bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pericyte-Derived Sphinogosine 1-Phosphate Induces the Expression of Adhesion Proteins and Modulates the Retinal Endothelial Cell Barrier
Authors: McGuire Paul G. , Rangasamy Sampathkumar , Maestas Joann , Das Arup 
Published: September 2011

Objective—
The mechanisms that regulate the physical interaction of pericytes and endothelial cells and the effects of these interactions on interendothelial cell junctions are not well understood. We determined the extent to which vascular pericytes could regulate pericyte-endothelial adhesion and the consequences that this disruption might have on the function of the endothelial barrier.

Methods and Results—
Human retinal microvascular endothelial cells were cocultured with pericytes, and the effect on the monolayer resistance of endothelial cells and expression of the cell junction molecules N-cadherin and VE-cadherin were measured. The molecules responsible for the effect of pericytes or pericyte-conditioned media on the endothelial resistance and cell junction molecules were further analyzed. Our results indicate that pericytes increase the barrier properties of endothelial cell monolayers. This barrier function is maintained through the secretion of pericyte-derived sphingosine 1-phosphate. Sphingosine 1-phosphate aids in maintenance of microvascular stability by upregulating the expression of N-cadherin and VE-cadherin, and downregulating the expression of angiopoietin 2.

Conclusion—
Under normal circumstances, the retinal vascular pericytes maintain pericyte-endothelial contacts and vascular barrier function through the secretion of sphingosine 1-phosphate. Alteration of pericyte-derived sphingosine 1-phosphate production may be an important mechanism in the development of diseases characterized by vascular dysfunction and increased permeability.
Presence of Intracranial Artery Calcification Is Associated With Mortality and Vascular Events in Patients With Ischemic Stroke After Hospital Discharge
Authors: Bugnicourt Jean-Marc , Leclercq Claire , Chillon Jean-Marc , Diouf Momar , Deramond Hervé , Canaple Sandrine , Lamy Chantal , Massy Ziad A. , Godefroy Olivier 
Published: September 2011

Background and Purpose—
Although intracranial artery calcification (IAC) has been reported to be a risk factor for ischemic stroke, the prognostic implications of IAC in stroke outcome are unknown. The purpose of this study was to determine the association between IAC and risk of vascular events and death in patients with stroke after hospital discharge.

Methods—
All patients with ischemic stroke over a 1-year period were included (n=302). IAC, assessed by multidetector CT, was defined as hyperdense foci (peak density >130 Hounsfield units) and assessed in the 7 major cerebral arteries. The IAC scores ranged from 0 (no calcification) to 7. Follow-up information on major clinical events (including fatal or nonfatal ischemic stroke, cardiac and peripheral artery events, and all-cause death) was obtained by means of a structured phone interview.

Results—

IAC was present in 260 patients (83%). With a mean follow-up of 773±223 days, 88 major clinical events occurred in 67 patients (22%): 45 new ischemic vascular events (ischemic stroke: n=22; cardiac event: n=15; peripheral artery event: n=8) and 43 deaths from any cause. Patients with the highest IAC scores had significantly higher rates of death and vascular events than those with the lowest IAC scores (log rank test,
P
=0.029). In the Cox proportional hazards regression model, the IAC score was significantly associated with major clinical events (hazard ratio, 1.34; 95% CI, 1.11–1.61;
P
=0.002).

Conclusions—
In patients with ischemic stroke, IAC detection may constitute a simple marker of a high risk of future major clinical events.
Carotid Intima-Media Thickness, Electrocardiographic Left Ventricular Hypertrophy, and Incidence of Intracerebral Hemorrhage
Authors: Folsom Aaron R. , Yatsuya Hiroshi , Psaty Bruce M. , Shahar Eyal , Longstreth W.T. 
Published: September 2011

Background and Purpose—
Carotid intima-media thickness and electrocardiographic left ventricular hypertrophy are 2 subclinical cardiovascular disease measures associated with increased risk of total and ischemic strokes. Increased intima-media thickness and electrocardiographic left ventricular hypertrophy also may reflect end-organ hypertensive effects. Information is scant on the associations of these subclinical measures with intracerebral hemorrhage (ICH). We hypothesized that greater carotid intima-media thickness and the presence of electrocardiographic left ventricular hypertrophy would be independently associated with increased ICH incidence.

Methods—
Among 18 155 participants initially free of stroke in the Atherosclerosis Risk in Communities Study (ARIC) and the Cardiovascular Health Study (CHS), we assessed carotid intima-media thickness, carotid plaque, and electrocardiographic left ventricular hypertrophy. Over a median of 18 years of follow-up, 162 incident ICH events occurred.

Results—

After adjustment for other ICH risk factors, carotid intima-media thickness was associated positively with incidence of ICH in both ARIC and CHS. The risk was lowest in study-specific Quartile 1, elevated 1.6- to 2.6-fold in Quartiles 2 to 3, and elevated 2.5 to 3.7-fold in Quartile 4 (
P
<0.05 for both studies). In CHS, having a carotid plaque was associated with a 2-fold (95% CI, 1.1–3.4) greater ICH risk than having no plaque, but only 1.2-fold (95% CI, 0.76–2.0) greater ICH risk in ARIC. Electrocardiographic left ventricular hypertrophy carried a hazard ratio of ICH of 1.7 (95% CI, 0.77–3.7) in CHS and 2.8 (95% CI, 1.2–6.4) in ARIC.

Conclusions—
Our data suggest that people with carotid atherosclerosis and possibly left ventricular hypertrophy are at increased risk not only of ischemic stroke, but also of ICH.
Fatalism, Optimism, Spirituality, Depressive Symptoms, and Stroke Outcome
Authors: Morgenstern Lewis B. , Sánchez Brisa N. , Skolarus Lesli E. , Garcia Nelda , Risser Jan M.H. , Wing Jeffrey J. , Smith Melinda A. , Zahuranec Darin B. , Lisabeth Lynda D. 
Published: September 2011

Background and Purpose—
We sought to describe the association of spirituality, optimism, fatalism, and depressive symptoms with initial stroke severity, stroke recurrence, and poststroke mortality.

Methods—
Stroke cases from June 2004 to December 2008 were ascertained in Nueces County, TX. Patients without aphasia were queried on their recall of depressive symptoms, fatalism, optimism, and nonorganizational spirituality before stroke using validated scales. The association between scales and stroke outcomes was studied using multiple linear regression with log-transformed National Institutes of Health Stroke Scale and Cox proportional hazards regression for recurrence and mortality.

Results—
Six hundred sixty-nine patients participated; 48.7% were women. In fully adjusted models, an increase in fatalism from the first to third quartile was associated with all-cause mortality (hazard ratio, 1.41; 95% CI, 1.06–1.88) and marginally associated with risk of recurrence (hazard ratio, 1.35; 95% CI, 0.97–1.88), but not stroke severity. Similarly, an increase in depressive symptoms was associated with increased mortality (hazard ratio, 1.32; 95% CI, 1.02–1.72), marginally associated with stroke recurrence (HR, 1.22; 95% CI, 0.93–1.62), and with a 9.0% increase in stroke severity (95% CI, 0.01–18.0). Depressive symptoms altered the fatalism–mortality association such that the association of fatalism and mortality was more pronounced for patients reporting no depressive symptoms. Neither spirituality nor optimism conferred a significant effect on stroke severity, recurrence, or mortality.

Conclusions—
Among patients who have already had a stroke, self-described prestroke depressive symptoms and fatalism, but not optimism or spirituality, are associated with increased risk of stroke recurrence and mortality. Unconventional risk factors may explain some of the variability in stroke outcomes observed in populations and may be novel targets for intervention.
Neuroprotection by Interleukin-6 Is Mediated by Signal Transducer and Activator of Transcription 3 and Antioxidative Signaling in Ischemic Stroke
Authors: Jung Joo Eun , Kim Gab Seok , Chan Pak H. 
Published: September 2011

Background and Purpose—
Interleukin-6 (IL-6) has been shown to have a neuroprotective effect in brain ischemic injury. However, its molecular mechanisms are still poorly understood. In this study, we investigated the neuroprotective role of the IL-6 receptor (IL-6R) by IL-6 in the reactive oxygen species defense system after transient focal cerebral ischemia (tFCI).

Methods—
IL-6 was injected in mice before and after middle cerebral artery occlusion. Coimmunoprecipitation assays were performed for analysis of an IL-6R association after tFCI. Primary mouse cerebral cortical neurons were transfected with small interfering RNA probes targeted to IL-6Rα or gp130 and were used for chromatin-immunoprecipitation assay, luciferase promoter assay, and cell viability assay. Reduction in infarct volumes by IL-6 was measured after tFCI.

Results—
IL-6R was disrupted through a disassembly between IL-6Rα and gp130 associated by protein oxidation after reperfusion after tFCI. This suppressed phosphorylation of signal transducer and activator of transcription 3 (STAT3) and finally induced neuronal cell death through a decrease in manganese–superoxide dismutase. However, IL-6 injections prevented disruption of IL-6R against reperfusion after tFCI, consequently restoring activity of STAT3 through recovery of the binding of STAT3 to gp130. Moreover, IL-6 injections restored the transcriptional activity of the manganese–superoxide dismutase promoter through recovery of the recruitment of STAT3 to the manganese–superoxide dismutase promoter and reduced infarct volume after tFCI.

Conclusions—
This study demonstrates that IL-6 has a neuroprotective effect against cerebral ischemic injury through IL-6R-mediated STAT3 activation and manganese–superoxide dismutase expression.
Plasma-Type Gelsolin Is Decreased in Human Blood and Cerebrospinal Fluid After Subarachnoid Hemorrhage
Authors: Chou Sherry H.-Y. , Lee Po-Shun , Konigsberg Rachael G. , Gallacci Dana , Chiou Terry , Arai Ken , Simmons Suzanne , Bauer David , Feske Steven K. , Lo Eng H. , Ning MingMing 
Published: September 2011

Background and Purpose—
Subarachnoid hemorrhage (SAH) pathophysiology involves neurovascular proteolysis and inflammation. How these 2 phenomena are related remains unclear. We hypothesize that matrix metalloproteinases (MMPs) mediate the depletion of anti-inflammatory plasma-type gelsolin (pGSN).

Methods—
We enrolled 42 consecutive SAH subjects and sampled cerebrospinal fluid (CSF) and blood on post-SAH Days 2 to 3, 4 to 5, 6 to 7, and 10 to 14. Control subjects were 20 consecutive non-SAH hydrocephalus patients with lumbar drains. Enzyme-linked immunosorbent assay, Western blotting, and zymography were used to quantify pGSN and MMP-9.

Results—

In CSF, pGSN was lower in SAH compared with control subjects on post-SAH Days 2 to 3 (
P
=0.0007), 4 to 5 (
P
=0.041), and 10 to 14 (
P
=0.007). In blood, pGSN decreased over time (
P
=0.001) and was lower in SAH compared with control subjects on post-SAH Days 4 to 5 (
P
=0.037), 6 to 7 (
P
=0.006), and 10 to 14 (
P
=0.006). Western blots demonstrated that SAH CSF had novel bands at 52 and 46 kDa, representing cleaved pGSN fragments. Gelatin zymography showed that CSF MMP-9 was elevated in SAH compared with control subjects. Higher CSF MMP-9 correlated with lower CSF pGSN on post-SAH Day 7
(r
=−0.38;
P
=0.05).

Conclusions—
SAH is associated with decreased CSF and blood pGSN and elevated CSF MMP-9. Novel cleaved pGSN fragments are present in CSF of SAH subjects, consistent with pGSN cleavage by MMPs. Because pGSN is known to inhibit inflammatory mediators, these findings suggest that MMPs may reduce pGSN and exacerbate inflammation after SAH. Further studies are warranted to investigate the mechanisms underlying MMP–pGSN signaling in SAH.
A Context-Theoretic Framework for Compositionality in Distributional Semantics
Authors: Clarke Daoud 
Published: September 2011

Formalizing “meaning as context” mathematically leads to a new, algebraic theory of meaning, in which composition is bilinear and associative. These properties are shared by other methods that have been proposed in the literature, including the tensor product, vector addition, point-wise multiplication, and matrix multiplication. Entailment can be represented by a vector lattice ordering, inspired by a strengthened form of the distributional hypothesis, and a degree of entailment is defined in the form of a conditional probability. Approaches to the task of recognizing textual entailment, including the use of subsequence matching, lexical entailment probability, and latent Dirichlet allocation, can be described within our framework.
Factor VIII alters tubular organization and functional properties of von Willebrand factor stored in Weibel-Palade bodies
Authors: Bouwens Eveline A. M. , Mourik Marjon J. , van den Biggelaar Maartje , Eikenboom Jeroen C. J. , Voorberg Jan , Valentijn Karine M. , Mertens Koen 
Published: September 2011

AbstractIn endothelial cells, von Willebrand factor (VWF) multimers are packaged into tubules that direct biogenesis of elongated Weibel-Palade bodies (WPBs). WPB release results in unfurling of VWF tubules and assembly into strings that serve to recruit platelets. By confocal microscopy, we have previously observed a rounded morphology of WPBs in blood outgrowth endothelial cells transduced to express factor VIII (FVIII). Using correlative light-electron microscopy and tomography, we now demonstrate that FVIII-containing WPBs have disorganized, short VWF tubules. Whereas normal FVIII and FVIII Y1680F interfered with formation of ultra-large VWF multimers, release of the WPBs resulted in VWF strings of equal length as those from nontransduced blood outgrowth endothelial cells. After release, both WPB-derived FVIII and FVIII Y1680F remained bound to VWF strings, which however had largely lost their ability to recruit platelets. Strings from nontransduced cells, however, were capable of simultaneously recruiting exogenous FVIII and platelets. These findings suggest that the interaction of FVIII with VWF during WPB formation is independent of Y1680, is maintained after WPB release in FVIII-covered VWF strings, and impairs recruitment of platelets. Apparently, intra-cellular and extracellular assembly of FVIII-VWF complex involves distinct mechanisms, which differ with regard to their implications for platelet binding to released VWF strings.
Anti–Escherichia coli asparaginase antibody levels determine the activity of second-line treatment with pegylated E coli asparaginase: a retrospective analysis within the ALL-BFM trials
Authors: Willer Andrea , Gerß Joachim , König Thorsten , Franke Dieter , Kühnel Hans-Jürgen , Henze Günter , von Stackelberg Arendt , Möricke Anja , Schrappe Martin , Boos Joachim , Lanvers-Kaminsky Claudia 
Published: September 2011

AbstractHypersensitivity reactions limit the use of the antileukemic enzyme asparaginase (ASE). We evaluated Ab levels against Escherichia coli ASE and ASE activity in 1221 serum samples from 329 patients with acute lymphoblastic leukemia who had received ASE treatment according to the ALL-BFM 2000 or the ALL-REZ BFM 2002 protocol for primary or relapsed disease. ASE activity during first-line treatment with native E coli ASE and second-line treatment with pegylated E coli ASE was inversely related to anti–E coli ASE Ab levels (P < .0001; Spearman rank order correlation). An effect on ASE activity during second-line treatment with pegylated E coli ASE was, however, only observed when anti–E coli ASE Ab levels were high (> 200 AU/mL). In the presence of moderate or intermediate Ab levels (6.25-200 AU/mL) the switch from native to pegylated E coli ASE resulted in a significant increase of ASE activity above the threshold of 100 U/L (P < .05). Erwinia chrysanthemi ASE activity was not correlated with anti–E coli ASE Ab levels. Erwinia ASE was found to be the best ASE alternative if Ab levels against E coli ASE exceed 200 AU/mL. This retrospective analysis is the first to describe the relationship between the level of anti–E coli ASE Abs and serum activity of pegylated E coli ASE used second-line after native E coli ASE. These studies are registered at http://clinicaltrials.org as NTC00430118 and NCT00114348.
Prevalence and risk factors of diabetes and impaired fasting glucose in Nauru
Authors: Khambalia Amina , Phongsavan Philayrath , Smith Ben J , Keke Kieren , Dan Li , Fitzhardinge Andrew , Bauman Adrian E 
Published: September 2011

Abstract

Background
No comprehensive assessment of diabetes prevalence in Nauru has been conducted since an extreme prevalence was documented more than two decades ago. This study aims to determine the prevalence and risk factors of diabetes and impaired fasting glucose.

Methods
A nationwide survey in 2004 of people aged 15- 64 years (n = 1592). Fasting plasma glucose levels were used to defined diabetes (≥7.0 mmol/l or 126 mg/dl) and prediabetes (6.1-6.9 mmol/l or 110-125 mg/dl).

Results
The sex-standardized prevalence of diabetes was 13.0% (95% CI: 10.6, 15.4) in men, 14.4% (11.9, 16.9) in women, and 13.7% (12.0, 15.4) combined. The sex-standardized prevalence of prediabetes was 6.4% (4.6, 8.2) for men, 5.5% (3.9, 7.2) for women, and 6.0% (4.8, 7.3) combined. The prevalence of diabetes for individuals 15-24, 25-34, 35-44, 45-54 and 55-64 years was 4.5%, 7.6%, 24.1%, 32.9%, and 42.7%, respectively. The prevalence of prediabetes for the same age categories was 4.2%, 8.8%, 5.9%, 6.6%, 7.1%, respectively. Multivariable, multinomial logit modeling found risk factors for prediabetes were high cholesterol levels (OR: 2.02, 95% CI: 1.66, 2.47) and elevated waist circumference (OR: 1.04, 95% CI: 1.00, 1.08), and for diabetes were age in years (OR: 1.06; 95% CI: 1.04, 1.07), cholesterol levels (OR: 1.84, 95% CI: 1.58, 2.14) and waist circumference (OR: 1.04, 95% CI: 1.02, 1.07).

Conclusions
Diabetes remains a major public health problem in Nauru, affecting one out of every ten people. While the prevalence of diabetes has declined, its burden has persisted among the old but also extended towards the younger age groups.
Primary care provider perceptions of intake transition records and shared care with outpatient cardiac rehabilitation programs
Authors: Yee Jonathan , Unsworth Karen , Suskin Neville , Reid Robert D , Jamnik Veronica , Grace Sherry L 
Published: September 2011

Abstract

Background
While it is recommended that records are kept between primary care providers (PCPs) and specialists during patient transitions from hospital to community care, this communication is not currently standardized. We aimed to assess the transmission of cardiac rehabilitation (CR) program intake transition records to PCPs and to explore PCPs' needs in communication with CR programs and for intake transition record content.

Method
144 PCPs of consenting enrollees from 8 regional and urban Ontario CR programs participated in this cross-sectional study. Intake transition records were tracked from the CR program to the PCP's office. Sixty-six PCPs participated in structured telephone interviews.

Results
Sixty-eight (47.6%) PCPs received a CR intake transition record. Fifty-eight (87.9%) PCPs desired intake transition records, with most wanting it transmitted via fax (n = 52, 78.8%). On a 5-point Likert scale, PCPs strongly agreed that the CR transition record met their needs for providing patient care (4.32 ± 0.61), with 48 (76.2%) reporting that it improved their management of patients' cardiac risk. PCPs rated the following elements as most important to include in an intake transition record: clinical status (4.67 ± 0.64), exercise test results (4.61 ± 0.52), and the proposed patient care plan (4.59 ± 0.71).

Conclusions
Less than half of intake transition records are reaching PCPs, revealing a large gap in continuity of patient care. PCP responses should be used to develop an evidence-based intake transition record, and procedures should be implemented to ensure high-quality transitional care.
Fusion with extracellular domain of cytotoxic T-lymphocyte-associated-antigen 4 leads to enhancement of immunogenicity of Hantaan virus DNA vaccines in C57BL/6 mice
Authors: Liu Feng , Liang Mifang , Cao Shouchun , Liu Qinzhi , Zhang Quanfu , Li Chuan , Zhang Shuo , Wang Shiwen , Li Dexin 
Published: September 2011

Abstract

Background
Hantaan virus (HTNV) is the causative agent of the most severe form of a rodent-borne disease known as hemorrhagic fever with renal syndrome (HFRS). A safe and effective HTNV vaccine is needed. Vaccination with DNA constructs expressing fused antigen with bioactive factors, has shown promising improvement of immunogenicity for viral agents in animal models, but the effect of fusion strategy on HTNV DNA vaccine has not been investigated.

Results
DNA plasmids encoding the HTNV nucleocapsid protein (N) and glycoprotein (Gn and Gc) in fusion to the extracellular domain of cytotoxic T-lymphocyte-associated-antigen 4 (eCTLA-4) targeting to antigen presenting cells (APCs) were constructed. Intramuscular immunization of mice with plasmids expressing eCTLA-4-HTNV-N/GP fusion proteins leads to a significant enhancement of the specific antibody response as well as cytotoxic T-lymphocyte (CTL) response in C57BL/6 mice. Moreover, this effect could be further augmented when co-administered with CpG motifs.

Conclusions
Modification of viral antigen in fusion to bioactive factor will be promising to confer efficient antigen presentation and improve the potency of DNA vaccine in mice.
Intravascular large B-cell lymphoma of the kidney: A case report
Authors: Bai Xiaoyan , Li Xiao , Wan Liyan , Wang Guobao , Jia Nan , Geng Jian 
Published: September 2011

Abstract
We report a 41-year-old Chinese woman with intravascular large B-cell lymphoma diagnosed by percutaneous renal biopsy. The patient was admitted to Nanfang Hospital of Southern Medical University, Guangzhou, China with complaints of high spiking fever for a month and bilateral lower limb fatigue with difficulty ambulating for the past 5 months.
She had renal dysfunction with a total urinary protein of 5.61 g/dL (56.1 g/L), serum albumin of 2.89 g/dL (28.9 g/L), urea nitrogen of 2.24 mg/dL (1.6 mmol/L), and serum creatinine of 0.54 mg/dL (48 μmol/L). Bone marrow biopsy revealed myeloproliferative disorder without abnormal myeloid or lymphocytic proliferation. Positron Emission Tomography-Computed Tomography (PET-CT) showed marked bilateral swelling and enlargement of the renal parenchyma with splenic enlargement and involvement of multiple vertebrae. Percutaneous renal biopsy showed island-like accumulations of medium to large lymphoid cells in many areas of the interstitium, with round vesicular nuclei containing distinct basophilic nucleoli. Immunohistochemical analysis together with other supportive investigation confirmed the diagnosis of intravascular large B-cell lymphoma. Ten days later, she was started on chemotherapy with CHOP (cyclophosphamide, doxorubicin, leurocristime and prednisone) for a week. Palliative radiotherapy DT 40Gy/20F with other supportive treatment was provided for metastatic foci in the medullary cavity of the sternum, T1-T7. The patient regained muscle strength in both lower limbs and was able to walk again after three weeks. The patient was discharged after hepatic and renal function and proteinuria values had returned to normal. Follow-up data shows the patient to be alive nine months after discharge.

Virtual Slides

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