bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Madness of the Mob? Explaining the ‘Irrationality’ and Destructiveness of Crowd Violence
Authors: Waddington David 
Published: February 2008

AbstractThis article responds to a recent suggestion by Borch (2006) that sociologists might profitably reconsider the ‘group mind’ explanation, propagated by nineteenth‐century French academics like Tarde and Le Bon, which emphasises the inherent suggestibility, amorality, and destructiveness of crowds as mechanisms of accounting for collective violence. In alluding to the recent French riots of October–November 2005 as an illustrative example, the article rejects the group mind approach (along with a host of other lay explanations appearing in the wake of the disorders) in favour of a multivariate analysis, loosely based on the Flashpoints Model of Public Disorder. The purpose of this analysis is to demonstrate how even the most intensely destructive, spontaneous and emotional acts of collective violence are typically underpinned by a guiding and restraining rationality.
A systematic review of epidemiological studies investigating risk factors for work-related road traffic crashes and injuries: Table 1
Authors: Robb G , Sultana S , Ameratunga S , Jackson R 
Published: February 2008

Objective:To critically appraise the published evidence for risk factors for injuries and deaths relating to work-related road traffic crashes.Design:Systematic review.Data sources:Electronic databases searched included Medline, EMBASE, PsycINFO, Transport database, and the Australian Transport and Road Index (ATRI) database. Additional searches included websites of relevant organizations, reference lists of included studies, and issues of major injury journals published within the past 5 years.Inclusion criteria:Studies were included if they investigated work-related traffic crashes or related injuries or deaths as the outcome, measured any potential risk factor for work-related road traffic crash as an exposure, included a relevant comparison group, and were written in English.Methods:Included studies were critically appraised using the GATE-lite critical appraisal form (www.epiq.co.nz). Meta-analysis was not attempted because of the heterogeneity of the included studies.Findings:Of 25 studies identified, three of four robust (case–control and case-crossover) studies found an increased injury risk (i) among workers after extended shifts, (ii) for tractor-trailers with brake and steering defects, and (iii) for “double configuration” trucks. The fourth study showed that alcohol and drug use were not risk factors in an industry with a random testing policy. The best cross-sectional studies showed associations between injury and sleepiness, time spent driving, occupational stress, non-insulin-dependent uncomplicated diabetes, and use of narcotics and antihistamines.Conclusions:Modifiable behavioral and vehicle-related risk factors are likely to contribute to work-related traffic injury. Fatigue and sleepiness—the most commonly researched topics—were consistently associated with increased risk.
Factors associated with hip protector adherence among older people in residential care
Authors: Cryer C , Knox A , Stevenson E 
Published: February 2008

Background:There is evidence to suggest that hip protectors (HPs) prevent fractures among older people living in nursing homes. Studies have found HP wearing rates (adherence) to be low.Objectives:To investigate factors that are associated with adherence and whether those factors account for the variation in adherence between residential care homes (RCHs).Design:Six-month prospective study.Subjects and Setting:299 people aged 65 years and over (80% female, mean age 86 years) living in 17 RCHs. 128 of these wore HPs at least once.Methods:All residents in the homes were offered three pairs of SAFEHIP HPs, and adherence was measured using diaries completed daily. A mixed model regression analysis was used to investigate predictive factors for wearing HPs and the effects of these factors on the between-home variability in adherence.Results:Increased HP adherence was associated with hypertension, incontinence, a previous history of falls and fractures, and hip fracture history in the RCH. Decreased adherence was associated with arthritis of the lower limbs and dizziness on first rising. The large variation in adherence between RCHs was almost completely explained by these factors.Discussion:The evidence for the efficacy of HPs is weakening. Low adherence compromises the power of trials to detect a real effect. The literature is inconsistent regarding what factors are associated with adherence. Nevertheless, it suggests that some people who are at increased risk of fracture are more likely to wear HPs. Variations in staff or resident knowledge and attitude towards HPs may explain some variation between homes.
Novel empirical disability weights to assess the burden of non-fatal injury
Authors: Haagsma J A , van Beeck E F , Polinder S , Hoeymans N , Mulder S , Bonsel G J 
Published: February 2008

Background:Disability weights are necessary to estimate the disability component (years lived with disability, YLDs) of disability-adjusted life years. The original global burden of disease approach to deriving disability weights ignores temporary consequences of injury.Objectives:To develop and apply novel empirical disability weights to improve estimates of the non-fatal burden of injury.Methods:A set of 45 disability weights was derived for both permanent and temporary consequences of injury, using the annual profile approach. A population panel (n = 143) provided the values. The novel set of disability weights was then linked to epidemiological surveillance data on the incidence of injury in The Netherlands to calculate YLD resulting from permanent and temporary consequences of injury.Results:The empirical disability weights for injury consequences varied from minor (corneal abrasion, 0.004) to very severe (quadriplegia, 0.719) health loss. Increasing disability weights by level of severity were found, as illustrated by concussion (0.02), versus moderate brain injury (0.193), versus severe brain injury (0.540). Application of these new disability weights showed a 36% increase in YLD as the result of unintentional injury.Conclusions:YLD calculations based on global burden of disease disability weights underestimate the size of the injury problem by ignoring temporary health consequences. Application of novel empirical disability weights, derived using the annual profile approach, may improve calculations on the burden of non-fatal injury.
When the rules of the game are broken: what proportion of high school sports-related injuries are related to illegal activity?
Authors: Collins C L , Fields S K , Comstock R D 
Published: February 2008

Objectives:To compare sport and gender differences in injury rates and proportions of injuries related to illegal activity and to describe the epidemiology of injuries related to illegal activity.Design:Descriptive epidemiology study.Setting:100 US high schools.Subjects:Athletes participating in nine sports: boys’ football, soccer, basketball, wrestling, and baseball plus girls’ soccer, volleyball, basketball, and softball.Main outcome measures:Illegal activity-related injuries were analyzed using data from the 2005–06 and 2006–07 National High School Sports-Related Injury Surveillance Study.Results:Nationally, an estimated 98 066 injuries were directly related to an action that was ruled illegal activity by a referee/official or disciplinary committee, giving an injury rate of 0.24 injuries per 1000 athletic competition-exposures. Boys’ and girls’ soccer had the highest rates of injuries related to illegal activity, and girls’ volleyball, girls’ softball, and boys’ baseball had the lowest. Overall, 6.4% of all high school sports-related injuries were related to illegal activity, with the highest proportion in girls’ basketball (14.0%), girls’ soccer (11.9%), and boys’ soccer (11.4%). A greater proportion of injuries related to illegal activity were to the head/face (32.3%) and were concussions (25.4%) than injuries not related to illegal activity (13.8% (injury proportion ratio 2.35; 95% CI 1.82 to 3.04; p<0.001) and 10.9% (injury proportion ratio 2.35; 95% CI 1.71 to 3.22; p<0.001), respectively).Conclusions:Illegal activity is an overlooked risk factor for sports-related injury. Reducing illegal activity through enhanced enforcement of sports’ rules and targeted education about the dangers of illegal activity for players, coaches, and referees/officials may reduce sports-related injuries.
Accuracy of medical and ambulance record restraint and crash data information for child occupants
Authors: Bilston L E , Brown J 
Published: February 2008

Objective:To correlate the accuracy of information on children’s restraint usage and crash characteristics recorded with medical data using in-depth crash investigation. Restraint and crash information within the medical and ambulance records is often available, but information on the accuracy of this data is limited.Methods:Comparison of restraint and crash characteristic data from medical and ambulance records with that obtained from in-depth crash investigation studies, for a case series of child occupants aged 2–8 years involved in motor vehicle crashes.Results:When restraint type, seating position, impact severity, and impact direction data were recorded in either the medical record or ambulance records, it tended to be at least partially correct. However, incompleteness or absence of specifics of restraint use and crash information in the medical record (7–17%) was common. Ambulance records were often not available (39%), but this data was more often complete (78–100%) and accurate (52–89%), when available, possibly due to the use of a standardized pro-forma.Conclusions:Ambulance and hospital records data can provide information on restraint type and usage for child occupants in motor vehicle crashes, as well as crash information. The use of a standardized pro-forma may encourage more complete and accurate reporting of restraint and crash data.
Prostate Stem Cell Antigen Vaccination Induces a Long-term Protective Immune Response against Prostate Cancer in the Absence of Autoimmunity
Authors: de la Luz Garcia-Hernandez Maria , Gray Andrew , Hubby Bolyn , Klinger Otto J. , Kast W. Martin 
Published: February 2008

AbstractProstate stem cell antigen (PSCA) is an attractive antigen to target using therapeutic vaccines because of its overexpression in prostate cancer, especially in metastatic tissues, and its limited expression in other organs. Our studies offer the first evidence that a PSCA-based vaccine can induce long-term protection against prostate cancer development in prostate cancer–prone transgenic adenocarcinoma mouse prostate (TRAMP) mice. Eight-week-old TRAMP mice displaying prostate intraepithelial neoplasia were vaccinated with a heterologous prime/boost strategy consisting of gene gun–delivered PSCA-cDNA followed by Venezuelan equine encephalitis virus replicons encoding PSCA. Our results show the induction of an immune response against a newly defined PSCA epitope that is mediated primarily by CD8 T cells. The prostates of PSCA-vaccinated mice were infiltrated by CD4-positive, CD8-positive, CD11b-positive, and CD11c-positive cells. Vaccination induced MHC class I expression and cytokine production [IFN-γ, tumor necrosis factor-α, interleukin 2 (IL-2), IL-4, and IL-5] within prostate tumors. This tumor microenvironment correlated with low Gleason scores and weak PSCA staining on tumor cells present in hyperplastic zones and in areas that contained focal and well-differentiated adenocarcinomas. PSCA-vaccinated TRAMP mice had a 90% survival rate at 12 months of age. In contrast, all control mice had succumbed to prostate cancer or had heavy tumor loads. Crucially, this long-term protective immune response was not associated with any measurable induction of autoimmunity. The possibility of inducing long-term protection against prostate cancer by vaccination at the earliest signs of its development has the potential to cause a dramatic paradigm shift in the treatment of this disease. [Cancer Res 2008;68(3):861–9]
CD43, but not P-Selectin Glycoprotein Ligand-1, Functions as an E-Selectin Counter-Receptor in Human Pre-B–Cell Leukemia NALL-1
Authors: Nonomura Chizu , Kikuchi Jiro , Kiyokawa Nobutaka , Ozaki Hidenori , Mitsunaga Kanae , Ando Hidenobu , Kanamori Akiko , Kannagi Reiji , Fujimoto Junichiro , Muroi Kazuo , Furukawa Yusuke , Nakamura Mitsuru 
Published: February 2008

AbstractB-cell precursor acute lymphoblastic leukemia (BCP-ALL/B-precursor ALL) is characterized by a high rate of tissue infiltration. The mechanism of BCP-ALL cell extravasation is not fully understood. In the present study, we have investigated the major carrier of carbohydrate selectin ligands in the BCP-ALL cell line NALL-1 and its possible role in the extravascular infiltration of the leukemic cells. B-precursor ALL cell lines and clinical samples from patients with BCP-ALL essentially exhibited positive flow cytometric reactivity with E-selectin, and the reactivity was significantly diminished by O-sialoglycoprotein endopeptidase treatment in NALL-1 cells. B-precursor ALL cell lines adhered well to E-selectin but only very weakly to P-selectin with low-shear-force cell adhesion assay. Although BCP-ALL cell lines did not express the well-known core protein P-selectin glycoprotein ligand-1 (PSGL-1), a major proportion of the carbohydrate selectin ligand was carried by a sialomucin, CD43, in NALL-1 cells. Most clinical samples from patients with BCP-ALL exhibited a PSGL-1neg/low/CD43high phenotype. NALL-1 cells rolled well on E-selectin, but knockdown of CD43 on NALL-1 cells resulted in reduced rolling activity on E-selectin. In addition, the CD43 knockdown NALL-1 cells showed decreased tissue engraftment compared with the control cells when introduced into γ-irradiated immunodeficient mice. These results strongly suggest that CD43 but not PSGL-1 plays an important role in the extravascular infiltration of NALL-1 cells and that the degree of tissue engraftment of B-precursor ALL cells may be controlled by manipulating CD43 expression. [Cancer Res 2008;68(3):790–9]
Enhanced Activation of Epidermal Growth Factor Receptor Caused by Tumor-Derived E-Cadherin Mutations
Authors: Bremm Anja , Walch Axel , Fuchs Margit , Mages Jörg , Duyster Justus , Keller Gisela , Hermannstädter Christine , Becker Karl-Friedrich , Rauser Sandra , Langer Rupert , von Weyhern Claus Hann , Höfler Heinz , Luber Birgit 
Published: February 2008

Abstract
Mutations of the tumor suppressor E-cadherin and overexpression of the receptor tyrosine kinase epidermal growth factor receptor (EGFR) are among the most frequent genetic alterations associated with diffuse-type gastric carcinoma. Accumulating evidence suggests a functional relationship between E-cadherin and EGFR that regulates both proteins. We report that somatic mutation of E-cadherin is associated with increased activation of EGFR followed by enhanced recruitment of the downstream acting signaling components growth factor receptor binding protein 2 and Shc, and activation of Ras. Reduced complex formation of mutant E-cadherin — with an in frame deletion of exon 8 in the extracellular domain resulting in reduced adhesion and increased motility — with EGFR was observed compared with wild-type E-cadherin. We conclude that reduced binding of mutant E-cadherin to EGFR in a multicomponent complex or reduced stability of the complex may enhance EGFR surface motility, thereby facilitating EGFR dimerization and activation. Furthermore, reduced surface localization due to enhanced internalization of mutant E-cadherin compared with the wild-type protein was observed. The internalization of EGFR was decreased in response to epidermal growth factor stimulation in cells expressing mutant E-cadherin, suggesting that mutation of E-cadherin also influences the endocytosis of EGFR. Moreover, we show increased activation of EGFR in gastric carcinoma samples with mutant E-cadherin lacking exons 8 or 9. In summary, we describe activation of EGFR by mutant E-cadherin as a novel mechanism in tumor cells that explains the enhanced motility of tumor cells in the presence of an extracellular mutation of E-cadherin. [Cancer Res 2008;68(3):707–14]
Direct Evidence for Epithelial-Mesenchymal Transitions in Breast Cancer
Authors: Trimboli Anthony J. , Fukino Koichi , de Bruin Alain , Wei Guo , Shen Lei , Tanner Stephan M. , Creasap Nicholas , Rosol Thomas J. , Robinson Michael L. , Eng Charis , Ostrowski Michael C. , Leone Gustavo 
Published: February 2008

Abstract
We developed stromal- and epithelial-specific cre-transgenic mice to directly visualize epithelial-mesenchymal transition (EMT) during cancer progression in vivo. Using three different oncogene-driven mouse mammary tumor models and cell-fate mapping strategies, we show in vivo evidence for the existence of EMT in breast cancer and show that myc can specifically elicit this process. Hierarchical cluster analysis of genome-wide loss of heterozygosity reveals that the incidence of EMT in invasive human breast carcinomas is rare, but when it occurs it is associated with the amplification of MYC. These data provide the first direct evidence for EMT in breast cancer and suggest that its development is favored by myc-initiated events. [Cancer Res 2008;68(3):937–45]
Tumor-Induced Senescent T Cells with Suppressor Function: A Potential Form of Tumor Immune Evasion
Authors: Montes Carolina L. , Chapoval Andrei I. , Nelson Jonas , Orhue Vbenosa , Zhang Xiaoyu , Schulze Dan H. , Strome Scott E. , Gastman Brian R. 
Published: February 2008

AbstractSenescent and suppressor T cells are reported to be increased in select patients with cancer and are poor prognostic indicators. Based on the association of these T cells and poor outcomes, we hypothesized that tumors induce senescence in T cells, which negatively effects antitumor immunity. In this report, we show that human T cells from healthy donors incubated with tumor for only 6 h at a low tumor to T-cell ratio undergo a senescence-like phenotype, characterized by the loss of CD27 and CD28 expression and telomere shortening. Tumor-induced senescence of T cells is induced by soluble factors and triggers increases in expression of senescence-associated molecules such as p53, p21, and p16. Importantly, these T cells are not only phenotypically altered, but also functionally altered as they can suppress the proliferation of responder T cells. This suppression requires cell-to-cell contact and is mediated by senescent CD4+ and CD8+ subpopulations, which are distinct from classically described natural T regulatory cells. Our observations support the novel concept that tumor can induce senescent T cells with suppressor function and may effect both the diagnosis and treatment of cancer. [Cancer Res 2008;68(3):870–9]
Multiple Alternative Splicing Markers for Ovarian Cancer
Authors: Klinck Roscoe , Bramard Anne , Inkel Lyna , Dufresne-Martin Geneviève , Gervais-Bird Julien , Madden Richard , Paquet Éric R. , Koh ChuShin , Venables Julian P. , Prinos Panagiotis , Jilaveanu-Pelmus Manuela , Wellinger Raymund , Rancourt Claudine , Chabot Benoit , Abou Elela Sherif 
Published: February 2008

Abstract
Intense efforts are currently being directed toward profiling gene expression in the hope of developing better cancer markers and identifying potential drug targets. Here, we present a sensitive new approach for the identification of cancer signatures based on direct high-throughput reverse transcription-PCR validation of alternative splicing events. This layered and integrated system for splicing annotation (LISA) fills a gap between high-throughput microarray studies and high-sensitivity individual gene investigations, and was created to monitor the splicing of 600 cancer-associated genes in 25 normal and 21 serous ovarian cancer tissues. Out of &gt;4,700 alternative splicing events screened, the LISA identified 48 events that were significantly associated with serous ovarian tumor tissues. In a further screen directed at 39 ovarian tissues containing cancer pathologies of various origins, our ovarian cancer splicing signature successfully distinguished all normal tissues from cancer. High-volume identification of cancer-associated splice forms by the LISA paves the way for the use of alternative splicing profiling to diagnose subtypes of cancer. [Cancer Res 2008;68(3):657–63]
Tumor Immunobiological Differences in Prostate Cancer between African-American and European-American Men
Authors: Wallace Tiffany A. , Prueitt Robyn L. , Yi Ming , Howe Tiffany M. , Gillespie John W. , Yfantis Harris G. , Stephens Robert M. , Caporaso Neil E. , Loffredo Christopher A. , Ambs Stefan 
Published: February 2008

AbstractThe incidence and mortality rates of prostate cancer are significantly higher in African-American men when compared with European-American men. We tested the hypothesis that differences in tumor biology contribute to this survival health disparity. Using microarray technology, we obtained gene expression profiles of primary prostate tumors resected from 33 African-American and 36 European-American patients. These tumors were matched on clinical variables. We also evaluated 18 nontumor prostate tissues from seven African-American and 11 European-American patients. The resulting datasets were analyzed for expression differences on the gene and pathway level comparing African-American with European-American patients. Our analysis revealed a significant number of genes, e.g., 162 transcripts at a false-discovery rate of ≤5% to be differently expressed between African-American and European-American patients. Using a disease association analysis, we identified a common relationship of these transcripts with autoimmunity and inflammation. These findings were corroborated on the pathway level with numerous differently expressed genes clustering in immune response, stress response, cytokine signaling, and chemotaxis pathways. Several known metastasis-promoting genes, including autocrine mobility factor receptor, chemokine (C-X-C motif) receptor 4, and matrix metalloproteinase 9, were more highly expressed in tumors from African-Americans than European-Americans. Furthermore, a two-gene tumor signature that accurately differentiated between African-American and European-American patients was identified. This finding was confirmed in a blinded analysis of a second sample set. In conclusion, the gene expression profiles of prostate tumors indicate prominent differences in tumor immunobiology between African-American and European-American men. The profiles portray the existence of a distinct tumor microenvironment in these two patient groups. [Cancer Res 2008;68(3):927–36]