAs) are being identified more frequently and endovascular coil embolization has become an increasingly popular treatment modality.
Our study evaluates patient outcomes with changing patterns of treatment of UIA.

Methods—
We conducted a retrospective, longitudinal cohort study of 3132 hospital discharges for UIA identified from the New York Statewide Database (SPARCS) in 2005 to 2007 and 2200 discharges from 1995 to 2000. The rates of endovascular coiling and surgical clipping were examined along with hospital variables and discharge outcome. Anatomic specifics of UIA were unavailable for analysis.

Results—

The case rate for treatment of UIA doubled from 1.59 (1995 to 2000) to 3.45 per 100 000 (2005 to 2007,
P
<0.0001) and increased in the case treatment rate for coiling of UIA (0.36 versus 1.98 per 100 000,
P
<0.0001). Compared with the old epoch, there were more UIAs clipped at high-volume centers (55.8% versus 78.8%,
P
<0.0001) but fewer coiled at high-volume centers (94.8% versus 84.5%,
P
<0.0001) in the new epoch. Coiling and increasing hospital UIA treatment volume were associated with good discharge outcome. However, there was no significant improvement in overall good outcome when comparing 1995 to 2000 versus 2005 to 2007 (79% versus 81%,
P
=0.168) and a worsening of good outcomes for clipping (76.3% versus 71.7%,
P
=0.0132).

Conclusions—
Despite coiling being associated with an increased incidence of good outcome relative to clipping of UIA, the increase in coiling has failed to improve overall patient outcome. The shift in coiling venue from high-volume centers to low-volume centers and decreasing microsurgical volume accompanied by a worsening in microsurgical results contribute to this. This argues for greater centralization of care.
Accumulation of Dietary Docosahexaenoic Acid in the Brain Attenuates Acute Immune Response and Development of Postischemic Neuronal Damage
Authors: Lalancette-Hébert Mélanie , Julien Carl , Cordeau Pierre , Bohacek Ivan , Weng Yuan-Cheng , Calon Frédéric , Kriz Jasna 
Published: August 2011

Background and Purpose—
Consumption of fish has been shown to reduce risk of coronary heart disease and, possibly, of ischemic stroke. Because docosahexaenoic acid (DHA) is the most likely neuroactive component within fish oil, we hypothesized that exposing mice to a DHA-enriched diet may reduce inflammation and protect neurons against ischemic injury.

Methods—
To visualize the effects of DHA on neuroinflammation after stroke, TLR2-fluc-GFP transgenic mice were exposed to either a control diet, a diet depleted in n-3 polyunsaturated fatty acid, or a diet enriched in DHA during 3 months. Real-time biophotonic/bioluminescence imaging of the TLR2 response was performed before and after middle cerebral artery occlusion, whereas cytokines concentrations and stroke area analyses were performed at 3 and 7 days after middle cerebral artery occlusion, respectively.

Results—
We show that a 3-month DHA treatment prevented microglial activation after ischemic injury, reduced the ischemic lesion size, and increased levels of the antiapoptotic molecule Bcl-2 in the brain. Additional analysis revealed a significant decrease in the levels of COX2 and IL-1β, but not in other proinflammatory cytokines. Importantly, long-term DHA supplementation significantly changed the n-3:n-6 polyunsaturated fatty acid ratio in the brain.

Conclusions—
Collectively, these data indicate that diet-induced accumulation of DHA in the brain protects against postischemic inflammation and injury. Because DHA is widely available at low cost and has an excellent safety profile, our data suggest that increased DHA intake may provide protection against acute immune response/brain damage in ischemic stroke.
Diabetes and Poor Outcomes Within 6 Months After Acute Ischemic Stroke
Authors: Jia Qian , Zhao Xingquan , Wang Chunxue , Wang Yilong , Yan Yu , Li Hao , Zhong Liyong , Liu Liping , Zheng Huaguang , Zhou Yong , Wang Yongjun 
Published: August 2011

Background and Purpose—
Diabetes mellitus (DM) is an independent risk factor for ischemic stroke. However, controversy exists with regard to the impact of DM on prognosis after ischemic stroke in the Chinese population. We investigated the associations between DM and death, dependency, and stroke recurrence in patients after ischemic stroke onset in a nationwide, prospective registry, the China National Stroke Registry.

Methods—
The China National Stroke Registry consecutively recruited patients hospitalized for acute ischemic stroke in 2007 to 2008 and who were prospectively followed up for clinical and functional outcomes (death, dependency, and stroke recurrence) at 3 and 6 months after disease onset. Multivariable logistic regression was performed to analyze the association between DM and stroke outcomes after adjusting for potential confounding including age, sex, National Institutes of Health Stroke Scale score, glucose level at admission, hypertension, coronary heart disease, smoking, urinary tract infection, and other factors.

Results—
DM was identified in 3483 (27.0%) of stroke patients. Compared with stroke patients without DM, patients with DM had a significantly higher incidence of death or dependency and of recurrent stroke at 3 and 6 months after stroke onset. DM was an independent risk factor for death or dependency (adjusted odds ratio=1.23; 95% confidence interval, 1.10 to 1.37) in patients with ischemic stroke at 6 months after onset.

Conclusions—
DM independently predicted poor outcomes in Chinese patients after acute ischemic stroke.
Optimizing Protocols for Risk Prediction in Asymptomatic Carotid Stenosis Using Embolic Signal Detection
Authors: King Alice , Shipley Martin , Markus Hugh 
Published: August 2011

Background and Purpose—
Improved methods are required to identify patients with asymptomatic carotid stenosis at high risk for stroke. The Asymptomatic Carotid Emboli Study recently showed embolic signals (ES) detected by transcranial Doppler on 2 recordings that lasted 1-hour independently predict 2-year stroke risk. ES detection is time-consuming, and whether similar predictive information could be obtained from simpler recording protocols is unknown.

Methods—
In a predefined secondary analysis of Asymptomatic Carotid Emboli Study, we looked at the temporal variation of ES. We determined the predictive yield associated with different recording protocols and with the use of a higher threshold to indicate increased risk (≥2 ES). To compare the different recording protocols, sensitivity and specificity analyses were performed using analysis of receiver-operator characteristic curves.

Results—

Of 477 patients, 467 had baseline recordings adequate for analysis; 77 of these had ES on 1 or both of the 2 recordings. ES status on the 2 recordings was significantly associated (
P
<0.0001), but there was poor agreement between ES positivity on the 2 recordings (κ=0.266). For the primary outcome of ipsilateral stroke or transient ischemic attack, the use of 2 baseline recordings lasting 1 hour had greater predictive accuracy than either the first baseline recording alone (
P
=0.0005), a single 30-minute (
P
<0.0001) recording, or 2 recordings lasting 30 minutes (
P
<0.0001). For the outcome of ipsilateral stroke alone, two recordings lasting 1 hour had greater predictive accuracy when compared to all other recording protocols (all
P
<0.0001).

Conclusions—
Our analysis demonstrates the relative predictive yield of different recording protocols that can be used in application of the technique in clinical practice. Two baseline recordings lasting 1 hour as used in Asymptomatic Carotid Emboli Study gave the best risk prediction.
Multimodality Monitoring for Cerebral Perfusion Pressure Optimization in Comatose Patients With Intracerebral Hemorrhage
Authors: Ko Sang-Bae , Choi H. Alex , Parikh Gunjan , Helbok Raimund , Schmidt J. Michael , Lee Kiwon , Badjatia Neeraj , Claassen Jan , Connolly E. Sander , Mayer Stephan A. 
Published: August 2011

Background and Purpose—
Limited data exist to recommend specific cerebral perfusion pressure (CPP) targets in patients with intracerebral hemorrhage. We sought to determine the feasibility of brain multimodality monitoring for optimizing CPP and potentially reducing secondary brain injury after intracerebral hemorrhage.

Methods—

We retrospectively analyzed brain multimodality monitoring data targeted at perihematomal brain tissue in 18 comatose intracerebral hemorrhage patients (median monitoring, 164 hours). Physiological measures were averaged over 1-hour intervals corresponding to each microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio >40 with a brain glucose concentration <0.7 mmol/L. Brain tissue hypoxia (BTH) was defined as P
bt
O
2
<15 mm Hg. Pressure reactivity index and oxygen reactivity index were calculated.

Results—

Median age was 59 years, median Glasgow Coma Scale score was 6, and median intracerebral hemorrhage volume was 37.5 mL. The risk of BTH, and to a lesser extent metabolic crisis, increased with lower CPP values. Multivariable analyses showed that CPP <80 mm Hg was associated with a greater risk of BTH (odds ratio, 1.5; 95% confidence interval, 1.1–2.1;
P
=0.01) compared to CPP >100 mm Hg as a reference range. Six patients died (33%). Survivors had significantly higher CPP and P
bt
O
2
and lower ICP values starting on postbleed day 4, whereas lactate/pyruvate ratio and pressure reactivity index values were persistently lower, indicating preservation of aerobic metabolism and pressure autoregulation.

Conclusions—

P
bt
O
2
monitoring can be used to identify CPP targets for optimal brain tissue oxygenation. In patients who do not undergo multimodality monitoring, maintaining CPP >80 mm Hg may reduce the risk of BTH.
Inhibition of Protein Kinase Cβ Reverses Increased Blood–Brain Barrier Permeability During Hyperglycemic Stroke and Prevents Edema Formation In Vivo
Authors: Cipolla Marilyn J. , Huang Quillan , Sweet Julie G. 
Published: August 2011

Background and Purpose—
We investigated the effect of circulating factors and protein kinase Cβ on blood–brain barrier permeability and edema during hyperglycemic stroke.

Methods—
Male Wistar rats that were hyperglycemic by streptozotocin (50 mg/kg) for 5 to 6 days underwent middle cerebral artery occlusion (MCAO) for 2 hours with 2 hours of reperfusion. Blood–brain barrier permeability was measured in middle cerebral arteries that were ischemic (MCAO) or nonischemic (CTL) and perfused with plasma (20% in buffer) from MCAO or CTL animals. A separate set of MCAO vessels was perfused with the protein kinase Cβ inhibitor CGP53353 (0.5 μmol/L) and permeability measured. Lastly, hyperglycemic rats were treated intravenously with CGP53353 (10 or 100 μg/kg or vehicle 15 minutes before reperfusion and edema formation measured by wet:dry weights (n=6/group).

Results—

MCAO vessels had increased permeability compared with controls regardless of the plasma perfusate. Permeability (water flux, μm
3
×10
8
) of CTL vessel/CTL plasma (n=8), CTL vessel/MCAO plasma (n=7), MCAO vessel/CTL plasma (n=6), and MCAO vessel/MCAO plasma (n=6) was 0.98±0.11, 1.13±0.07, 1.36±0.02, and 1.34±0.06;
P
<0.01). Inhibition of protein kinase Cβ in MCAO vessels (n=6) reversed the increase in permeability (0.92±0.1;
P
<0.01). In vivo, hyperglycemia increased edema versus normoglycemia after MCAO (water content=78.84%±0.11% versus 81.38%±0.21%;
P
<0.01). Inhibition of protein kinase Cβ with 10 or 100 μg/kg CGP53353 during reperfusion prevented the increased edema in hyperglycemic animals (water content=79.54%±0.56% and 79.99%±0.43%;
P
<0.01 versus vehicle).

Conclusions—
These results suggest that the pronounced vasogenic edema that occurs during hyperglycemic stroke is mediated in large part by activation of protein kinase Cβ.
A Model of Motion Transparency Processing with Local Center-Surround Interactions and Feedback
Authors: Raudies Florian , Mingolla Ennio , Neumann Heiko 
Published: August 2011

Motion transparency occurs when multiple coherent motions are perceived in one spatial location. Imagine, for instance, looking out of the window of a bus on a bright day, where the world outside the window is passing by and movements of passengers inside the bus are reflected in the window. The overlay of both motions at the window leads to motion transparency, which is challenging to process. Noisy and ambiguous motion signals can be reduced using a competition mechanism for all encoded motions in one spatial location. Such a competition, however, leads to the suppression of multiple peak responses that encode different motions, as only the strongest response tends to survive. As a solution, we suggest a local center-surround competition for population-encoded motion directions and speeds. Similar motions are supported, and dissimilar ones are separated, by representing them as multiple activations, which occurs in the case of motion transparency. Psychophysical findings, such as motion attraction and repulsion for motion transparency displays, can be explained by this local competition. Besides this local competition mechanism, we show that feedback signals improve the processing of motion transparency. A discrimination task for transparent versus opaque motion is simulated, where motion transparency is generated by superimposing large field motion patterns of either varying size or varying coherence of motion. The model’s perceptual thresholds with and without feedback are calculated. We demonstrate that initially weak peak responses can be enhanced and stabilized through modulatory feedback signals from higher stages of processing.
Computing Confidence Intervals for Point Process Models
Authors: Sarma Sridevi V. , Nguyen David P. , Czanner Gabriela , Wirth Sylvia , Wilson Matthew A. , Suzuki Wendy , Brown Emery N. 
Published: August 2011

Abstract
Characterizing neural spiking activity as a function of intrinsic and extrinsic factors is important in neuroscience. Point process models are valuable for capturing such information; however, the process of fully applying these models is not always obvious. A complete model application has four broad steps: specification of the model, estimation of model parameters given observed data, verification of the model using goodness of fit, and characterization of the model using confidence bounds. Of these steps, only the first three have been applied widely in the literature, suggesting the need to dedicate a discussion to how the time-rescaling theorem, in combination with parametric bootstrap sampling, can be generally used to compute confidence bounds of point process models. In our first example, we use a generalized linear model of spiking propensity to demonstrate that confidence bounds derived from bootstrap simulations are consistent with those computed from closed-form analytic solutions. In our second example, we consider an adaptive point process model of hippocampal place field plasticity for which no analytical confidence bounds can be derived. We demonstrate how to simulate bootstrap samples from adaptive point process models, how to use these samples to generate confidence bounds, and how to statistically test the hypothesis that neural representations at two time points are significantly different. These examples have been designed as useful guides for performing scientific inference based on point process models.