bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validation of a home safety questionnaire used in a randomised controlled trial
Authors: Watson M , Kendrick D , Coupland C 
Published: June 2003

Objective:To measure the validity of self reported safety practices from a questionnaire, completed by families participating in a home safety randomised controlled trial.Methods:The postal questionnaire was used to measure secondary outcomes in a randomised controlled trial. The answers to 26 questions that could be assessed by observation were checked by a home visit. Families were invited to take part in a “home safety check”; they were not told that the visit was part of a validation study. At the time of the visit the researcher was blind to the self reports in the questionnaires.Results:Sixty four questionnaires were validated by visits to 64 households. Percentage agreement ranged from 58% to 100%. Sensitivity was high (68% or above) for most safety practices. The positive predictive value was also high for most safety practices (78% or above for 15 of the 16 practices).Conclusions:This study found a fairly high degree of consistency between self reported data and actual observations. The findings from this relatively small study need confirmation from larger studies.
Routine narrative analysis as a screening tool to improve data quality
Authors: Jones S J , Lyons R A 
Published: June 2003

Aim:To determine whether narrative information in emergency department surveillance systems can be systematically interrogated to improve our understanding of the causes of injury.Methods:Screening algorithms for location, intent, and activity were developed from structured analysis of narrative data from 98 999 records. The algorithms were then tested on a 50 000 record database containing entries in both of the two narrative fields. A proxy gold standard was defined as the total extract using both code and narrative. Sensitivity and specificity of the emergency department coding and narrative algorithms was calculated.Results:The proportion of records carrying an informative emergency department code was higher in records containing narrative—the percentage of causes coded “not know” dropped by 28.3%. The sensitivity of coded data varied from 42% to 98 % and from 33% to 99% for narrative data. Narrative analysis increased the percentage of home injuries identified by 19%, assaults by 26%, and rugby injuries by 137%.Conclusions:Using a small amount of narrative is a practical and effective means of developing more informative injury causation data in an emergency department based surveillance system. It allows for internal validation of the codes and for the identification of emerging hazards without adding more “tick boxes” or further burdening data entry clerks.
Violent attacks on Middle Easterners in the United States during the month following the September 11, 2001 terrorist attacks: Figure 1
Authors: Swahn M H , Mahendra R R , Paulozzi L J , Winston R L , Shelley G A , Taliano J , Frazier L , Saul J R 
Published: June 2003

Objectives:To document and describe hate related violent attacks on Middle Easterners or those perceived to be Middle Easterners during the month following the September 11, 2001 terrorist attacks in New York City and Washington, DC.Methods:The LexisNexis database of newspaper reports were used to identify incidents of hate related violent acts against Middle Easterners or those perceived to be Middle Easterners in the US between September 1 and October 11, 2001. A total of 100 incidents of hate related violence were identified in the 2659 news articles that were reviewed.Results:Of the 100 incidents of violent victimization that took place during the period September 1 to October 11, only one incident occurred before September 11. The 99 incidents that occurred after September 11 involved at least 128 victims and 171 perpetrators. Most violent victimizations occurred within 10 days of the attacks, involved male perpetrators and male victims, and occurred in convenience stores, on the streets, at gas stations, at schools/colleges, and at places of worship.Discussion:Most violent victimizations occurred in the 10 days immediately following the terrorist attacks indicating that interventions that promote tolerance and understanding of diversity need to be implemented quickly in order to be effective. In addition, patrolling by police and Neighborhood Watch programs around convenience stores and gas stations may also be effective strategies for reducing hate related violent crimes.
CLASSIFICATION OF RESPIRATORY SOUNDS BY USING AN ARTIFICIAL NEURAL NETWORK
Authors: DOKUR ZÜMRAY , ÖLMEZ TAMER 
Published: June 2003

In this paper, a classification method for respiratory sounds (RSs) in patients with asthma and in healthy subjects is presented. Wavelet transform is applied to a window containing 256 samples. Elements of the feature vectors are obtained from the wavelet coefficients. The best feature elements are selected by using dynamic programming. Grow and Learn (GAL) neural network, Kohonen network and multi-layer perceptron (MLP) are used for the classification. It is observed that RSs of patients (with asthma) and healthy subjects are successfully classified by the GAL network.
Oxidized Phospholipid-Induced Endothelial Cell/Monocyte Interaction Is Mediated by a cAMP-Dependent R-Ras/PI3-Kinase Pathway
Authors: Cole Amy L. , Subbanagounder Ganesamoorthy , Mukhopadhyay Srirupa , Berliner Judith A. , Vora Devendra K. 
Published: June 2003

Objective—Previous studies have demonstrated the importance of endothelial apical expression of connecting segment-1 (CS-1) fibronectin in mediating the entry of monocytes into atherosclerotic lesions and other sites of chronic inflammation. We previously demonstrated that oxidized PAPC (OxPAPC) increases monocyte-specific binding to arterial endothelium by causing deposition of CS-1 fibronectin on apical α5β1integrin. The present studies identify important signal transduction components regulating this pathway.Methods and Results—Using endothelial cells in culture, we demonstrate that activation of R-Ras is responsible for CS-1–mediated monocyte binding. Although few natural activators of R-Ras have been demonstrated, OxPAPC activated endothelial R-Ras by 2.5-fold but decreased levels of activated H-Ras. The importance of R-Ras/H-Ras balance in regulating monocyte binding was shown by overexpression studies. Constitutively active R-Ras enhanced monocyte adhesion, whereas coexpression with constitutively active H-Ras was inhibitory. Elevated cAMP, mediated by OxPAPC and specific components POVPC and PEIPC, was responsible for R-Ras activation, and dibutyryl cAMP and pertussis toxin were also effective activators of R-Ras. Using inhibitor and dominant-negative constructs, we demonstrated that phosphatidylinositol 3-kinase (PI3K) was a key downstream effector of R-Ras in this pathway.Conclusions—OxPAPC, POVPC, and PEIPC induce a cAMP/R-Ras/PI3K signaling pathway that contributes to monocyte/endothelial cell adhesion and potentially atherosclerosis.
Constitutively Active Glycogen Synthase Kinase-3β Gene Transfer Sustains Apoptosis, Inhibits Proliferation of Vascular Smooth Muscle Cells, and Reduces Neointima Formation After Balloon Injury in Rats
Authors: Park Kyung-Woo , Yang Han-Mo , Youn Seock-Won , Yang Hyun-Ju , Chae In-Ho , Oh Byung-Hee , Lee Myoung-Mook , Park Young-Bae , Choi Yun-Shik , Kim Hyo-Soo , Walsh Kenneth 
Published: June 2003

Objective—Glycogen synthase kinase (GSK)-3β is a crucial factor in many cellular signaling pathways and may play an important role in smooth muscle proliferation and apoptosis after angioplasty.Methods and Results—To investigate the effect of GSK-3β modulation on neointima formation, smooth muscle proliferation, and apoptosis after balloon injury in vivo, we delivered adenoviral vectors expressing the constitutively active form of GSK-3β (GSK-S9A: 9th serine switched to alanine) or a control gene into rat carotid arterial segments after balloon injury with a 2F Fogarty catheter. Viral infusion mixtures (5×108pfu) were incubated in the arterial lumen for 20 minutes, and the effects of gene delivery were evaluated 3 days and 2 weeks after gene delivery with morphometry and immunohistochemical staining for proliferating and apoptotic cells. There were no significant differences in intimal, medial, and lumen areas at 3 days after the procedure. However, 2 weeks after gene delivery, the active GSK-3β gene transfer resulted in a significantly lower intima to media ratio (0.29±0.06 versus 0.86±0.09,P<0.01) and a greater lumen area (0.41±0.02 versus 0.31±0.01 mm2,P<0.01) compared with the control gene transfected group. This was attributable to a significant reduction in intimal area (0.05±0.01 versus 0.15±0.02 mm2,P<0.01), whereas the medial area was similar (0.17±0.01 versus 0.18±0.01 mm2,P=0.21). Proliferation index was significantly reduced both at 3 days and 2 weeks in the active GSK-3β gene transferred group (2.97±0.29% versus 5.71±0.50%,P<0.01). In addition, apoptotic index, which was not significantly different between the 2 groups at 3 days, was significantly higher in the active GSK-3β gene transferred group at 2 weeks (3.14±0.68% versus 22.7±1.63%, n=10,P<0.01, for control versus active GSK-3β gene transfer).Conclusions—In vivo delivery of the active GSK-3β gene inhibits smooth muscle proliferation, sustains apoptosis, and reduces neointima formation after balloon injury in rats and may be a future therapeutic target to limit neointima hyperplasia after angioplasty.
Novel Proangiogenic Effect of Factor XIII Associated With Suppression of Thrombospondin 1 Expression
Authors: Dardik Rima , Solomon Arieh , Loscalzo Joseph , Eskaraev Regina , Bialik Ann , Goldberg Iris , Schiby Ginette , Inbal Aida 
Published: June 2003

Objective—Factor XIII (FXIII), a plasma transglutaminase that stabilizes fibrin clots at the final stages of blood coagulation by crosslinking fibrin monomers, is essential for embryo implantation and participates in tissue remodeling and wound healing, processes that involve angiogenesis. The aim of our study was to analyze the effect of FXIII on angiogenesis using in vitro and in vivo models and to examine the role of FXIII in the basic steps of angiogenesis, ie, migration, proliferation, and apoptosis/cell survival.Methods and Results—In the Matrigel tube formation model, only FXIIIa caused a dose-dependent enhancement of array formation. This proangiogenic effect was not associated with alterations in vascular endothelial growth factor (VEGF) protein levels nor VEGF or VEGFR2 mRNA levels. FXIIIa, but not nonactivated or transglutaminase-inactivated FXIII, significantly enhanced endothelial cell migration and proliferation and inhibited apoptosis. After treatment of HUVECs with FXIIIa, almost complete disappearance of mRNA of thrombospondin 1 (TSP-1) and a marked reduction in the secretion of TSP-1 protein were observed. A reduction in TSP-1 protein synthesis, although to a lesser extent, was observed on treatment of microvascular endothelial cells with FXIIIa. In a rabbit cornea model, injection of FXIIIa caused neovascularization associated with almost complete disappearance of TSP-1 in the cornea.Conclusions—These results show that FXIIIa exhibits a novel proangiogenic activity that is associated with downregulation of TSP-1 and also involves stimulation of endothelial cell proliferation and migration and inhibition of apoptosis. These findings might shed light on the mechanism by which FXIII mediates tissue repair and remodeling.
Interaction of Oxidative Stress and Inflammatory Response in Coronary Plaque Instability
Authors: Kobayashi Seiichi , Inoue Nobutaka , Ohashi Yoshitaka , Terashima Mitsuyoshi , Matsui Kiyoko , Mori Takao , Fujita Hideki , Awano Kojiro , Kobayashi Katsuya , Azumi Hiroshi , Ejiri Junya , Hirata Ken-ichi , Kawashima Seinosuke , Hayashi Yoshitake , Yokozaki Hiroshi , Itoh Hiroshi , Yokoyama Mitsuhiro 
Published: June 2003

Objective—C-reactive protein (CRP), a predictor of cardiovascular events, localizes in atherosclerotic arteries and exerts proinflammatory effects on vascular cells. Reactive oxygen species (ROS) have been implicated in atherogenesis and plaque instability.Methods and Results—Expressional pattern of CRP in directional coronary atherectomy specimens from 39 patients was examined. Characteristics of histological plaque instability and higher levels of serum CRP and fibrinogen were associated with the CRP immunoreactivity. In situ hybridization revealed the presence of CRP mRNA in coronary vasculature. Furthermore, the expression of CRP mRNA and protein was detected in cultured human coronary artery smooth muscle cells (CASMCs) by reverse transcriptase–polymerase chain reaction and Western blotting. In addition, CRP was frequently colocalized with p22phox, an essential component of NADH/NADPH oxidase, which is an important source of ROS in vasculature. Moreover, the incubation of cultured CASMCs with CRP resulted in the enhanced p22phoxprotein expression and in the generation of intracellular ROS.Conclusions—The expression of CRP in coronary arteries was associated with histological and clinical features of vulnerable plaque, and it had a prooxidative effect on cultured CASMCs, suggesting that it might play a crucial role in plaque instability and in the pathogenesis of acute coronary syndrome via its prooxidative effect.
Infection and the Risk of Spontaneous Cervical Artery Dissection
Authors: Guillon Benoît , Berthet Karine , Benslamia Lamia , Bertrand Marion , Bousser Marie-Germaine , Tzourio Christophe 
Published: June 2003

Background and Purpose—Several constitutional and environmental risk factors may be involved in the occurrence of spontaneous cervical artery dissection (SCAD). This work explored the association between recent infection and SCAD in an hospital-based case-control study.Methods—Forty-seven patients with SCAD and 52 with ischemic stroke from another cause were prospectively and consecutively recruited by 2 neurology departments. A specially designed questionnaire was used to assess the history of an acute infection that could have occurred within a month before the vascular event.Results—Acute infection was more frequent in patients with SCAD (31.9%) than in control subjects (13.5%) (crude odds ratio, 3.0; 95% confidence interval, 1.1 to 8.2;P=0.032). This association was stronger in patients with multiple (odds ratio, 6.4) than single artery (odds ratio, 2.1) dissection.Conclusions—Recent infection is a risk factor and could be a trigger for SCAD.
Endogenous CCL2 (monocyte chemotactic protein-1) modulates human immunodeficiency virus type-1 replication and affects cytoskeleton organization in human monocyte–derived macrophages
Authors: Fantuzzi Laura , Spadaro Francesca , Vallanti Giuliana , Canini Irene , Ramoni Carlo , Vicenzi Elisa , Belardelli Filippo , Poli Guido , Gessani Sandra 
Published: June 2003

AbstractCC chemokine ligand 2 (CCL2) is constitutively expressed at high levels in human peripheral blood monocytes, and its expression is further up-modulated during their differentiation into macrophages as well as in the course of HIV infection. To investigate the role of endogenous CCL2 on HIV replication and macrophage function, CCL2's activity was neutralized by specific antibodies. Infection of monocyte-derived macrophages with laboratory-adapted HIV-1 or primary viral isolates in the continuous presence of anti-CCL2 antibody resulted in significantly lower p24 Gag antigen release with respect to control cultures. Interestingly, CCL2 neutralization did not affect the early steps of the HIV life cycle but resulted in the intracellular accumulation of p24 Gag antigen. Simultaneously, remarkable changes in cell morphology and size occurred in cell cultures maintained in the presence of anti-CCL2 antibody. These results suggest that CCL2 may represent an autocrine factor important for enhancing virion production likely by affecting the macrophage cytoskeleton. (Blood. 2003;102:2334-2337)
A novel MyD-1 (SIRP-1α) signaling pathway that inhibits LPS-induced TNFα production by monocytes
Authors: Smith Rosemary E. , Patel Vanshree , Seatter Sandra D. , Deehan Maureen R. , Brown Marion H. , Brooke Gareth P. , Goodridge Helen S. , Howard Christopher J. , Rigley Kevin P. , Harnett William , Harnett Margaret M. 
Published: June 2003

AbstractMyD-1 (CD172) is a member of the family of signal regulatory phosphatase (SIRP) binding proteins, which is expressed on human CD14+ monocytes and dendritic cells. We now show a novel role for MyD-1 in the regulation of the innate immune system by pathogen products such as lipopolysaccharide (LPS), purified protein derivative (PPD), and Zymosan. Specifically, we demonstrate that ligation of MyD-1 on peripheral blood mononuclear cells (PBMCs) inhibits tumor necrosis factor alpha (TNFα) secretion but has no effect on other cytokines induced in response to each of these products. In an attempt to understand the molecular mechanisms underlying this surprisingly selective effect we investigated signal transduction pathways coupled to MyD-1. Ligation of the SIRP was found to recruit the tyrosine phosphatase SHP-2 and promote sequential activation of phosphatidylinositol (PI) 3-kinase, phospholipase D, and sphingosine kinase. Inhibition of LPS-induced TNFα secretion by MyD-1 appears to be mediated by this pathway, as the PI 3-kinase inhibitor wortmannin restores normal LPS-driven TNFα secretion. MyD-1-coupling to this PI 3-kinase-dependent signaling pathway may therefore present a novel target for the development of therapeutic strategies for combating TNFα production and consequent inflammatory disease. (Blood. 2003;102:2532-2540)
Green fluorescent protein selectively induces HSP70-mediated up-regulation of COX-2 expression in endothelial cells
Authors: Zhang Fan , Hackett Neil R. , Lam George , Cheng Joseph , Pergolizzi Robert , Luo Lan , Shmelkov Sergey V. , Edelberg Jay , Crystal Ronald G. , Rafii Shahin 
Published: June 2003

AbstractReporter genes, including green fluorescent protein (GFP), have been used to monitor the expression of transgenes introduced into vascular cells by gene transfer vectors. Here, we demonstrate that GFP by itself can selectively induce expression of certain genes in endothelial cells. Elevation of the cytoplasmic concentration of GFP in endothelial cells, specifically, resulted in a robust upregulation of heat shock protein 70 (HSP70). GFP induced both mRNA and protein expression of HSP70 in a dose-dependent manner. GFP-mediated up-regulation of HSP70 resulted in induction of cyclooxygenase-2 (COX-2) followed by prostaglandin E2 (PGE2) production. GFP-mediated up-regulation of HSP70 is independent of mitogen-activated protein kinase and phosphatidylinositol-3-kinase signaling cascades because inhibition of these pathways had no effect on HSP70 increases. Adenoviral delivery of GFP into murine vasculature significantly enhanced blood flow, suggesting that sufficient PGE2 is produced to induce vasodilation. Identification of the molecular partners that interact with GFP will increase our understanding of the vascular-specific factors that regulate stress angiogenesis and hemostasis.
Phenotype and hematopoietic potential of side population cells throughout embryonic development
Authors: Nadin Brian M. , Goodell Margaret A. , Hirschi Karen K. 
Published: June 2003

AbstractAdult murine bone marrow hematopoietic stem cells (HSCs) can be purified by sorting Hoechst 33342-extruding side population (SP) cells. Herein we investigated whether SP cells reside within embryonic tissues and exhibit hematopoietic progenitor activity. We isolated yolk sac (YS) and embryonic tissues 7.5 to 11.5 days after coitus (dpc), resolved an SP in each, and demonstrated that these SP cells exhibit distinct phenotypic and functional characteristics throughout development. YS and embryonic SP isolated 8.0 dpc expressed vascular endothelial-cadherin (VE-cadherin) and vascular endothelial receptor 2 (Flk-1), markers not expressed by bone marrow SP but expressed by endothelial cells and progenitors. SP at this stage did not express CD45 or produce hematopoietic colonies in vitro. In contrast, SP isolated 9.5 to 11.5 dpc contained a significantly higher proportion of cells expressing cKit and CD45, markers highly expressed by bone marrow SP. Furthermore, YS SP isolated 9.5 to 11.5 dpc demonstrated 40- to 90-fold enrichment for hematopoietic progenitor activity over unfractionated tissue. Our data indicate that YS and embryonic SP cells detected prior to the onset of circulation express the highest levels of endothelial markers and do not generate blood cells in vitro; however, as development progresses, they acquire hematopoietic potential and phenotypic characteristics similar to those of bone marrow SP. (Blood. 2003;102:2436-2443)
IL-15 induces antigen-independent expansion and differentiation of human naive CD8+ T cells in vitro
Authors: Alves Nuno L. , Hooibrink Berend , Arosa Fernando A. , van Lier René A. W. 
Published: June 2003

Abstract
Recent studies in mice have shown that although interleukin 15 (IL-15) plays an important role in regulating homeostasis of memory CD8+ T cells, it has no apparent function in controlling homeostatic proliferation of naive T cells. We here assessed the influence of IL-15 on antigen-independent expansion and differentiation of human CD8+ T cells. Both naive and primed human T cells divided in response to IL-15. In this process, naive CD8+ T cells successively down-regulated CD45RA and CD28 but maintained CD27 expression. Concomitant with these phenotypic changes, naive cells acquired the ability to produce interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α), expressed perforin and granzyme B, and acquired cytotoxic properties. Primed CD8+ T cells, from both noncytotoxic (CD45RA-CD27+) and cytotoxic (CD45RA+CD27-) subsets, responded to IL-15 and yielded ample numbers of cytokine-secreting and cytotoxic effector cells. In summary, all human CD8+ T-cell subsets had the ability to respond to IL-15, which suggests a generic influence of this cytokine on CD8+ T-cell homeostasis in man. (Blood. 2003;102:2541-2546)
Recombinant BβArg14His fibrinogen implies participation of N-terminus of Bβ chain in desA fibrin polymerization
Authors: Moen Jennifer L. , Gorkun Oleg V. , Weisel John W. , Lord Susan T. 
Published: June 2003

AbstractWe synthesized BβArg14His fibrinogen with histidine substituted for arginine at the Bβ thrombin-cleavage site. This substitution led to a 300-fold decrease in the rate of thrombin-catalyzed fibrinopeptide B (FpB, Bβ 1-14) release, whereas the rate of FpA release was normal with either thrombin or the FpA-specific enzyme, batroxobin. Both thrombin- and batroxobincatalyzed polymerization of BβArg14His fibrinogen were significantly impaired, with a longer lag time, slower rate of lateral aggregation, and decreased final turbidity. Moreover, desA monomer polymerization was similarly impaired, demonstrating that the histidine substitution itself, and not the lack of FpB cleavage, caused the abnormal polymerization of BβArg14His fibrin. Scanning electron microscopy showed BβArg14His fibrin fibers were thinner than normal (BβArg14His, approximately 70 nm; normal, approximately 100 nm; P &lt; .0001), as expected from the decreased final turbidity. We conclude that the N-terminus of the Bβ chain is involved in the lateral aggregation of normal desAprotofibrils and that the Arg→His substitution disrupts these interactions in BβArg14His fibrinogen. (Blood. 2003;102:2466-2471)