bluuebunny/crossref_metadata_2025_split huggingface dataset:
Race and Gender Differences in 1-Year Outcomes for Community-Dwelling Stroke Survivors With Family Caregivers
Authors: Roth David L. , Haley William E. , Clay Olivio J. , Perkins Martinique , Grant Joan S. , Rhodes J. David , Wadley Virginia G. , Kissela Brett , Howard George 
Published: January 2011

Background and Purpose—
Previous research has reported worse outcomes after stroke for women and for African Americans, but few prospective population-based studies have systematically examined demographic differences on long-term stroke outcomes. Race and gender differences in 1-year stroke outcomes were examined using an epidemiologically derived sample of first-time stroke survivors from the national REasons for Geographic and Racial Differences in Stroke (REGARDS) study.

Methods—
Participants of REGARDS who reported a first-time stroke event during regular surveillance calls were interviewed by telephone and then completed an in-home evaluation approximately 1 year after the verified first-time stroke event (N=112). A primary family caregiver was also enrolled and interviewed for each stroke survivor. Measures from the in-home evaluation included previously validated stroke outcomes assessments of neurological deficits, functional impairments, and patient-reported effects of stroke in multiple domains.

Results–
African American stroke survivors were less likely to be living with their primary family caregivers than white participants. Analyses that controlled for age, education, and whether the stroke survivors lived with their primary family caregivers indicated that African Americans and women showed significantly greater deficits on multiple 1-year outcome measures compared to whites and men, respectively.

Conclusions—
Among community-dwelling stroke survivors with family caregivers, women and African Americans are at heightened risk for poor long-term outcomes 1 year after first-time stroke events. Rehabilitation services and public health policies aimed at enhancing stroke recovery rates should address these disparities in poststroke outcomes.
Stromal-Derived Factor-1α Correlates With Circulating Endothelial Progenitor Cells and With Acute Lesion Volume in Stroke Patients
Authors: Bogoslovsky Tanya , Spatz Maria , Chaudhry Aneeka , Maric Dragan , Luby Marie , Frank Joseph , Warach Steven 
Published: January 2011

Background and Purpose—
Endothelial progenitor cells (EPC) are important participants of neovascularization and are mobilized through signaling with stromal-derived factor (SDF-1α), vascular endothelial growth factor (VEGF), granulocyte colony-stimulating factor, and stem cell factor. The association between EPC levels and these growth factors (GF) in acute stroke has not been previously established. We aimed to determine the association between EPC and these GF, and to elucidate a relationship between these GF and stroke severity in acute stroke patients.

Methods—
Seventeen patients were selected from 175 patients with imaging-confirmed acute ischemic stroke. EPC were quantified using CD34, CD133, and VEGF-R2 markers. Plasma VEGF, SDF-1α, granulocyte colony-stimulating factor, and stem cell factor were determined by enzyme-linked immunosorbent assay on days 1 and 3, and brain MRI was performed at baseline and on days 1 and 5 after the stroke onset.

Results—

Levels of SDF-1α strongly (
r
=0.6) correlated with the numbers of EPC subsets CD133
+
VEFG-R2
+
(
P
<0.004), CD34
+
VEGF-R2
+
(
P
<0.01), and CD34
+
CD133
+
VEGF-R2
+
(
P
<0.01) on day 1. Stem cell factor strongly (
r
=0.5) correlated with CD133
+
VEGF-R2
+
(
P
<0.05). SDF-1α moderately inversely (
r
=−0.49) correlated with baseline diffusion-weighted imaging lesion volumes (
P
<0.04). Median levels of SDF-1α (1561 pg/mL) increased (
P
<0.04) on day 3 compared to day 1 (1379 pg/mL). Similarly, VEGF at day 3 (95 pg/mL) increased (
P
<0.03) compared to day 1 (64 pg/mL).

Conclusions—
These results indicate that SDF-1α and stem cell factor correlate with an increase in EPC early in ischemic stroke patients.
Granulocyte Colony-Stimulating Factor Enhances Arteriogenesis and Ameliorates Cerebral Damage in a Mouse Model of Ischemic Stroke
Authors: Sugiyama Yukio , Yagita Yoshiki , Oyama Naoki , Terasaki Yasukazu , Omura-Matsuoka Emi , Sasaki Tsutomu , Kitagawa Kazuo 
Published: January 2011

Background and Purpose—
Enhancing collateral artery growth is a potent therapeutic approach to treat cardiovascular ischemic disease from occlusive artery. Granulocyte–macrophage colony-stimulating factor (GM-CSF) has gained attention for its ability to promote arteriogenesis, ameliorating brain damage, by the mechanisms involving monocyte upregulation. However, the recent clinical study testing its efficacy in myocardial ischemia has raised the question about its safety. We tested alternative colony-stimulating factors for their effects on collateral artery growth and brain protection.

Methods—
Brain hypoperfusion was produced by occluding the left common carotid artery in C57/BL6 mice. After the surgery, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, or GM-CSF (100 μg/kg/day) was administered daily for 5 days. The angioarchitecture for leptomeningeal anastomoses and the circle of Willis were visualized after the colony-stimulating factor treatment. Circulating blood monocytes and Mac-2-positive cells in the dorsal surface of the brain were determined. A set of animals underwent subsequent ipsilateral middle cerebral artery occlusion and infarct volume was assessed.

Results—
Granulocyte colony-stimulating factor as well as GM-CSF promoted leptomeningeal collateral growth after common carotid artery occlusion. Both granulocyte colony-stimulating factor and GM-CSF increased circulating blood monocytes and Mac-2-positive cells in the dorsal brain surface, suggesting the mechanisms coupled to monocyte upregulation might be shared. Infarct volume after middle cerebral artery occlusion was reduced by granulocyte colony-stimulating factor, similarly to GM-CSF. Macrophage colony-stimulating factor showed none of theses effects.

Conclusions—
Granulocyte colony-stimulating factor enhances collateral artery growth and reduces infarct volume in a mouse model of brain ischemia, similarly to GM-CSF.
High Frequency of Silent Pulmonary Embolism in Patients With Cryptogenic Stroke and Patent Foramen Ovale
Authors: Tanislav Christian , Puille Maximilian , Pabst Wolfgang , Reichenberger Frank , Grebe Mathias , Nedelmann Max , Kaps Manfred , Allendörfer Jens 
Published: January 2011

Background and Purpose—
Deep vein thrombosis and pulmonary embolism (PE) prove venous embolic activity and enforce the suspicion of paradoxical embolism in patients with stroke with patent foramen ovale. Because it has implications in secondary prevention, we investigated the frequency of silent PE in such a cohort of patients.

Methods—
Patients with cryptogenic stroke or transient ischemic attack and patent foramen ovale who underwent a ventilation perfusion scintigraphy were identified from a stroke registry. Blinded from clinical data, ventilation perfusion scintigraphy scans were re-evaluated independently by 2 experts. Patients showing at least a subsegmental defect were considered as having silent PE. Factors potentially associated with PE were analyzed.

Results—

The evaluation included 151 patients. Median age was 55.2 years and 59.9% were male. In 56 (37%) patients, silent PE was found; a deep vein thrombosis was evident in 11 (7%) patients. Atrial septal aneurysm was identified in 39 patients and hypermobile atrial septum in 37 patients. Atrial septal aneurysm and hypermobile atrial septum were independently associated with PE. In females, intake of oral contraceptives showed certain association with PE (6 of 25 versus 3 of 40;
P
=0.07).

Conclusions—
Silent PE frequently occurs in patients with cryptogenic stroke and patent foramen ovale, particularly when atrial septal aneurysm or hypermobile atrial septum are present.
Clopidogrel Versus Dipyridamole in Addition to Aspirin in Reducing Embolization Detected With Ambulatory Transcranial Doppler
Authors: King Alice , Bath Philip M.W. , Markus Hugh S. 
Published: January 2011

Background and Purpose—
After stroke and transient ischemic attack there is a high early risk of recurrent stroke, particularly in large artery disease. It has been suggested more intensive antiplatelet regimens are required, but trial data are lacking. Treatment efficacy can be evaluated using transcranial Doppler detection of embolic signals. Ambulatory transcranial Doppler has recently been developed; prolonged recording may reduce subject numbers required to determine therapeutic efficacy. In a randomized trial (ISRCTN68019845) with blinded end point evaluation, we determined whether treatment with dipyridamole or clopidogrel, in addition to aspirin, was more effective at reducing embolization.

Methods—
Consecutive patients with recent symptomatic carotid stenosis were recruited. Ambulatory transcranial Doppler and platelet aggregometry were performed at baseline and 48 hours. Patients, all on aspirin, were randomized to dipyridamole or clopidogrel. Recordings were analyzed offline masked to subject identity.

Results—

Sixty patients were recruited, 30 in each arm. The primary end point of change in embolic signal frequency did not differ between groups (
P
=0.36). In patients with embolic signals at baseline, there was no difference in reduction in embolic signal frequency: dipyridamole (75.5; SD 17.7%) versus clopidogrel (77.5; SD 20.5%;
P
=0.77). Baseline platelet aggregation was not different between regimens, but at 48 hours, adenosine 5′-diphosphate aggregation rate (but not collagen) was lower with clopidogrel (
P
<0.001).

Conclusions—
Both dipyridamole and clopidogrel reduced embolization to a similar extent. Embolic signals are strong predictors of future stroke rate in this patient group. Our results suggest these 2 treatment regimens have similar efficacy in early secondary prevention of stroke, although this now needs testing in large Phase III trials.
Syntactic Processing Using the Generalized Perceptron and Beam Search
Authors: Zhang Yue , Clark Stephen 
Published: January 2011

We study a range of syntactic processing tasks using a general statistical framework that consists of a global linear model, trained by the generalized perceptron together with a generic beam-search decoder. We apply the framework to word segmentation, joint segmentation and POS-tagging, dependency parsing, and phrase-structure parsing. Both components of the framework are conceptually and computationally very simple. The beam-search decoder only requires the syntactic processing task to be broken into a sequence of decisions, such that, at each stage in the process, the decoder is able to consider the top-n candidates and generate all possibilities for the next stage. Once the decoder has been defined, it is applied to the training data, using trivial updates according to the generalized perceptron to induce a model. This simple framework performs surprisingly well, giving accuracy results competitive with the state-of-the-art on all the tasks we consider. The computational simplicity of the decoder and training algorithm leads to significantly higher test speeds and lower training times than their main alternatives, including log-linear and large-margin training algorithms and dynamic-programming for decoding. Moreover, the framework offers the freedom to define arbitrary features which can make alternative training and decoding algorithms prohibitively slow. We discuss how the general framework is applied to each of the problems studied in this article, making comparisons with alternative learning and decoding algorithms. We also show how the comparability of candidates considered by the beam is an important factor in the performance. We argue that the conceptual and computational simplicity of the framework, together with its language-independent nature, make it a competitive choice for a range of syntactic processing tasks and one that should be considered for comparison by developers of alternative approaches.
The Risk of Torture as a Basis for Refusing Extradition and the Use of Diplomatic Assurances to Protect against Torture after 9/11
Authors: Johnston Jeffrey 
Published: January 2011

AbstractDiplomatic assurances have become increasingly common since 9/11 as conditions of removing suspected terrorists to other countries, including through the process of extradition, in response to claims that these individuals will be tortured following their return. Assurances have sometimes been relied upon by states to justify the removal of persons to countries where these individuals have been tortured despite the existence of assurances. Focusing on the extradition context, this article will explore the debate surrounding the use of diplomatic assurances to protect against torture. The article will demonstrate that the use of assurances to address a risk of torture is permissible under international law. With a view to strengthening human rights protection, the article will propose the establishment of minimum standards for the use of assurances and common criteria to be applied in assessing whether assurances can be viewed as sufficiently reliable in protecting against a risk of torture.
Genocide in Rwanda – Is It Really Finland's Concern?
Authors: Kimpimäki Minna 
Published: January 2011

AbstractIn June 2010, a Rwandan citizen, Francois Bazaramba, was sentenced in a Finnish court of first instance, to life imprisonment for acts of genocide committed in Rwanda in 1994. This was the first time that the provisions of Finnish law dealing with genocide had ever been applied in a court. This article examines the details of this case, as well as the Finnish legislation on genocide, jurisdiction and extradition. Many of the questions considered in this article are not only typical for Finland, but have a more general bearing as well. For instance, the issues relating to the transfer or extradition of fugitives to Rwanda have recently been considered in several national and international jurisdictions. A trial conducted in a national court on the basis of universal jurisdiction reveals in a concrete way the advantages and disadvantages of this form of prosecution.
Low doses of natural killer T cells provide protection from acute graft-versus-host disease via an IL-4–dependent mechanism
Authors: Leveson-Gower Dennis B. , Olson Janelle A. , Sega Emanuela I. , Luong Richard H. , Baker Jeanette , Zeiser Robert , Negrin Robert S. 
Published: January 2011

AbstractCD4+ natural killer T (NKT) cells, along with CD4+CD25+ regulatory T cells (Tregs), are capable of controlling aberrant immune reactions. We explored the adoptive transfer of highly purified (> 95%) CD4+NKT cells in a murine model of allogeneic hematopoietic cell transplantation (HCT). NKT cells follow a migration and proliferation pattern similar to that of conventional T cells (Tcons), migrating initially to secondary lymphoid organs followed by infiltration of graft-versus-host disease (GVHD) target tissues. NKT cells persist for more than 100 days and do not cause significant morbidity or mortality. Doses of NKT cells as low as 1.0 × 104 cells suppress GVHD caused by 5.0 × 105 Tcons in an interleukin-4 (IL-4)–dependent mechanism. Protective doses of NKT cells minimally affect Tcon proliferation, but cause significant reductions in interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production by donor Tcons and in skin, spleen, and gastrointestinal pathology. In addition, NKT cells do not impact the graft-versus-tumor (GVT) effect of Tcons against B-cell lymphoma-1 (BCL-1) tumors. These studies elucidate the biologic function of donor-type CD4+NKT cells in suppressing GVHD in an allogeneic transplantation setting, demonstrating clinical potential in reducing GVHD in HCT.
Hypoxia-inducible factors in human pulmonary arterial hypertension: a link to the intrinsic myeloid abnormalities
Authors: Farha Samar , Asosingh Kewal , Xu Weiling , Sharp Jacqueline , George Deepa , Comhair Suzy , Park Margaret , Tang W. H. Wilson , Loyd James E. , Theil Karl , Tubbs Raymond , Hsi Eric , Lichtin Alan , Erzurum Serpil C. 
Published: January 2011

AbstractPulmonary arterial hypertension (PAH) is a proliferative vasculopathy characterized by high circulating CD34+CD133+ proangiogenic progenitors, and endothelial cells that have pathologic expression of hypoxia-inducible factor 1 α (HIF-1α). Here, CD34+CD133+ progenitor cell numbers are shown to be higher in PAH bone marrow, blood, and pulmonary arteries than in healthy controls. The HIF-inducible myeloid-activating factors erythropoietin, stem cell factor (SCF), and hepatocyte growth factor (HGF) are also present at higher than normal levels in PAH blood, and related to disease severity. Primary endothelial cells harvested from human PAH lungs produce greater HGF and progenitor recruitment factor stromal-derived factor 1 α (SDF-1α) than control lung endothelial cells, and thus may contribute to bone marrow activation. Even though PAH patients had normal numbers of circulating blood elements, hematopoietic alterations in myeloid and erythroid lineages and reticulin fibrosis identified a subclinical myeloproliferative process. Unexpectedly, evaluation of bone marrow progenitors and reticulin in nonaffected family members of patients with familial PAH revealed similar myeloid abnormalities. Altogether, the results show that PAH is linked to myeloid abnormalities, some of which may be related to increased production of HIF-inducible factors by diseased pulmonary vasculature, but findings in nonaffected family suggest myeloid abnormalities may be intrinsic to the disease process.
Protein kinases modulate store-operated channels in pulmonary artery smooth muscle cells
Authors: Chen I-Shan , Dai Zen-Kong , Welsh Donald G , Chen Ing-Jun , Wu Bin-Nan 
Published: January 2011

Abstract

Background
This study investigates whether protein kinase G (PKG), protein kinase A (PKA) and protein kinase C (PKC) are involved in the regulatory mechanisms of store-operated channel (SOC) in pulmonary arteries.

Methods
Pulmonary artery smooth muscle cells (PASMCs) were enzymatically dissociated from rat intralobar pulmonary arteries. Whole cell, cell-attached and inside-out patch-clamp electrophysiology were used to monitor SOCs in isolated PASMCs.

Results
Initially the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA, 10 μM) initiated a whole cell current that was reduced by the SOC blocker SKF-96365 (10 μM). Subsequent work using both cell-attached and whole cell configurations revealed that the PKG and PKA inhibitors, KT5823 (3 μM) and H-89 (10 μM), also stimulated SOC activity; this augmentation was attenuated by the SOC blockers SKF-96365 (10 μM) and Ni2+ (0.1 mM). Finally using the inside-out configuration, the PKC activator phorbol 12-myristate 13-acetate (PMA, 10 μM) was confirmed to modestly stimulate SOC activity although this augmentation appeared to be more substantial following the application of 10 μM inositol 1,4,5-triphosphate (Ins(1,4,5)P3).

Conclusions
SOC activity in PASMCs was stimulated by the inhibition of PKG and PKA and the activation of PKC. Our findings suggest that the SOC could be a substrate of these protein kinases, which therefore would regulate the intracellular concentration of calcium and pulmonary arteriopathy via SOC.
Macrophage presence is essential for the regeneration of ascending afferent fibres following a conditioning sciatic nerve lesion in adult rats
Authors: Aguilar Salegio Ernesto A , Pollard Anthony N , Smith Malcolm , Zhou Xin-Fu 
Published: January 2011

AbstractBackgroundInjury to the peripheral branch of dorsal root ganglia (DRG) neurons prior to injury to the central nervous system (CNS) DRG branch results in the regeneration of the central branch. The exact mechanism mediating this regenerative trigger is not fully understood. It has been proposed that following peripheral injury, the intraganglionic inflammatory response by macrophage cells plays an important role in the pre-conditioning of injured CNS neurons to regenerate. In this study, we investigated whether the presence of macrophage cells is crucial for this type of regeneration to occur. We used a clodronate liposome technique to selectively and temporarily deplete these cells during the conditioning phase of DRG neurons.ResultsRetrograde and anterograde tracing results indicated that in macrophage-depleted animals, the regenerative trigger characteristic of pre-conditioned DRG neurons was abolished as compared to injury matched-control animals. In addition, depletion of macrophage cells led to: (i) a reduction in macrophage infiltration into the CNS compartment even after cellular repopulation, (ii) astrocyte up-regulation at rostral regions and down-regulation in brain derived neurotrophic factor (BDNF) concentration in the serum.ConclusionActivation of macrophage cells in response to the peripheral nerve injury is essential for the enhanced regeneration of ascending sensory neurons.
Apoptosis-related deregulation of proteolytic activities and high serum levels of circulating nucleosomes and DNA in blood correlate with breast cancer progression
Authors: Roth Carina , Pantel Klaus , Müller Volkmar , Rack Brigitte , Kasimir-Bauer Sabine , Janni Wolfgang , Schwarzenbach Heidi 
Published: January 2011

Abstract

Background
As cell-free circulating DNA exists predominantly as mono- and oligonucleosomes, the focus of the current study was to examine the interplay of circulating nucleosomes, DNA, proteases and caspases in blood of patients with benign and malignant breast diseases.

Methods
The concentrations of cell-free DNA and nucleosomes as well as the protease and caspase activities were measured in serum of patients with benign breast disease (n = 20), primary breast cancer (M0, n = 31), metastatic breast cancer (M1, n = 32), and healthy individuals (n = 28) by PicoGreen, Cell Death Detection ELISA, Protease Fluorescent Detection Kit and Caspase-Glo®3/7 Assay, respectively.

Results
Patients with benign and malignant tumors had significantly higher levels of circulating nucleic acids in their blood than healthy individuals (p = 0.001, p = 0.0001), whereas these levels could not discriminate between benign and malignant lesions. Our analyses of all serum samples revealed significant correlations of circulating nucleosome with DNA concentrations (p = 0.001), nucleosome concentrations with caspase activities (p = 0.008), and caspase with protease activities (p = 0.0001). High serum levels of protease and caspase activities associated with advanced tumor stages (p = 0.009). Patients with lymph node-positive breast cancer had significantly higher nucleosome levels in their blood than node-negative patients (p = 0.004). The presence of distant metastases associated with a significant increase in serum nucleosome (p = 0.01) and DNA levels (p = 0.04), and protease activities (p = 0.008).

Conclusion
Our findings demonstrate that high circulating nucleic acid concentrations in blood are no indicators of a malignant breast tumor. However, the observed changes in apoptosis-related deregulation of proteolytic activities along with the elevated serum levels of nucleosomes and DNA in blood are linked to breast cancer progression.